neurology and neuroscience

Question 1

what are the 4 main characteristics of the cerebral cortex?

Answer 1

covers entire surface (very thin)

together with deep nuclei (such as in the thalamus) contains grey matter

highly folded with gyri and solci

organised into lobes

Question 2

what is the microscopic organisation of the cerebral cortex?

Answer 2

6 layers

(I closest to surface, VI deepest)

also columns

Question 3

how are regions of the cortex classified?

Answer 3

based on cytoarchitecture - cell size, space/packing density, layers

often correlates with function

Question 4

what are the functions of the frontal lobe?

Answer 4

regulate and initiate motor function

language

cognitive function - e.g planning

attention

memory

Question 5

what are the functions of the parietal lobe?

Answer 5

sensation - touch, pain

sensory language aspects

spatial orientation and self perception

Question 6

what are the functions of the occipital lobe?

Answer 6

visual input

Question 7

what are the functions of the temporal lobe?

Answer 7

processing auditory information

emotions

forming memories

Question 8

what are the functions of the limbic lobe?

Answer 8

learning

memory

emotion

motivation and reward

Question 9

what are the functions of the insular cortex (under lateral fissure between temporal and frontal lobe)?

Answer 9

concerned with visceral sensations

autonomic control, and interoception, auditory processing, visual-vestibular integration
(inputs coming in from visual pathway and balance organs)

Question 10

what is grey matter (outside)?

Answer 10

neuronal cell bodies and glial cells

Question 11

what is white matter(inside)?

Answer 11

Myelinated neuronal axons arranged in tracts

neuronal cell bodies make their way out of brain to spinal cord/ peripheral nerves

Question 12

what are the 3 main types of white matter tract?

Answer 12

association, commissural and projection fibres

Question 13

which cortical areas do association fibres connect?

Answer 13

connect areas within the same hemisphere

Question 14

which cortical areas do commissural fibres connect?

Answer 14

connect homologous structure in left and right hemispheres (cross the midline)

Question 15

which cortical areas do projection fibres connect?

Answer 15

connect cortex with lower brain structures (e.g. thalamus, brain stem and spinal cord)

Question 16

what do short association fibres/U fibres connect?

Answer 16

adjacent cortical regions (usually same lobe)

Question 17

what are the 4 types of long association fibres?

Answer 17

superior longitudinal fasciculus

arcuate fasciculus

inferior longitudinal fasciculus

uncinate fasciculus

Question 18

what two lobes does the superior longitudinal fasciculus connect?

Answer 18

frontal and occipital

Question 19

what two lobes does the arcuate fasciculus connect?

Answer 19

frontal and temporal

Question 20

what two lobes does the inferior longitudinal fasciculus connect?

Answer 20

temporal and occipital

Question 21

what two lobes does the uncinate fasciculus connect?

Answer 21

anterior frontal and temporal

Question 22

what is the corpus callosum an example of?

Answer 22

commissural fibres (connects left and right hemispheres)

Question 23

what is the structure inferior to the corpus callosum that connects the left and right hemispheres?

Answer 23

anterior commissure

Question 24

how are projection fibres arranged?

Answer 24

make way down from cortical layers down towards deeper structures

converge through internal capsule between thalamus and basal ganglia

go down into spina cord to go out to structures such as limbs

Question 25

what is the function of afferent projection fibres?

Answer 25

bring information to brain from outside world via spinal cord and cortex

sensory impulses

Question 26

what is the function of efferent projection fibres?

Answer 26

take information out from the cortex down to brain stem, spinal cord and out

motor impulses

Question 27

what are the afferent and efferent projection fibres collectively known as?

Answer 27

corona radiata

Question 28

what are the 3 differences between primary and secondary/association cortices?

Answer 28

primary: predictable function
secondary: function less predictable

primary: organised topographically
secondary: not organised topographically

primary: symmetry between left and right
secondary: left-right symmetry weak or absent

Question 29

what is the function of the primary motor cortex in the frontal lobe?

Answer 29

controls fine, discrete, precise voluntary movements

provides descending signals to execute movements

Question 30

what is the function of the supplementary cortex of the frontal lobe?

Answer 30

involved in planning movements (e.g. externally cued - the plan to move an arm to pick up an object, for example)

Question 31

what is the function of the premotor cortex of the frontal lobe?

Answer 31

involved in planning complex movements (e.g. internally cued - the plan to co ordinate fibres to generate speech by making muscles contract, for example)

Question 32

what is the function of the primary somatosensory cortex in the parietal lobe?

Answer 32

processes somatic sensations arising from receptors in the body

(e.g. fine touch, vibration, two-point discrimination, proprioception, pain and temperature)

Question 33

what is the function of the somatosensory association cortex in the parietal lobe?

Answer 33

interpret significance of sensory information, e.g. recognizing an object placed in the hand.
Awareness of self and awareness of personal space

Question 34

what is the function of the primary visual cortex in the parietal lobe?

Answer 34

processes visual stimuli - input from retina reaches here

Question 35

what is the function of the visual association cortex in the parietal lobe?

Answer 35

gives meaning and interpretation of visual input

Question 36

what is the function of the primary auditory cortex in the temporal lobe?

Answer 36

processes auditory stimuli

Question 37

what is the function of the auditory association cortex in the temporal lobe?

Answer 37

gives meaning and interpretation of auditory input

Question 38

what are the functions of the prefrontal cortex?

Answer 38

attention

adjusting social behaviour

planning

personality expression

decision making

Question 39

where are Broca’s and Wernicke’s areas found?

Answer 39

left hemisphere only (association/secondary cortex)

Question 40

what is the function of Broca’s area?

Answer 40

production of language (motor region - i.e motor commands and movement to generate speech)

Question 41

what is the function of Wernicke’s area?

Answer 41

understanding of language (sensory region - i.e information about language is understood)

Question 42

what may a frontal lobe lesion cause?

Answer 42

personality changes

socially inappropriate behaviour

Question 43

what may a parietal lobe lesion cause?

Answer 43

contralateral neglect

lesion in right hemisphere causes lack of awareness of self and extrapersonal space on the left side

Question 44

what are the 2 types of temporal lobe lesion?

Answer 44

lateral and medial

Question 45

what may a temporal lobe lesion cause?

Answer 45

agnosia - inability to recognise things

Question 46

what is the effect of a lesion to Broca’s area?

Answer 46

expressive aphasia - poor production of speech, comprehension intact

Question 47

what is the effect of a lesion to Wernicke’s area?

Answer 47

receptive aphasia - poor comprehension of speech, production intact

Question 48

what structure connects Broca’s and Wernicke’s areas?

Answer 48

arcuate fasciculus

Question 49

what is the effect of a lesion on the primary visual cortex?

Answer 49

blindness in the corresponding part of the visual field

Question 50

what is the effect of a lesion on the visual association cortex?

Answer 50

deficits in interpretation of visual information e.g. prosopagnosia: inability to recognise familiar faces or learn new faces (face blindness)

Question 51

how can cortical function be assessed?

Answer 51

positron emission tomography (PET)

functional magnetic resonance imaging (fMRI)

electroencephalography/magnetoencephalography (EEG/MEG)

Question 52

how does a positron emission tomography (PET) work?

Answer 52

track blood flow directly to a brain region using radioactive label (e.g radioactive glucose) and then asking the person to undertake a task

obvious risk of using radioactive substance

Question 53

how does functional magnetic resonance imaging (fMRI) work?

Answer 53

amount of blood oxygen in a brain region

relative use of oxygen and determines that increase of oxygen use implies increased activity in that area

Question 54

what is temporal resolution?

Answer 54

how quickly can it be ascertained that things are changing

Question 55

what is spatial resolution?

Answer 55

how detailed a picture can be obtained at the level of individual cells vs groups of cells etc.

Question 56

how does an EEG work?

Answer 56

measures electrical signals produced by brain using electrodes in a standard arrangement (no need to use all electrodes, can only put electrodes on areas that are relevant to the function being tested)

Question 57

how does an MEG work?

Answer 57

measures magnetic signals produced by brain

Question 58

where is an EEG often used and why?

Answer 58

epilepsy, sleep disorders

can look at rhythms being produced during sleep/wakefulness

can look at onset of events that correlate with clinical symptoms (e.g seizure)

Question 59

how are somatosensory evoked potentials used to assess cortical function?

Answer 59

stimulus to peripheral nerve

series of waves that reflect sequential activation of neural structures along somatosensory pathways

Question 60

when are somatosensory evoked potentials used to assess cortical function?

Answer 60

e.g spinal cord injury

when checking where along the pathway the injury occurred - if fully intact, signal will travel up to CNS, then thalamus and sensory cortex

Question 61

when are transcranial magnetic stimulations (TMS) used?

Answer 61

assess the functional integrity of neural circuits

uses electromagnetic induction to stimulate neurons

Question 62

how does a transcranial magnetic stimulation (TMS) work?

Answer 62

stimulates brain and assesses signal as it arrives at the effector (almost the opposite of somatosensory evoked potentials)

relies on production of changing magnetic fields/changing electric fields giving rise to magnetic fields by using a magnetic coil to stimulate areas of the brain

Question 63

what conditions may transcranial magnetic stimulation (TMS) also be used to treat and why?

Answer 63

epilepsy

tinnitus

migraine

depression

all are associated with firing of cortical neurones - magnetic pulses can also modulate overactive brain regions by interfering with transmission

Question 64

what is transcranial direct current stimulation (tDCS) and how does it work?

Answer 64

brain stimulation, affects cortical function

uses low direct current over scalp to increase or decrease neuronal firing rates

used in chronic pain and epilepsy treatment

Question 65

how can the structure of the brain be assessed?

Answer 65

diffusion tensor imaging (DTI)

DTI with tractography

Question 66

why is assessing brain structure important?

Answer 66

understanding connection between brain regions

e.g if two linked regions are functioning individually but the pathway between them is damaged

Question 67

how does diffusion tensor imaging (DTI) work?

Answer 67

based on diffusion of water molecules

Question 68

what is diffusion tensor imaging (DTI) with tractography?

Answer 68

3D reconstruction to assess neural tracts

Question 69

why is the brain vulnerable if blood supply is impaired?

Answer 69

high metabolic demands therefore extensive vascular supply needed for function

(uses around 20% of all cardiac output, oxygen consumption, 2/3 of liver glucose)

Question 70

what arteries supply the brain?

Answer 70

vertebral

internal carotid

Question 71

what is the path of the common carotid artery?

Answer 71

branches from brachiocephalic artery, runs up side of the neck

at about the level of laryngeal prominence (Adam’s apple), common carotid divides into internal carotid and external carotid (supplies structures of the face)

Question 72

what is the path of the internal carotid artery?

Answer 72

branches off from common carotid

carries on with no branches, passes through base of skull (so-called carotid canal) and into cranial cavity

Question 73

what is the path of the vertebral artery?

Answer 73

first branch off subclavian artery

goes upwards posteriorly through transverse foramen of survival vertebrae ( protected by bone architecture)

passes through foramen magnum at base of skull to reach cranial cavity

Question 74

what is the arrangement of vessels at the base of the brain called?

Answer 74

circle of Willis, vessels are adjoined

Question 75

what is the structure of the circle of Willis?

Answer 75

posterior - 2 vertebral arteries that come up through foramen magnum and fuse to form basilar artery (base of pons)

basilar artery divides into 2 posterior cerebral arteries

internal carotid branches into:

• middle cerebral artery (main)
• anterior cerebral artery

anterior communicating artery between anterior cerebral arteries in the long latitudinal fissure anteriorly

posterior communicating artery between posterior cerebral artery and middle cerebral artery

Question 76

what is the advantage of the arrangement of the circle of Willis?

Answer 76

blockage in anterior carotid can cause atherosclerotic build up in the common carotid, especially where it divides

theoretically there is a chance of compensatory flow from the other side - can flow through communicating arteries and supply both sides of the brain

Question 77

why is the advantage of the arrangement of the circle of Willis not always effective?

Answer 77

not universal

compensation between posterior circulation and anterior circulation is often weak because posterior communicating arteries are very thin

Question 78

how does blood exit the brain?

Answer 78

cerebral veins in brain itself

venous blood drains in the cranial cavity via dural sinuses in the dura mater (outer meningeal layer)

internal jugular vein

Question 79

what is the structure of the dural sinuses?

Answer 79

dura mater is made up of two layers that are usually closely pressed together

when these layers separate they form the venous sinuses

Question 80

how does venous blood drain through the sinuses?

Answer 80

venous blood drains in the cranial cavity via dural sinuses in the dura mater (outer meningeal layer)

drains through superior sagittal sinus, blood drains down the back of the head

large cerebral vein (vein of Gaylan) drains down “straight” sinus to confluence formed by superior sagittal sinus and inferior sagittal sinus on lower edge of falx cerebri

reaches occipital area (occipital conflicts of the sinuses)

drains transversely then down through sigmoid sinus going down through jugular frame (foramen in base of skull)

sigmoid sinus into internal jugular vein going back to the heart

Question 81

what are the 4 types of intercranial haemorrhage?

Answer 81

extradural

subdural

subarachnoid

intracerebral

Question 82

what causes extradural haemorrhage?

Answer 82

nearly always trauma

main artery supplying dura is right behind pterion so trauma is likely to rupture this artery

Question 83

what is the effect of an extradural haemorrhage?

Answer 83

acute onset arterial bleed - high pressure

strips dura away from inside of skull and builds pressure within intracranial cavity

puts pressure on brain stem and eventually closes down cardiorespiratory centres

Question 84

why are subdural bleeds dangerous and how can the potential effects be prevented?

Answer 84

effects are slightly delayed (as low pressure venous blood)

for head injuries with loss of consciousness patients are kept for observation overnight in case symptoms start to show

Question 85

what causes subarachnoid haemorrhage?

Answer 85

circle of Willis has weaknesses in blood vessels called aneurysms (generally congenital)

these may burst (especially if hypertensive) and produces subarachnoid bleed

Question 86

people with which pre-existing condition are more at risk of intracerebral haemorrhage?

Answer 86

hypertension

Question 87

what is an intracerebral haemorrhage?

Answer 87

bleed in substance of brain itself

Question 88

what is the definition of a stroke/cerebrovascular accident?

Answer 88

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

Question 89

what are the two main types of stroke and how common are they?

Answer 89

thrombo-embolic (85%)

haemorrhagic (15%)

Question 90

what is the definition of a transient ischaemic attack (TIA)?

Answer 90

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

Question 91

what is the definition of an infarction?

Answer 91

degenerative changes which occur in tissue following occlusion of an artery

Question 92

what is the definition of cerebral ischaemia?

Answer 92

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

Question 93

what could a transient ischaemic attack indicate?

Answer 93

risk of stroke further on

Question 94

what is the difference between ischaemia and anoxia/hypoxia?

Answer 94

anoxia/hypoxia only refers to oxygen deficit in blood

ischaemia refers to loss of all required metabolites in blood (e.g. glucose etc.)

Question 95

what is thrombosis?

Answer 95

formation of a blood clot (thrombus)

Question 96

what is an embolism?

Answer 96

plugging of small vessel by material carried from larger vessel

e.g. thrombi from the heart or atherosclerotic debris from the internal carotid

Question 97

what are the risk factors for stroke?

Answer 97

age (inefficiency of vascular system and brain itself)

hypertension (risk of haemorrhage)

cardiac disease (formation of clots due to inefficient vascular or cardiac function)

smoking (effect on vasculature)

diabetes mellitus (effect on vasculature)

Question 98

what is the perfusion field of the middle cerebral artery?

Answer 98

much of the brain’s lateral surface

subcortical deep structures of the brain

Question 99

what is the perfusion field of the anterior cerebral artery?

Answer 99

midline structures all the way back

perfuses all the way back to parietal-occipital fissure

Question 100

what is the perfusion field of the posterior cerebral artery?

Answer 100

occipital lobe

inferior part of temporal lobe

Question 101

why are perfusion fields important?

Answer 101

can judge where in the brain a stroke might have occurred

Question 102

what symptoms indicate an anterior cerebral artery issue?

Answer 102

paralysis of contralateral structures - leg > arm, face (since arm and face are mostly supplied by middle cerebral artery)

disturbance of intellect, executive function and judgement (abulia - breakdown in frontal lobe function)

loss of appropriate social behaviour (damaged frontal lobe)

Question 103

what symptoms indicate a middle cerebral artery issue?

Answer 103

“classic stroke”

middle cerebral artery supplies deep motor structures therefore contralateral hemiplegia: arm > leg

sensory cortex also affected

• contralateral hemisensory deficits
• hemianopia
• aphasia (L sided lesion)
• if on the left side - may affect speech (Broca’s and Wernicke’s)

Question 104

what symptoms indicate a posterior cerebral artery issue?

Answer 104

supply to occipital lobe is cut off so-

homonymous hemianopia

visual agnosia

Question 105

what are the broad principles of motor control?

Answer 105

hierarchical organisation

higher order areas of hierarchy are involved in more complex tasks
(e.g. programme and decide on movements, coordinate muscle activity)

lower level areas of hierarchy perform lower level tasks (e.g. execution of movement)

Question 106

what is functional segregation?

Answer 106

motor system organised in a number of different areas that interact to control different aspects of movement (voluntary and automatic)

motor cortex receives information from other cortical areas and sends commands to thalamus and brainstem

cerebellum and basal ganglia adjust commands received from other parts of the motor system

brainstem passes commands from cortex to spinal cord

Question 107

what are the 2 major descending tracts?

Answer 107

pyramidal

extrapyramidal

Question 108

what are the pathways of the pyramidal tracts?

Answer 108

pass through pyramids of medulla

output neurones in motor cortex, project down to spinal cord or cranial nerve nuclei in brainstem

Question 109

what are the 2 pyramidal tracts?

Answer 109

corticospinal

corticobulbar`

Question 110

what do the pyramidal tracts control?

Answer 110

voluntary movements of body and face

Question 111

what are the pathways of the extrapyramidal tract?

Answer 111

do not pass through pyramids of medulla

upper motor neurones in cortex, lower motor neurones in brainstem nuclei - project down to muscles

Question 112

what do the extrapyramidal tracts control?

Answer 112

involuntary (automatic) movements for balance, posture and locomotion

Question 113

what are the 4 extrapyramidal tracts?

Answer 113

vestibulospinal

tectospinal

reticulospinal
`
rubrospinal

Question 114

where is the primary motor cortex situated?

Answer 114

precentral gyrus, anterior to central sulcus

Question 115

what does the primary motor cortex control?

Answer 115

controls fine, discrete, precise voluntary movements

provides descending signals to execute movements - final common pathway from brain to lower motor neurones in brainstem/spinal cord

Question 116

where is the premotor area located?

Answer 116

anterior to primary motor cortex

Question 117

what does the premotor area control?

Answer 117

involved in planning movements

regulates externally cued movements
e.g. seeing an apple and reaching for it

Question 118

where is the supplementary motor area located?

Answer 118

anterior and medial to primary motor cortex

Question 119

what does the supplementary motor area control?

Answer 119

involved in planning complex movements (e.g. internally cued, speech)

becomes active prior to voluntary movement

Question 120

what is the pathway of the corticospinal tract?

Answer 120

upper motor neurones in primary motor cortex

midbrain contains cerebral peduncle

most fibres decussate, about 10% do not

Question 121

what is the function of decussated fibres in the corticospinal tract?

Answer 121

make up lateral corticospinal tract

responsible for limb muscle control

Question 122

what is the function of non-decussated fibres in the corticospinal tract?

Answer 122

make up anterior corticospinal tract

responsible for trunk muscle control

Question 123

what is the main function of the corticobulbar tract?

Answer 123

principal motor pathway for voluntary movements of the face (and neck)

Question 124

which nuclei control the function of extraocular muscles (corticobulbar tract)?

Answer 124

oculomotor

trochlear

abducens

Question 125

which nuclei control the function of jaw muscles (muscles of mastication) (corticobulbar tract)?

Answer 125

trigeminal motor nucleus

Question 126

which nuclei control the facial muscles (corticobulbar tract)?

Answer 126

facial

Question 127

which nuclei control the tongue (corticobulbar tract)?

Answer 127

hypoglossal

Question 128

what is the function of the vestibulospinal (extrapyramidal) tract?

Answer 128

stabilise head during body movements, or as head moves

coordinate head movements with eye movements

mediate postural adjustments

Question 129

what is the function of the reticulospinal (extrapyramidal) tract?

Answer 129

(most primitive descending tract - from medulla and pons)

changes in muscles tone associated with voluntary movement

postural stability

Question 130

what is the function of the tectospinal (extrapyramidal) tract?

Answer 130

(from superior colliculus of midbrain)

orientation of the head and neck during eye movements

Question 131

what is the function of the rubrospinal (extrapyramidal) tract?

Answer 131

(From red nucleus of midbrain - in humans mainly taken over by corticospinal tract)

innervate lower motor neurons of flexors of the upper limb

Question 132

what are the negative signs of an upper motor neurone lesion?

Answer 132

loss of voluntary motor function

paresis: graded weakness of movements

paralysis (plegia): complete loss of voluntary muscle activity

Question 133

what are the positive signs of an upper motor neurone lesion?

Answer 133

increased abnormal motor function due to loss of inhibitory descending inputs

spasticity: increased muscle tone

hyper-reflexia: exaggerated reflexes

clonus: abnormal oscillatory muscle contraction

Babinski’s sign

Question 134

what is apraxia?

Answer 134

disorder of skilled movement

patients are not paretic but have lost information about how to perform skilled movements

Question 135

disease of which areas (including stroke and dementia) can cause apraxia?

Answer 135

inferior parietal lobe

frontal lobe (premotor cortex, supplementary motor area - SMA)

Question 136

what are the effects of a lower motor neurone lesion?

Answer 136

weakness

hypotonia (reduced muscle tone)

hyporeflexia (reduced reflexes)

muscle atrophy

fasciculations: damaged motor units produce spontaneous action potentials, resulting in a visible twitch
fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination

Question 137

what is motor neurone disease (MND)/amyotrophic lateral sclerosis (ALS)?

Answer 137

progressive neurodegenerative disorder of motor system - affects both upper and lower motor neurones

Question 138

which muscles have trouble contracting in motor neurone disease (MND)?

Answer 138

tongue

intercostal muscles - eventual death caused by lack of respiratory function

upper and lower limb

Question 139

what are the upper motor neurone signs of motor neurone disease?

Answer 139

spasticity (increased tone of limbs and tongue)

brisk limbs and jaw reflexes

Babinski’s sign

loss of dexterity

dysarthria (difficulty speaking)

dysphagia (difficulty swallowing)

Question 140

what are the lower motor neurone signs of motor neurone disease?

Answer 140

weakness

muscle wasting

tongue fasciculations and wasting

nasal speech

dysphagia

Question 141

what are the structures that make up the basal ganglia?

Answer 141

caudate nucleus

lentiform nucleus (putamen + external globus pallidus) – together caudate and putamen are known as the striatum

nucleus accumbens

subthalamic nuclei

substantia nigra (midbrain)

ventral pallidum, claustrum, nucleus basalis (of Meynert)

Question 142

what are the functions of the basal ganglia?

Answer 142

decision to move

elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)

moderating and coordinating movement (suppressing unwanted movements)

performing movements in order

Question 143

what causes Parkinson’s disease?

Answer 143

degeneration of dopaminergic neurons originating in the substantia nigra and projecting to the striatum

Question 144

what are the symptoms of Parkinson’s disease?

Answer 144

bradykinesia - slowness of (small) movements (doing up buttons, handling a knife)

hypomimic face - expressionless, mask-like (absence of movements that normally animate the face)

akinesia - difficulty in the initiation of movements because cannot initiate movements internally

rigidity - muscle tone increase, causing resistance to externally imposed joint movements

tremor at rest - 4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body

Question 145

what causes Huntington’s disease?

Answer 145

degeneration of GABAergic neurons in the striatum, caudate and then putamen

chromosome 4,
autosomal dominant

CAG repeat

Question 146

what are the symptoms of Huntington’s disease?

Answer 146

choreic movements (chorea - dance) -
rapid jerky involuntary movements of the body; hands and face affected first; then legs and rest of body

speech impairment

difficulty swallowing

unsteady gait

later stages - cognitive decline and dementia

Question 147

what is ballism?

Answer 147

sudden uncontrolled flinging of the extremities

usually from stroke affecting the subthalamic nucleus

symptoms occur contralaterally

Question 148

what are the functions of the vestibulocerebellum?

Answer 148

regulation of gait, posture and equilibrium

coordination of head movements with eye movements

Question 149

what does damage (tumour) to the vestibulocerebellum cause?

Answer 149

syndrome similar to vestibular disease

leads to gait ataxia, tendency to fall (even when patient sitting and eyes open)

Question 150

what are the functions of the spinocerebellum?

Answer 150

coordination of speech

adjustment of muscle tone

coordination of limb movements

Question 151

what does damage (degeneration and atrophy associated with chronic alcoholism) to the spinocerebellum cause?

Answer 151

affects mainly legs

causes abnormal gait and stance (wide-based)

Question 152

what are the functions of the cerebrocerebellum?

Answer 152

coordination of skilled movements

cognitive function

attention

processing of language

emotional control

Question 153

what does damage to the cerebrocerebellum cause?

Answer 153

affects mainly arms/skilled coordinated movements (tremor)

speech

Question 154

what are the main signs of cerebellar dysfunction?

Answer 154

ataxia

• general impairments in movement coordination and accuracy
• disturbances of posture or gait: wide-based, staggering (“drunken”) gait

dysmetria
- inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)

intention tremor
- increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)

dysdiadochokinesia
- inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)

scanning speech
- staccato, due to impaired coordination of speech muscles

Question 155

what is an alpha motor neuron?

Answer 155

lower motor neuron of brainstem and spinal cord

occupy anterior/ventral horn of grey matter of spinal cord

Question 156

what is the function of alpha motor neurons?

Answer 156

innervate extrafusal muscle fibres (fibres with contractile elements) of skeletal muscles (i.e. activation causes muscle contraction)

Question 157

what is a motor neuron pool?

Answer 157

contains all alpha motor neurons innervating a single muscle

Question 158

what are the intrafusal muscle fibres?

Answer 158

contain sensory organs which respond to stretch and tension within the muscle - convey information about sensitivity to bring about reflex activity

Question 159

what is a motor unit?

Answer 159

single motor neuron together with all the muscle fibres that it innervates

smallest functional unit with which to produce force

stimulation of one motor unit causes contraction of all the muscle fibres in that unit

Question 160

what are the 3 types of motor unit?

Answer 160

slow (S, type I)

fast, fatigue resistant (FR, type IIa)

fast, fatigable (FF, type IIb)

Question 161

what are the characteristics of a slow motor unit?

Answer 161

smallest diameter cell bodies

small dendritic trees

thinnest axons

slowest conduction velocity

Question 162

what are the characteristics of a fast motor unit (both fatigue resistant and fatigable?

Answer 162

larger diameter cell bodies

larger dendritic trees

thicker axons

faster conduction velocity

Question 163

how are the 3 different types of motor unit classified?

Answer 163

amount of tension generated

speed of contraction

fatigability

Question 164

what is the difference between the response to single motor neuron action potential between the 3 types of motor unit?

Answer 164

slow motor unit - very little force, generated slowly

fatigue resistant - 5x more force than slow, generated quickly

fatigable - almost 10x more force than slow, generated quickly

Question 165

what is the difference between the response to repeated stimulation at a level that evokes maximum tension between the 3 types of motor unit?

Answer 165

fast, fatigable: loses ability to generate force very quickly (within 2 mins)

fast, fatigue resistant - progressively loses ability to generate force gradually over time

slow - generates maximal force for a long time (over 1hr)

Question 166

where would a slow motor unit be found? why?

Answer 166

muscles used for postural stability

no need to generate large amounts of force, but need to maintain maximal force for many hours

Question 167

where would a fast motor unit be found? why?

Answer 167

gastrocnemius (calf)

can generate a lot of force quite quickly

Question 168

what are the two mechanisms by which the brain regulates the force that a single muscle can produce?

Answer 168

recruitment

rate coding

Question 169

how does recruitment work in regulating muscle force?

Answer 169

motor units not randomly recruited - order governed by “size principle”

smaller units recruited first (generally slow twitch units)

as more force is required, more units are recruited

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

Question 170

how does rate coding work to regulate muscle force?

Answer 170

motor unit can fire at a range of frequencies

slow units fire at a lower frequency - as firing rate increases, force produced by the unit increases

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

Question 171

what is a neurotrophic factor?

Answer 171

are a type of growth factor

prevent neuronal death

promote growth of neurons after injury

(if a muscle retains arterial supply but has its nerve supply cut, muscle will start to waste due to lack of neurotrophic factors)

Question 172

how can it be determined that the motor neurone has some effect on the properties of the muscle fibres that it innervates?

Answer 172

motor unit and fibre characteristics are dependent on the nerve which innervates them

if a fast twitch muscle and a slow muscle are cross innervated, the soleus becomes fast and the FDL becomes slow

Question 173

what is the most common change from one type of neurone to another?

Answer 173

IIB to IIA (fast fatigue to fatigue resistant)

most common following training

Question 174

when is a change from a type I neurone to a type II neurone possible?

Answer 174

in cases of severe deconditioning or spinal cord injury

microgravity during spaceflight results in shift from slow to fast muscle fibre types

Question 175

what kind of change in motor units/muscle fibres occurs during the ageing process?

Answer 175

associated with loss of type I and II fibres (preferential loss of type II fibres)

therefore larger proportion of type I fibres in aged muscle (evidence from slower contraction times)

Question 176

what is a reflex?

Answer 176

automatic response to a stimulus

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

magnitude and timing determined respectively by intensity and onset of stimulus

Question 177

how do reflexes differ from voluntary movements?

Answer 177

cannot be stopped once they are released

Question 178

what is the path of the monosynaptic (stretch) reflex?

Answer 178

stimulus at sensory receptor

transmitted through sensory neuron to spinal cord (CNS)

motor neuron carries impulse to effector

different motor neuron carries impulse to antagonist

Question 179

what is the Jendrassik manoeuvre?

Answer 179

pulling against locked fingers when having patellar tendon tapped - reflex becomes larger

work by reducing amount of inhibition that brain and upper regions of CNS exert over reflexes under normal conditions

Question 180

why is the Jendrassik manoeuvre important?

Answer 180

reflexes are thought of as being entirely automatic and stereotyped behaviours in response to stimulation of peripheral receptors

Jendrassik manoeuvre (also things like clenching teeth and making a fist) prove that reflexes can be influenced

Question 181

what is the role of higher centres of the CNS in the stretch reflex?

Answer 181

exert inhibitory and excitatory regulation

inhibitory - dominates in normal conditions (i.e. if muscle is stretched, control is exerted to tense it straight away)

decerebration (cortex separated from lower brain stem and lower spinal cord) reveals excitatory control from supraspinal areas - causes greater reflex response, muscle has elevated level of tonic contraction before muscle comes back to normal

Question 182

what can cause an overactive or tonic stretch reflex?

Answer 182

brain damage

causes rigidity and spasticity

Question 183

what is the pathway of descending (supraspinal) control of reflexes?

Answer 183

activating alpha motor neurons

activating inhibitory interneurons

activating propriospinal neurons (interneurons going up and down the spinal cord - few segments each way activated to activate nearby muscles)

activating gamma motor neurons

activating terminals of afferent fibres

Question 184

what is hyper-reflexia?

Answer 184

overactive reflexes

loss of descending inhibition (associated with loss of voluntary movement)

associated with upper motor neuron lesions

Question 185

what is clonus in hyper-reflexia?

Answer 185

involuntary and rhythmic muscle contraction

loss of descending inhibition

associated with upper motor neuron lesions

Question 186

what is Babinski’s sign (hyper-reflexia)?

Answer 186

when sole of foot is stimulated with a blunt instrument big toe curls downwards in normal response

toe curling upwards - positive Babinski sign (abnormal in adults, but normal in infants)

associated with upper motor neuron lesions

Question 187

what is hypo-reflexia?

Answer 187

below normal or absent reflexes

associated with lower motor neuron disease

Question 188

what are gamma motor neurones?

Answer 188

responsible for altering sensitivity of sensory organs in muscle - when organs stretch a signal travels to spinal cord to generate reflex contraction

sensitise organ so that it remains sensitive to stretch when muscle is at a different level in intrafusal muscle fibres

Question 189

where is the ear located?

Answer 189

embedded in petrous portion of temporal bone (hardest in body)

Question 190

what are the functions of the outer ear?

Answer 190

capture sound and focus it to tympanic membrane

amplify some frequencies by resonance in the canal

protect the ear from external threats

• hair: stops any mechanical or external element entering
• wax: traps any mechanical/external element entering, pH will kill anything live entering ear

Question 191

what does the outer ear consist of?

Answer 191

pinna

external auditory canal`

Question 192

what are the functions of the middle ear?

Answer 192

(2 mechanisms of amplification)

focusing vibrations from large surface area (tympanic membrane) to smaller surface area (oval window) - change in surface area increases pressure

using leverage from the incus-stapes joint to increase the force on the oval window

Question 193

what makes up the middle ear?

Answer 193

tympanic membrane to oval window

ossicles - articulated with each other to allow transmission of sound to inner ear

Question 194

what makes up the inner ear?

Answer 194

cochlea

Question 195

what are the functions of the inner ear?

Answer 195

transduces vibration into nervous impulses

simultaneously produces frequency and intensity analysis of the sound

Question 196

what are the 3 compartments of the cochlea?

Answer 196

scala media (innermost)

scala tympani (near basilar membrane, next to stapes and oval window at base)

scala vestibuli (near vestibular membrane, next to round window at base)

Question 197

what is the structure of the scala vestibuli and the scala tympani?

Answer 197

bone structures

contain perilymph (high in sodium)

Question 198

what is the structure of the scala media?

Answer 198

membranous structure

contains endolymph (high in potassium)

hearing organ/organ of Corti located here

Question 199

where is the structure where the organ of Corti lies?

Answer 199

basilar membrane

Question 200

how is the basilar membrane of the ear arranged?

Answer 200

tonotopically

i.e. sensitive to different frequencies at different points along its length

high frequencies near base, low frequencies near apex

Question 201

what are the 2 types of hair cells in the organ of Corti?

Answer 201

inner hair cells (IHC)

outer hair cells (OHC)

Question 202

how are the inner and outer hair cells arranged in the organ of Corti?

Answer 202

IHC arranged on 1 column

OHC arranged on 3 columns

Question 203

how does the tectorial membrane interact with inner and outer hair cells in the organ of Corti?

Answer 203

tectorial membrane is located above the hair cells - allow the hair deflection, which in turn will depolarise the cell

only OHCs are in constant contact with the tectorial membrane

these OHCs assist the contact with the IHCs

Question 204

what is the function of the inner hair cells (IHC) in the organ of Corti?

Answer 204

transduction of sound into nerve impulses

carry 95% of afferent information of auditory nerve

Question 205

what is the function of the outer hair cells (OHC) in the organ of Corti?

Answer 205

modulation of the sensitivity of the response

carry 95% of efferent information of auditory nerve

Question 206

how does transduction work in the auditory system?

Answer 206

deflection of the stereocilia (hairs of hair cells) towards the longest cilium will open K+ channels

ionic interchange depolarises the cell and neurotransmitter is liberated

higher amplitudes (louder) of sound will cause greater deflection of stereocilia and K+ channel opening

(hyper-polarisation closes K+ channels)

Question 207

what is the structure of the auditory pathways?

Answer 207

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

auditory information crosses at the superior olive level

after this point all connections are bilateral

Question 208

how is hearing organised (central auditory pathways)?

Answer 208

tonotopically organised

Question 209

what is frequency?

Answer 209

pitch (Hz)

cycles per second, perceived tone

Question 210

what is amplitude?

Answer 210

loudness (dB)

sound pressure, subjective attribute correlated with physical strength

Question 211

why is the decibel scale useful in measuring the amplitude of sounds?

Answer 211

logarithmic scale

range of sensitivity is very large

allows us to compress the scale on a graph - reflect the fact that many physiological processes are non-linear (i.e. respond to both very low and very high values)

Question 212

how does hearing change with age?

Answer 212

hearing acuity decreases with age, (particularly higher frequencies)

medium and low frequencies could be affected with the progression of hearing loss

Question 213

what are the aims of a hearing assessment?

Answer 213

determine:
is there a hearing loss?
- of what degree?
- of what type?

Question 214

what procedures are used in a hearing assessment?

Answer 214

tuning fork

audiometry

central processing assessment

tympanometry

otoacustic emission

electrocochleography

evoked potentials

Question 215

how is a tuning fork used in a hearing assessment?

Answer 215

used to establish probable presence/absence of a hearing loss with a significant conductive component

used to provide early and general information, when audiometry is not available or possible

Weber test:
Rinne test:

Question 216

how is pure tone audiometry (PTA) used in a hearing assessment?

Answer 216

science of measuring hearing acuity for variations in sound intensity and frequency

audiometer: device used to produce sound of varying intensity and frequency

Question 217

what is an audiogram?

Answer 217

graph plotting hearing thresholds to determine if there is hearing loss (normal threshold: 0 - 20 dB)

Question 218

how is a central processing assessment used in a hearing assessment?

Answer 218

assessment of hearing abilities other than detection using verbal and non-verbal tests

e.g. sound localization, filtered speech, speech in noise

Question 219

how is tympanometry used in a hearing assessment?

Answer 219

examination used to test middle ear condition and mobility of tympanic membrane and conduction bones by creating variations of air pressure in the ear canal

Question 220

how are otoacoustic emissions (OAEs) used in a hearing assessment?

Answer 220

normal cochlea produces low-intensity sounds called OAEs produced specifically by the outer hair cells as they expand and contract

(test is often part of the new born hearing screening and hearing loss monitoring)

Question 221

how are auditory evoked potentials used in a hearing assessment?

Answer 221

electrocochleography
– 0.2-4.0 ms, electrical activity from the cochlea and eighth nerve. Evoked by clicks or tone burst.

auditory brainstem response (ABR)
– 1.5-10.0 ms, electrical activity from the eighth nerve and brainstem nuclei and tracts. Evoked by clicks.

late responses (N1-P2, P300, MMN, and more)
– 80-500+ ms, electrical activity from the primary auditory and association cortex. Evoked by tone burst and oddball paradigm.

Question 222

what is the auditory brainstem response and how is it used in a hearing assessment?

Answer 222

electrical responses from the auditory pathway (often used in babies and children)

alterations in latency of waves can point to location of the deficit

Question 223

what would affect cortical potentials?

Answer 223

neurological conditions

processing problems

Question 224

what are the 2 types of hearing loss?

Answer 224

conductive hearing loss: problem is located in outer or middle ear

sensorineural hearing loss: problem is located in the inner ear or the auditory nerve

mixed hearing loss: conduction and transduction of sound are affected (problem affects more than one part of the ear)

Question 225

how is the degree of hearing loss classified?

Answer 225

mild - profound

Question 226

what are the causes of outer ear conductive hearing loss?

Answer 226

wax

foreign body

Question 227

what are the causes of middle ear conductive hearing loss?

Answer 227

otitis

otosclerosis

Question 228

what are the causes of inner ear sensorineural hearing loss?

Answer 228

presbycusis

ototoxicity

Question 229

what are the causes of nerve sensorineural hearing loss?

Answer 229

VIII tumour

Question 230

what treatments are available for hearing loss?

Answer 230

treat cause

hearing aids

cochlear implants

brainstem implants

Question 231

how do hearing aids work in treating hearing loss?

Answer 231

amplify the sound, does not replace any structure

Question 232

how do cochlear implants work in treating hearing loss?

Answer 232

replaces function of the hair cells by receiving sound, analysing it, transform it into electrical signals and sending an electric impulse directly to the auditory nerve

(needs functional auditory nerve)

Question 233

how do brainstem implants work in treating hearing loss?

Answer 233

when the auditory nerves are the affected structures, the electrical signals can be send to a set of electrodes placed directly into the brainstem

very risky, then it is advised for people with bilateral important auditory nerve damage

Question 234

what are the 3 main inputs of the vestibular system?

Answer 234

visual

proprioceptive

vestibular

Question 235

what are the outputs of the vestibular system?

Answer 235

ocular reflex (maintain stable gaze)

postural control (maintain stable posture)

(unwanted output: nausea)

Question 236

what are the inputs of the vestibular system?

Answer 236

visual (eye)

rotation and gravity (inner and middle ear)

pressure (feet)

Question 237

how do the inputs generate the outputs in the vestibular system?

Answer 237

CNS integrates input information and generates the responses

Question 238

where is the vestibular organ located?

Answer 238

posterior area of inner ear

inner ear contains hair cells for hearing and balance

Question 239

where are the utricle and saccule located?

Answer 239

vestibule

joined by a conduit

saccule is also joined to the cochlea

Question 240

how are the semi-circular canals arranged?

Answer 240

three semi-circular canals on each ear (anterior, posterior, lateral)

have an ampulla on one side, and they are connected to the utricle

Question 241

what is the labyrinth in the skull?

Answer 241

superior projection of right bony labyrinth on base of skull

Question 242

why is the location of the vestibular organ important?

Answer 242

location of the vestibular organ draws planes for anterior and posterior canals

these planes determine which structure will be stimulated with a specific head movement

Question 243

what is the structure of vestibular hair cells?

Answer 243

have a kinocilium (the biggest cilium) and stereocilia

Question 244

what is the function of the cilia on vestibular hair cells?

Answer 244

cilia allows the cells to depolarise the cell with movement of the endolymph generated by head movement

Question 245

what are the the otolith organs?

Answer 245

utricle and saccule

Question 246

where are the cells of the otolith organs located?

Answer 246

on the maculae

placed horizontally in the utricle

placed vertically in the saccule

Question 247

what is the structure of the maculae?

Answer 247

contain the hair cells

gelatinous matrix

otoliths on top

Question 248

what are otoliths?

Answer 248

carbonate crystals that help the deflection of the hairs

Question 249

what is the structure of the semi-circular canals of the ear?

Answer 249

hair cells in the canals are located in ampulla

rest of the canal only has endolymph (high potassium)

Question 250

what is the structure of the ampulla?

Answer 250

has crista where hair cells are located

cells surrounded by cupula (helps hair cell movement)

Question 251

how are the semi-circular canals oriented?

Answer 251

defines 3 planes

anterior and posterior form a 90° angle

lateral is horizontal to other canals

Question 252

where do vestibular nuclei have projections to?

Answer 252

spinal cord (postural control)

nuclei of the extraocular muscles (eye movement)

cerebellum (feedback)

centres for cardiovascular + respiratory control

Question 253

where do the primary afferents in the vestibular system end?

Answer 253

vestibular nuclei

cerebellum

Question 254

which vestibular nuclei are associated with the ventroposterior nucleus and vestibular cortex?

Answer 254

superior and lateral

Question 255

which vestibular nuclei are associated with the vestibulospinal reflexes?

Answer 255

lateral, medial, inferior

Question 256

what are the 3 reflexes produced by vestibular pathways?

Answer 256

vestibulo-ocular reflex (VOR)

vestibulocerebellar reflexes

vestibulospinal reflexes

Question 257

where is the vestibular cortex located?

Answer 257

not one specific area - since many inputs and integrators are involved, many cortical areas participate

main processing centre thought to be in the parietal lobe (in parieto-insular vestibular cortex (PIVC))

Question 258

what does the vestibular physiology look like?

Answer 258

sensory input

• visual
• vestibular
• proprioceptive

input travels for central processing in primary processor (vestibular nuclear complex) and adaptive processor (cerebellum), which interact with each other

information travels from primary processor (vestibular nuclear complex) to motor neurons

eye movements and positional movements produced

Question 259

what are the functions of the vestibular system?

Answer 259

to detect and inform about head movements

to keep images fixed in the retina during head movements

postural control

Question 260

how do hair cells alter potential?

Answer 260

hair cells have a resting potential which has a basal discharge to the nerve

hairs moving towards the kinocilium generates depolarization and an increase in nerve discharge

hairs moving away from the kinocilium generates hyperpolarization and a reduction in nerve discharge

Question 261

how do the otolith organs work?

Answer 261

linear acceleration and tilt cause otolith movement and therefore detection

utricle - horizontal movement

saccule - vertical movement

Question 262

how do the semi-circular canals work?

Answer 262

angular acceleration causes cupula to move and displace hair cells

output signal on cranial nerve VIII (vestibulocochlear) is velocity

work in pairs according to the planes

• laterals logether
• anterior from one side with posterior of opposite side

Question 263

how does the vestibulo-ocular reflex (VOR) work?

Answer 263

keeps images fixed in the retina

connection between vestibular nuclei and oculomotor nuclei

eye movement in opposite direction to head movement, but same velocity and amplitude

Question 264

how does the vestibulo-spinal reflex (VSR) work?

Answer 264

motor neurons to limb muscles (lateral tract)

motor neurons to neck and back muscles (medial tract)

postural control, avoidance of falls and compensatory body movement according to the head position

Question 265

how is the vestibular system assessed?

Answer 265

medical history, posture and gait, cerebellar function, eye movements

vestibular tests

• caloric test
• video head impulse test (vHIT)
• vestibular evoked myogenic potential (VEMP)
• rotational test

imaging

• CT
• MRI

symptoms and impact assessment

Question 266

what is the main symptom of a balance disorder?

Answer 266

dizziness/vertigo (very common - 25% of ENT and neurological referrals)

can be categorised based on location of the affected structure and evolution of signs and symptoms

Question 267

what are some peripheral vestibular disorders (labyrinth and/or VIII nerve)?

Answer 267

vestibular neuritis

benign paroxysmal positional vertigo (BPPV)

Meniere’s disease

unilateral and bilateral vestibular hypofunction

Question 268

what are some central vestibular disorders (CNS - brainstem/cerebellum)?

Answer 268

stroke

MS

tumour

Question 269

what are 2 examples of an acute balance disorder?

Answer 269

vestibular neuritis (‘labyrinthitis’)

stroke

Question 270

what is an example of an intermittent balance disorder?

Answer 270

Benign Paroxysmal Positional Vertigo (BPPV)

Question 271

what are 2 examples of a recurrent balance disorder?

Answer 271

Meniere’s disease

migraine

Question 272

what are 2 examples of a progressive balance disorder?

Answer 272

schwannoma vestibular (VIIIth nerve)

degenerative conditions (MS)

Question 273

what are some non-vestibular causes of dizziness?

Answer 273

heart disorders

presyncopal episodes

orthostatic hypotension

anaemia

hypoglycaemia

psychological

gait disorders

Question 274

what are the bases for a headache?

Answer 274

structural (not just brain, could be scalp, skull, meninges, spinal fluid, blood vessels, eyeballs, ear apparatus, veins etc.)

pharmacological

psychological

Question 275

what are some things that may cause an acute single headache?

Answer 275

febrile illness, sinusitis

first attack of migraine

following a head injury

subarachnoid haemorrhage

meningitis

tumour

drugs

toxins

stroke

thunderclap (sudden onset), low pressure

Question 276

what are some things that may cause a dull headache, increasing in severity?

Answer 276

(usually benign)

overuse of medication (e.g. codeine)

contraceptive pill, hormone replacement therapy

neck disease

temporal arteritis

benign intracranial hypertension

cerebral tumour

cerebral venous sinus thrombosis

Question 277

what are some things that may cause a dull headache, unchanged over months?

Answer 277

chronic tension headache

depressive, atypical facial pain

Question 278

what are some things that may cause a triggered headache?

Answer 278

coughing, straining, exertion

coitus

food and drink

Question 279

what are some things that may cause a recurrent headache?

Answer 279

migraine

cluster headache

episodic tension headache

trigeminal or post-herpetic neuralgia

Question 280

what are the red flags associated with onset of a headache?

Answer 280

“thunderclap” headache (like patient has been struck by thunder or lightning suddenly)

acute

subacute

Question 281

what are the red flags associated with meningism?

Answer 281

photophobia

phonophobia

stiff neck

vomiting

Question 282

what are red flag systemic symptoms that may occur in conjunction with a headache?

Answer 282

fever

rash

weight loss

Question 283

what are red flag neurological symptoms/focal signs that may occur in conjunction with a headache?

Answer 283

visual loss

confusion

seizures

hemiparesis

double vision (focal sign)

3rd nerve palsy (focal sign - droopy eyelid)

Horner syndrome (focal sign)

papilloedema

Question 284

what are some red flags for a headache in general?

Answer 284

orthostatic (better lying down

strictly unilateral

Question 285

what are the signs of a subarachnoid silhouette?

Answer 285

sudden generalised headache - “blow to the head”

meningism - stiff neck and photophobia

Question 286

what causes a subarachnoid haemorrhage?

Answer 286

most caused by a ruptured aneurysm

a few from arteriovenous malformations

some are unexplained

Question 287

how are subarachnoid haemorrhages treated?

Answer 287

around 50% are instantly fatal

vasospasm may stop the leak

nimodipine and BP control.

high risk of a further bleed.

early neurosurgical assessment will confirm bleed
and establish cause

CT brain, lumbar puncture (RBC and xanthochromia) and MRA, angiogram

Question 288

how are aneurysms treated?

Answer 288

filled with platinum coils

used to be clipped or wrapped

Question 289

how are aneurysms treated?

Answer 289

filled with platinum coils

used to be clipped or wrapped

Question 290

what is an acute intracerebral bleed?

Answer 290

fatal haemorrhage due to coning

mechanism of coning - raised intracranial pressure (ICP)

Question 291

what is papilloedema?

Answer 291

optic disc swelling due to raised intracranial pressure

Question 292

how likely is a carotid and vertebral artery dissection to lead to stroke?

Answer 292

20% of ischaemic strokes under 45 years old

mean age 40 - carotid > vertebral

Question 293

how is a carotid and vertebral artery dissection diagnosed?

Answer 293

headache and neck pain

MRI/MRA

Doppler

angiography

(test if traumatic vs. spontaneous)

Question 294

how is a carotid and vertebral artery dissection treated?

Answer 294

aspirin or anticoagulation

Question 295

what are the symptoms of temporal arteritis?

Answer 295

(happens over the age of 55, 3x commoner in females)

constant unilateral headache

scalp tenderness

jaw claudication

25% polymyalgia rheumatica-proximal muscle tenderness

involvement of posterior ciliary arteries causes blindness

elevated ESR and CRP

temporal artery usually inflamed and tortuous

visible on ultrasound

biopsy shows inflammation and giant cells

Question 296

how is temporal arteritis treated?

Answer 296

high dose steroids

aspirin

Question 297

what is cerebral venous thrombosis?

Answer 297

thrombosis in dural venous sinus or cerebral vein

Question 298

what can cause cerebral venous thrombosis?

Answer 298

non-territorial ischaemia “venous infarcts”

haemorrhage

thrombophilia

pregnancy

dehydration

Behcets

Question 299

what causes headaches in cerebral venous thrombosis?

Answer 299

raised ICP

Question 300

what can cause viral meningitis?

Answer 300

coxsackie

ECHO

mumps

EBV

Question 301

what can cause bacterial meningitis?

Answer 301

Meningococci

Pneumococci

Haemophilus tuberculous

Question 302

what can cause fungal meningitis?

Answer 302

Cryptococci

Question 303

what can cause granulomatous meningitis?

Answer 303

sarcoid

Lyme

Brucella

Behcet’s

syphilis

Question 304

what are the types of meningitis?

Answer 304

viral

bacterial

fungal

tuberculous

granulomatous

carcinomatous

Question 305

what are the presenting symptoms of meningitis?

Answer 305

malaise

headache

fever

neck stiffness

photophobia

confusion

alteration of consciousness

Question 306

what is herpes simplex encephalitis?

Answer 306

classic haemorrhagic changes in temporal lobes

Question 307

how is meningitis treated?

Answer 307

(treat then diagnose)

antibiotics

blood and urine culture

lumbar puncture (CSF looks white -increased white cell count, decreased glucose due to brain using up large quantities)

antigens

cytology

bacterial culture

CT or MRI scan

Question 308

what does bacterial meningitis look like?

Answer 308

cerebral oedema

effacement of ventricles and sulci

inflamed meninges

Question 309

what are the symptoms of sinusitis?

Answer 309

malaise

headache

fever

blocked nasal passages

loss of vocal resonance

anosmia

nasal or postnasal catarrh

local pain and tenderness.

frontal pain characteristically starts 1-2 hours after rising and clears up during the afternoon

Question 310

brain tumour

Answer 310

glioblastoma multiforme

Question 311

what demographic often suffers from pseudotumour cerebri?

Answer 311

young obese women

Question 312

what are the symptoms of a pseudotumour cerebri?

Answer 312

headache

visual obscurations

diplopia

tinnitus

papilloedema with or without visual field loss

Question 313

what drugs are used in pseudotumour cerebri?

Answer 313

hormones

steroids

antibiotics

vitamin E

Question 314

what treatments are needed for pseudotumour cerebri?

Answer 314

weight loss

diuretics

optic nerve sheath decompression

lumboperitoneal shunt

stenting of stenosed venous sinuses

Question 315

what does raised intracranial pressure look like on an MRI?

Answer 315

cerebral oedema

effacement of ventricles and sulci

no mass lesion

Question 316

what can cause a low pressure headache?

Answer 316

CSF leak due to tear in dura

traumatic (post-lumbar puncture) or spontaneous

Question 317

how can a low pressure headache be identified on an MRI?

Answer 317

meningeal enhancement

Question 318

how is a low pressure headache treated?

Answer 318

rehydration

caffeine

blood patch

Question 319

what is a Chiari malformation?

Answer 319

brain sits low within skull

Question 320

how does a Chiari malformation cause triggered headaches?

Answer 320

cerebellar tonsils descending through foramen magnum

descend further when patient coughs - tugs on the meninges causing cough headache

Question 321

what are the signs of obstructive sleep apnoea?

Answer 321

often characteristic body habitus

history of loud snoring and apnoeic spells

hypoxia, CO2 retention

non-refreshing sleep

depression

impotence

poor performance at work

Question 322

how is obstructive sleep apnoea treated?

Answer 322

require sleep study

nocturnal NI

surgery

Question 323

what is trigeminal neuralgia?

Answer 323

electric shock like pain in the distribution of a sensory nerve

often triggered by innocuous stimuli

any division of the trigeminal can be affected

can be symptom of M.S.

Question 324

what causes trigeminal neuralgia?

Answer 324

neurovascular conflict at the point of entry of the nerve into the pons

Question 325

how is trigeminal neuralgia treated?

Answer 325

carbamazepine

lamotrigine

gabapentin

posterior fossa decompression

Question 326

what are the symptoms of atypical facial pain?

Answer 326

(most commonly in middle aged women - depressed or anxious)

daily, constant, poorly localised deep aching or burning

facial or jaw bones, but may extend to the neck, ear or throat

not lancinating

not conforming to the strict anatomical distribution of any nerve

no sensory loss

(pathology in teeth, temporomandibular joints, eye, nasopharynx and sinuses must be excluded)

Question 327

how is atypical facial pain treated?

Answer 327

unresponsive to conventional analgesics, opiates and nerve blocks

mainstay of management tricyclics

Question 328

how likely is a post traumatic headache?

Answer 328

depends on nature of injury

• high in victims of car accidents
• low in perpetrators of car accidents
• low in sports injuries

Question 329

what are the mechanisms that may cause post traumatic headache?

Answer 329

neck injury

scalp injury

vasodilation - autonomic damage

depression - often delayed

Question 330

how is a post traumatic headache managed?

Answer 330

explain, prevent analgesic abuse

non-steroidal anti-inflammatories - ibuprofen, naproxen

tricyclic antidepressants - Amitriptyline

will take 3-4 years

Question 331

what causes cervical spondylosis?

Answer 331

narrowing of joint space due to worn disk

commonest cause of new headache in older patients

Question 332

what are the characteristics of a headache caused by cervical spondylosis?

Answer 332

usually bilateral

occipital pain can radiate forwards to the frontal region

steady pain

no nausea or vomiting

worsened by moving the neck

Question 333

how is a headache caused by cervical spondylosis treated?

Answer 333

rest, deep heat, massage

anti-inflammatory analgesics

(NB over-manipulation may be harmful)

Question 334

what are the 3 types of tears?

Answer 334

basal

reflex

emotional

Question 335

where is the lacrimal gland located?

Answer 335

within orbit

latero-superior to globe

Question 336

what are basal tears?

Answer 336

lacrimal gland produces tears at a constant level (even in the absence of irritation or stimulation)

Question 337

what are reflex tears?

Answer 337

refers to increased tear production in response to ocular irritation

Question 338

what makes up the tear reflex pathway?

Answer 338

afferent pathway (cornea, cranial nerve V1, ophthalmic trigeminal)

CNS

efferent (parasympathetic nerve)

lacrimal gland

Question 339

how is the cornea innervated?

Answer 339

sensory nerve fibres via ophthalmic branch of trigeminal nerve

Question 340

how are tears produced?

Answer 340

afferent pathway: trigeminal nerve relays signal to CNS from cornea

efferent pathway: mediated by parasympathetic nerve, innervates lacrimal gland

tear film drains through the two puncta (tiny openings on upper and lower medial lid margins)

puncta form opening of superior and inferior canaliculi within upper and lower eyelids

both canaliculi converge as one single common canaliculus, drain tear into tear sac

tear is finally drained out of the tear sac,
into the nasal cavity through the tear duct

Question 341

what are the functions of the tear film?

Answer 341

maintains smooth cornea-air surface

source of oxygen and nutrient supply to the anterior segment (normal cornea has no blood vessels)

bactericide

Question 342

why is a smooth cornea-air surface important?

Answer 342

maintaining clear vision

removing surface debris during blinking

Question 343

what are the 3 layers of the tear film?

Answer 343

lipid layer (superficial)

aqueous layer (forms bulk of film)

mucinous (deep)

Question 344

how is the lipid layer of the tear film formed?

Answer 344

secreted by Meibomian Glands (situated along the eyelid margins)

Question 345

what is the function of the lipid layer of the tear film?

Answer 345

responsible for protecting the tear film from rapid evaporation

Question 346

what are the functions of the aqueous layer of the tear film?

Answer 346

delivers oxygen and nutrient to surrounding tissue

contains factors against potentially harmful bacteria (bactericide)

Question 347

what is the function of the mucinous layer of the tear film?

Answer 347

ensures that tear film sticks to the eye surface

maintains surface wetting

Question 348

how does the mucinous layer of the tear film carry out its function?

Answer 348

mucin molecules act by binding water molecules to hydrophobic corneal epithelial cell surface

Question 349

what is the conjunctiva?

Answer 349

thin, transparent tissue that covers eye’s outer surface

nourished by tiny blood vessels that are nearly invisible to the naked eye

Question 350

what area does the conjunctiva cover?

Answer 350

begins at outer edge of cornea

covers visible part of eye

lines inside of eyelids

Question 351

what are the 3 layers of the coat of the eye?

Answer 351

outermost - sclera (white of the eye)

choroid

innermost - retina (neurosensory tissue)

Question 352

what is the function of the sclera?

Answer 352

protecting the eye

maintaining the shape of the eye

Question 353

what is the function of the choroid?

Answer 353

providing circulation to the eye

shielding out unwanted scattered light

Question 354

what is the function of the retina?

Answer 354

converting light into neurological impulses

to be transmitted to the brain via the optic nerve

Question 355

what are the structural properties of the sclera?

Answer 355

hard

fibrous

opaque

high water content

Question 356

what are the structural properties of the choroid?

Answer 356

pigmented

vascular - layers of blood vessels that nourish the back of the eye

Question 357

what is the cornea?

Answer 357

transparent, dome-shaped window covering the front of the eye

Question 358

what is the function of the cornea?

Answer 358

powerful refracting surface (providing 2/3 of eye’s focusing power)

gives us a clear window to look through

Question 359

what are the 5 layers of the cornea?

Answer 359

epithelium

Bowman’s membrane

stroma

Descemet’s membrane

endothelium

Question 360

what feature of the stroma of the cornea contributes towards transparency?

Answer 360

its regularity

Question 361

what is the function of the endothelium of the cornea?

Answer 361

pumps fluid out of cornea, prevents corneal oedema

cornea has low water content

Question 362

what is the uvea?

Answer 362

vascular coat of eyeball

lies between the sclera and retina

Question 363

what are the 3 parts that make up the uvea?

Answer 363

iris

ciliary body

choroid

(intimately connected - disease of one part also affects the other portions though not necessarily to the same degree)

Question 364

what is the function of the iris?

Answer 364

controls light levels inside the eye

similar to the aperture on a camera

Question 365

how does the iris control pupil size?

Answer 365

embedded with tiny muscles

dilate and constrict pupil size

Question 366

what is the structure of the lens?

Answer 366

outer acellular capsule

regular inner elongated cell fibres – transparency

Question 367

how does the lens change with age?

Answer 367

may lose its transparency with age

results in an opaque lens (cataract)

Question 368

what is the function of the lens of the eye?

Answer 368

refractive Power

1/3 of the eye focusing power - higher refractive index than aqueous fluid and vitreous

accommodation

elasticity

Question 369

what is the function of the optic nerve?

Answer 369

transmits electrical impulses from the retina to the brain

Question 370

how is the optic nerve arranged?

Answer 370

connects to the back of the eye near the macula

visible portion is called the optic disc

where the optic nerve meets the retina there are no light sensitive cells - it is a blind spot

Question 371

where is the macula located?

Answer 371

roughly in the centre of the retina

temporal to the optic nerve

Question 372

what is the function of the macula?

Answer 372

small and highly sensitive part of the retina responsible for detailed central vision

allows us to perform tasks such as reading

Question 373

what is the fovea?

Answer 373

centre of macula

most sensitive part of the retina

Question 374

what is the arrangement of cells on the fovea?

Answer 374

highest concentration of cones (low concentration of rods)

this is why stars out of the corner of your eye are brighter than when you look at them directly

Question 375

why is the high concentration of cones on the fovea important?

Answer 375

allow perception in detail

Question 376

what are the 2 types of visual function?

Answer 376

central

peripheral

Question 377

what is central vision responsible for?

Answer 377

detailed day vision

colour vision – fovea has the highest concentration of cone photoreceptors

(reading, facial recognition)

Question 378

what problems will people with loss of central vision have?

Answer 378

poor visual acuity (loss of foveal vision)

problems with reading and recognising faces

Question 379

what is peripheral vision responsible for?

Answer 379

shape

movement

night vision

navigation vision

Question 380

what problems will people with loss of peripheral vision have?

Answer 380

extensive loss of visual field – unable to navigate in environment, patient may need white stick even with perfect visual acuity

problems navigating the world

Question 381

how is central vision assessed?

Answer 381

visual acuity assessment

Question 382

how is peripheral vision assessed?

Answer 382

visual field assessment

Question 383

what are the 2 layers of the retina?

Answer 383

retinal pigment epithelium (in front of choroid)

neuroretina (inner, thicker layer)

Question 384

what are the functions of the retinal pigment epithelium?

Answer 384

transports nutrient from the choroid to the photo-receptor cells

removes metabolic waste from the retina

Question 385

what are the 3 layers of the neuroretina?

Answer 385

outer, middle, inner

Question 386

what cells are present on the outer layer of the neuroretina?

Answer 386

photoreceptors (1st order neuron)

Question 387

what is the the function of the outer layer of the neuroretina?

Answer 387

detection of light

Question 388

what cells are present on the middle layer of the neuroretina?

Answer 388

bipolar cells (2nd order neuron)

Question 389

what is the the function of the middle layer of the neuroretina?

Answer 389

local signal processing to improve contrast sensitivity, regulate sensitivity

Question 390

what cells are present on the inner layer of the neuroretina?

Answer 390

retinal ganglion cells (3rd order neuron)

axon runs along optic nerve into brain

Question 391

what is the the function of the inner layer of the neuroretina?

Answer 391

transmission of signal from the eye to the brain

Question 392

what are the 2 classes of photoreceptor?

Answer 392

rods and cones

Question 393

what are rods responsible for?

Answer 393

night vision (scotopic vision)

peripheral vision

recognises motion

more photoreceptors, more pigment - higher spatial and temporal summation

Question 394

what are cones responsible for?

Answer 394

daylight fine vision and colour vision (photopic vision)

Question 395

how do rods and cones differ in terms of sensitivity to light?

Answer 395

rods 100x more sensitive than cones

Question 396

how do rods and cones differ in terms of response to light?

Answer 396

rods have slower response than cones

Question 397

how do rods and cones differ in terms of their outer segment?

Answer 397

rods have longer outer segment (therefore more photosensitive pigment) than cones

Question 398

where are photopigments synthesised?

Answer 398

inner photo-receptor segment of rods and cones

then transported to outer segment

Question 399

how is the outer segment of rods and cones arranged?

Answer 399

stacks of discs

Question 400

how are photopigments regenerated?

Answer 400

distal discs (outer segment) with deactivated photo-pigments are shed from the tips

discs phagocytosed by the retinal epithelial cells

deactivated photopigments regenerated inside retinal epithelial cells

photopigments transported back to photo-receptors

Question 401

where are rod photoreceptors distributed?

Answer 401

widely distributed all over the retina,
highest density just outside the macula

density tails off towards the periphery

completely absent within the macula

Question 402

where are cone photoreceptors distributed?

Answer 402

only within macula

Question 403

where is the peak of rod vison light sensitivity?

Answer 403

498nm wavelength

rods used for night vision and spatial recognition, not really sensitive to any particular colour

Question 404

what are the 3 cone photopigment sub-types?

Answer 404

S-cones

M-cones

L- cones

Question 405

what wavelengths are S-cones sensitive to?

Answer 405

short wavelength (blue)

peak sensitivity: 430nm

Question 406

what wavelengths are M-cones sensitive to?

Answer 406

medium wavelength (green)

peak sensitivity: 540nm

Question 407

what wavelengths are L-cones sensitive to?

Answer 407

long wavelength (red)

peak sensitivity: 570nm

Question 408

how is yellow light experienced?

Answer 408

wavelength between peak sensitivity of M-cones and L-cones

equal stimulation of M and L cones

therefore yellow light experienced as a combination of green and red light

Question 409

what is deuteranomaly/Daltonism (most common form of colour vision deficiency) caused by?

Answer 409

shifting of the M-cone sensitivity peak towards that of the L-cone curve

causes red-green confusion

Question 410

what 2 things can cause colour vision deficits?

Answer 410

colour vision deficits caused by a shift in the photo-pigment peak sensitivity (anomalous trichromatism)

absence of one or more of the 3 cone photo-pigments

Question 411

what is dichromatism?

Answer 411

only two cone photo-pigment sub-types are present

Question 412

what is monochromatism?

Answer 412

complete absence of colour vision

Question 413

what is blue cone monochromatism?

Answer 413

presence of only blue L-cones

normal daylight visual acuity

Question 414

what is rod monochromatism?

Answer 414

a total absence of all cone photo-receptors

no functional day vision

Question 415

what is achromatopsia?

Answer 415

full colour blindness (occurs in very small percentage of the population)

Question 416

what is the Ishihara test?

Answer 416

colour blindness test

Question 417

what is the basis of refraction?

Answer 417

as light goes from one medium to another, velocity changes

path of light changes

some light reflects off the boundary (angle of incidence = angle of reflection)

some refracts through the boundary (angle of incidence > or < angle of reflection depending on direction of light)

Question 418

what is the index of refraction?

Answer 418

speed of light in a vacuum/speed of light in a medium

speed of light in a medium will always be smaller and produces a value greater than or equal to 1

Question 419

what are the 2 types of lens?

Answer 419

convex (takes light rays and brings them to a point)

concave (takes light rays and spreads them outward)

Question 420

when might a convex lens be used practically?

Answer 420

camera

focus image on film

Question 421

what is emmetropia?

Answer 421

adequate correlation between axial length and refractive power (functioning eye)

parallel light rays fall on the retina (no accommodation)

Question 422

what is ametropia?

Answer 422

mismatch between axial length and refractive power

parallel light rays don’t fall on the retina (no accommodation)

Question 423

what are some ametropic errors?

Answer 423

near-sightedness (myopia)

farsightedness (hyperopia)

astigmatism

presbyopia

Question 424

how does the path of light lead to myopia?

Answer 424

parallel rays converge at a focal point anterior to the retina

Question 425

what causes myopia?

Answer 425

excessive long globe (axial myopia) - more common

excessive refractive power (refractive myopia)

Question 426

what is the etiology of myopia and hyperopia?

Answer 426

unclear

genetic factor

Question 427

what are the symptoms of myopia?

Answer 427

blurred distance vision

squint in an attempt to improve uncorrected visual acuity when gazing into the distance

headache

Question 428

how is myopia treated?

Answer 428

correction with diverging lenses (negative lenses)

correction with contact lens

correction by removing the lens to reduce refractive power of the eye

Question 429

how does the path of light lead to hyperopia?

Answer 429

parallel rays converge at a focal point posterior to the retina

Question 430

what causes hyperopia?

Answer 430

excessive short globe (axial hyperopia) -more common

insufficient refractive power (refractive hyperopia)

Question 431

what are the symptoms of hyperopia?

Answer 431

visual acuity at near tends to blur relatively early

• nature of blur varies from inability to read fine print to clear near vision that suddenly and intermittently blurs
• blurred vision is more noticeable if person is tired, printing is weak or light inadequate

asthenopic symptoms

• eye pain
• headache in frontal region
• burning sensation in the eyes
• blepharoconjunctivitis

amblyopia – uncorrected hyperopia > 5D

Question 432

how is hyperopia treated?

Answer 432

correction with converging (positive lenses)

correction with positive lens + cataract extraction

correction with contact lens

correction with intraocular lens

Question 433

how does the path of light lead to astigmatism?

Answer 433

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

Question 434

what causes astigmatism?

Answer 434

refractive media is not spherical

refraction different along one meridian than along meridian perpendicular to it

2 focal points (punctiform object is represent as 2 sharply defined lines)

Question 435

what is the etiology of astigmatism?

Answer 435

heredity

Question 436

what are the symptoms of astigmatism?

Answer 436

asthenopic symptoms

• headache
• eyepain

blurred vision

distortion of vision

head tilting and turning

Question 437

how is regular astigmatism treated?

Answer 437

cylinder lenses with or without spherical lenses (convex or concave), Sx

Question 438

how is irregular astigmatism treated?

Answer 438

rigid cylinder lenses

surgery

Question 439

what is the near response triad?

Answer 439

adaptation for near vision

Question 440

what 3 things form the near response triad? what is their function?

Answer 440

pupillary miosis (sphincter pupillae) to increase depth of field

convergence (medial recti from both eyes) to align both eyes towards a near object

accommodation (circular ciliary muscle) to increase the refractive power of lens for near vision

Question 441

what is presbyopia?

Answer 441

naturally occurring loss of accommodation (focus for near objects), distant vision intact

onset from age 40 years

Question 442

how is presbyopia treated?

Answer 442

convex lenses in near vision

• reading glasses
• bifocal glasses
• trifocal glasses
• progressive power glasses

Question 443

what are the 2 types of spectacle lens?

Answer 443

monofocal lenses

• spherical lenses
• cylindrical lenses

multifocal lenses

Question 444

what is the difference between contact lenses and spectacle lenses?

Answer 444

higher quality of optical image and less influence on the size of retinal image than spectacle lenses

Question 445

when are contact lenses used?

Answer 445

cosmetic

athletic activities

occupational

irregular corneal astigmatism

high anisometropia

corneal disease

Question 446

what are the disadvantages of contact lenses?

Answer 446

careful daily cleaning and disinfection

expense

complications

• infectious keratitis
• giant papillary conjunctivitis
• corneal vascularization
• severe chronic conjunctivitis

Question 447

what are intraocular lenses?

Answer 447

replacement of cataract crystalline lens

Question 448

what are the advantages of intraocular lenses?

Answer 448

give best optical correction for aphakia

avoid significant magnification and distortion caused by spectacle lenses

Question 449

what are the types of keratorefractive surgery?

Answer 449

RK

AK

PRK

LASIK

ICR

thermokeratoplasty

Question 450

what are the types of intraocular surgery?

Answer 450

clear lens extraction (with or without IOL)

phakic IOL

Question 451

how is surgical correction carried out?

Answer 451

pre operative eye

initial cutting of corneal flap

cutting of corneal flap

flipping of corneal flap

photorefractive treatment (laser)

corneal stroma reshaped post laser

corneal flap back in position

treatment completed

Question 452

what is the process of clear lens extraction and addition of an intraocular lens?

Answer 452

cataract extraction

implantation of artificial lens

Question 453

what occurs as a result of clear lens extraction and addition of an intraocular lens?

Answer 453

loss of accommodation (patient needs reading glasses)

Question 454

what is the function of the visual pathway?

Answer 454

transmits signal from eye to the visual cortex

Question 455

what are the visual pathway landmarks?

Answer 455

eye

optic nerve – ganglion nerve fibres with cell bodies originating in the retina

optic chiasm – half of the nerve fibres cross here and exit along the contra-lateral optic tract,
while the remaining ganglion nerve fibres exit along the optic Tract on the same side

optic tract – ganglion nerve fibres exit as optic tract

lateral geniculate nucleus – ganglion nerve fibres synapse at lateral geniculate nucleus (relay centre in thalamus)

optic radiation – 4th order neuron, relaying signal from lateral geniculate ganglion to primary visual cortex for lower visual processing

primary visual cortex or striate cortes – within the occipital lobe, relays visual information to the extra-striate cortex
(region adjacent to primary visual cortex)
for further higher visual processing

Question 456

what are first order neurons within the visual pathway?

Answer 456

photoreceptors

Question 457

what are second order neurons within the visual pathway?

Answer 457

phototreceptors synapse on retinal bipolar cells

Question 458

what are third order neurons within the visual pathway?

Answer 458

retinal ganglion cells

Question 459

what feature of retinal ganglion nerve fibres allows better signal transmission of visual information out of the eye to the brain?

Answer 459

myelination after entering optic nerve

Question 460

what is decussation in the visual pathway?

Answer 460

half of the retina ganglion nerve fibres cross to the opposite side at the optic chiasm

Question 461

what are fourth order neurons within the visual pathway?

Answer 461

retinal ganglion Fibres terminate at the lateral geniculate ganglion (thalamus)
and synapse upon the fourth order neurons, or optic radiation

Question 462

what will a lesion anterior to the optic chiasma affect?

Answer 462

visual field in one eye

Question 463

what will a lesion posterior to the optic chiasma affect?

Answer 463

visual field simultaneously in both eyes because of fibre crossing at chiasma

Question 464

where do the crossed fibres at the optic chiasma predominantly originate from?

Answer 464

nasal retina

Question 465

which half of the visual field are the crossed fibres at the optic chiasma responsible for?

Answer 465

temporal

Question 466

where do the uncrossed fibres at the optic chiasma predominantly originate from?

Answer 466

temporal retina

Question 467

which half of the visual field are the uncrossed fibres at the optic chiasma responsible for?

Answer 467

nasal

Question 468

what will a lesion at the optic chiasma affect?

Answer 468

damages crossed ganglion fibres from nasal retina in both eyes

temporal field deficit in both eyes – bitemporal hemianopia

Question 469

what will a right sided lesion (optic tract, optic radiation or visual cortex) posterior to the optic chiasma affect?

Answer 469

left homonymous hemianopia (both eyes)

Question 470

what will a left sided lesion (optic tract, optic radiation or visual cortex) posterior to the optic chiasma affect?

Answer 470

right homonymous hemianopia (both eyes)

Question 471

what is a bitemporal hemianopia generally caused by?

Answer 471

enlargement of benign pituitary gland tumour pressing on optic chiasma from above

Question 472

what is a homonymous hemianopia generally caused by?

Answer 472

stroke

cerebrovascular accidents in the brain

Question 473

when does contralateral homonymous hemianopia with macular sparing occur?

Answer 473

damage to the primary visual cortex due to stroke

Question 474

why does contralateral homonymous hemianopia with macular sparing occur?

Answer 474

area within primary visual cortex representing macula is well protected -
receives blood supply from both right and left posterior cerebral arteries

Question 475

what is the function of the pupil?

Answer 475

regulates light input to the eye

Question 476

what is pupillary constriction mediated by?

Answer 476

parasympathetic nerve within cranial nerve III

Question 477

what happens to the pupil in light conditions?

Answer 477

iris circular muscles contract, decreased pupil size (less light entering eye)

Question 478

what happens to the pupil in dark conditions?

Answer 478

iris radial muscles contract, pupil dilation (more light entering eye)

Question 479

why does the pupil contract in light conditions?

Answer 479

decreases spherical aberrations and glare

increases depth of field – near response triad

reduces bleaching of photo-pigments

Question 480

what is the afferent pathway of the pupillary reflex?

Answer 480

rod and cone photoreceptors synapsing on bipolar bells synapsing on retinal ganglion cells

pupil-specific ganglion cells exit at posterior third of optic tract before entering lateral geniculate nucleus

afferent pathway from each eye synapses on Edinger-Westphal nuclei on both sides in dorsal brainstem

Question 481

what is the efferent pathway of the pupillary reflex?

Answer 481

parasympathetic nerve (Edinger-Westphal nucleus) on brainstem (oculomotor nerve efferent)

synapses at ciliary ganglion on short posterior ciliary nerve

short posterior ciliary nerve directly innervates pupillary sphincter

Question 482

what does the pathway of the pupillary reflex mean?

Answer 482

only one eye needs to be stimulated with light to elicit pupillary constriction response in both eyes

afferent pathway on either side alone will stimulate efferent pathway on both sides

Question 483

what will a right afferent defect (e.g. damaged right optic nerve) in the pupillary reflex pathway cause?

Answer 483

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 484

what will a right efferent defect (e.g. damaged right 3rd nerve) in the pupillary reflex pathway cause?

Answer 484

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 485

what is the relative afferent pupillary defect?

Answer 485

damage to afferent pathway is usually incomplete, or relative

some degree of of pupillary constriction remains (albeit weaker response when damaged side is stimulated)

Question 486

how can a relative afferent pupillary defect be demonstrated?

Answer 486

swinging torch test – alternating stimulation of right and left eye with light

both pupils constrict when light swings to undamaged side

both pupils paradoxically dilate when light swings to damaged side

Question 487

why is eye movement necessary?

Answer 487

acquiring and tracking visual stimuli

Question 488

what is eye movement facilitated by?

Answer 488

six extraocular muscles innervated by the three cranial nerves (III, IV and VI)

Question 489

what is duction (eye movements)?

Answer 489

eye movement in one eye

Question 490

what is version (eye movements)?

Answer 490

simultaneous movement of both eyes in the same direction

dextroversion: both eyes looking right
levoversion: both eyes looking left

Question 491

what is vergence (eye movements)?

Answer 491

movement of both eyes in opposite directions

convergence: simultaneous adduction (inward) movement in both eyes when viewing a near object as part of near response triad

Question 492

what is saccade?

Answer 492

short fast burst eye movement (up to 900 degrees per second)

Question 493

what are the different types of saccade?

Answer 493

reflexive saccade to external stimuli (acquired new target)

scanning saccade (e.g. when reading)

predictive saccade to track objects

memory-guided saccade (absence of external stimuli)

Question 494

what is smooth pursuit?

Answer 494

slow sustained eye movement (up to 60 degrees per second)

involuntary movement, driven by motion of moving target across retina

Question 495

which extraocular muscles allow straight movement?

Answer 495

superior, inferior, lateral, medial rectus

Question 496

where do the extraocular muscles come from?

Answer 496

all except inferior oblique come from a cone in the back of the orbit

inferior oblique comes in nasally

Question 497

how does the superior rectus move the eye?

Answer 497

upwards

Question 498

how does the inferior rectus move the eye?

Answer 498

downwards

Question 499

how does the lateral rectus move the eye?

Answer 499

towards the outside of the head (towards temple)

Question 500

how does the medial rectus move the eye?

Answer 500

towards the middle of the head (towards the nose)

Question 501

how is the superior oblique arranged?

Answer 501

attached high on temporal side of eye

passes under superior rectus

travels through the trochlea

Question 502

how does the superior oblique move the eye?

Answer 502

diagonal pattern (down and out)

Question 503

how is the inferior oblique arranged?

Answer 503

attached low on nasal side of eye.

passes over inferior rectus

Question 504

how does the inferior oblique move the eye?

Answer 504

diagonal pattern (up and out)

Question 505

what does the superior branch of the third cranial nerve innervate?

Answer 505

superior rectus – elevates eye

levator palpebrae superioris

Question 506

what does the inferior branch of the third cranial nerve (oculomotor) innervate?

Answer 506

inferior rectus - depresses eye

medial rectus – adducts eye

inferior oblique – elevates eye

parasympathetic nerve – constricts pupil

Question 507

what does the fourth cranial nerve (trochlear) innervate?

Answer 507

superior oblique – depresses eye

Question 508

what does the sixth cranial nerve (abducens) innervate?

Answer 508

lateral rectus - abducts eye

Question 509

how is eye movement tested?

Answer 509

isolate muscle to be tested by maximizing its action and minimizing the action of other muscles

lateral rectus - abducted

medial rectus - adducted

superior rectus - elevated and abducted

inferior rectus - depressed and abducted

inferior oblique - elevated and adducted

superior oblique - depressed and adducted

Question 510

how can upwards, downwards, inwards, outwards and rotating movements of the eye be described?

Answer 510

elevation

• supraduction – one eye
• supraversion – both eyes

depression

• infraduction – one eye
• infraversion – both eyes

right movement – dextroversion

• right abduction
• left adduction

left movement– levoversion

• right adduction
• left abduction

torsion – rotation of eye around its anterior-posterior axis

Question 511

what does third nerve (oculomotor) palsy cause?

Answer 511

unopposed action of lateral rectus and superior oblique (causes eye to stay down and out)

ptosis (eyelid drooping) - levator palpabrae superioris loses innervation

Question 512

what does sixth nerve (abducens) palsy cause?

Answer 512

lateral rectus loses innervation

affected eye cannot abduct, deviates inwards

double vision worsens on gazing to side of affected eye

Question 513

what is nystagmus?

Answer 513

oscillatory movement of the eye (physiological or pathological)

Question 514

what is optokinetic nystagmus?

Answer 514

physiological nystagmus

triggered by the presentation of a constantly moving grating pattern

eyes track along the grating motion,
with smooth pursuit up to a limit,
and resets the eye position to the centre,
with a burst of fast saccade motion

results in cycles of slow phase smooth pursuit,
alternating with fast phase reset saccade in the opposite direction

Question 515

why is optokinetic nystagmus useful?

Answer 515

testing pre-verbal children visual acuity

observe nystagmus movement in response to moving grating patterns of various spatial frequencies

presence of opto-kinetic nystagmus signifies that the subject has sufficient visual acuity to perceive the grating

Question 516

what are the features of a migraine disorder?

Answer 516

tendency to repeated attacks

triggers

easily hung-over

visual vertigo

motion sickness

Question 517

what are the 3 forms of attack of a migraine disorder?

Answer 517

pain

focal symptoms

both pain and focal symptoms

Question 518

what are the 5 phases of a migraine?

Answer 518

prodrome

aura

headache

resolution

recovery

(about 48 hours in total)

Question 519

what happens in the prodrome phase of a migraine?

Answer 519

changes in mood

changes in urination and fluid retention

food craving

yawning

Question 520

what happens in the aura phase of a migraine?

Answer 520

visual, sensory (numbness/paraesthesia)

weakness

speech arrest

Question 521

what happens in the headache phase of a migraine?

Answer 521

head and body pain

nausea

photophobia

Question 522

what happens in the resolution phase of a migraine?

Answer 522

rest and sleep

Question 523

what happens in the recovery phase of a migraine?

Answer 523

mood disturbed

food intolerance

feeling hungover

Question 524

how do positive and negative symptoms together during the aura phase of a migraine present?

Answer 524

scintillations

blindspot

Question 525

what things are seen by the patient during the aura phase of a migraine?

Answer 525

expanding ‘C’s’

elemental visual disturbance

Question 526

how is an acute migraine attack treated?

Answer 526

hit the headache hard and fast

aspirin/ibuprofen (non-steroidals)

paracetamol, metoclopramide (anti-emetic)
(soluble preparations to aid absorption
Triptans-tablets, melts, nasal sprays, s/c injections (vasoconstrictors), synergise with NSAIDS)

(be wary of analgesic abuse potential with opiates)

short nap

TMS - interrupts complex networks that trigger and perpetuate migraine, which is caused by spreading electrical depression across the cerebral cortex

Question 527

what are the lifestyle issues caused by migraines?

Answer 527

migraineurs have sensitive heads even in between attacks

over-react to any sort of stimulation

can’t ignore the world around them, it overstimulates their brains

Question 528

how can environmental issues that trigger migraines be controlled?

Answer 528

(dietary, environmental, hormonal, weather, dehydration, stress)

drink 2 litres water/day

avoid caffeinated drinks

don’t skip meals

fresh food- avoid ready meals, take-aways

don’t oversleep or have late nights (electronics downstairs)

be aware of potential for analgesic abuse

Question 529

what are the prophylactic methods of controlling migraines?

Answer 529

over-the-counter preparations: feverfew, coenzyme Q10, riboflavin, magnesium, EPO, nicotinamide

tricyclic antidepressants (TCAs): amitriptyline 7pm

beta-blockers - Propranolol, Atenolol

serotonin antagonists: pizotifen, methysergide

calcium channel blockers: flunarazine, verapamil

anticonvulsants: valproate, topiramate, gabapentin

greater occipital nerve blocks

Botox: crown of thorns

suppress ovulation (progesterone only pill or implant/injection)

Question 530

how is erenumab used as a prophylactic for migraines?

Answer 530

used for episodic migraine, chronic migraine, or cluster headache

injectable (also known as Aimovig)

cut number of days people had migraines from an average of 8 a month to 4-5 a month

monoclonal antibody
disables calcitonin gene-related peptide or its receptor (CGRP mAbs)

Question 531

what is a tension type headache?

Answer 531

tight muscles around head and neck bilaterally, as though head is in a vice

Question 532

how is a tension type headache treated?

Answer 532

NSAIDs preferred:
(ibuprofen, naproxen, diclofenac)

paracetamol

tricyclic antidepressants: amitriptyline 50-75mg daily, 30-60% derive some symptomatic relief

SSRI’s probably less effective

biofeedback and relaxation unproven

Question 533

what is a cluster headache?

Answer 533

severe unilateral pain lasting 15-180 minutes untreated

classified as a trigeminal autonomic cephalgia

Question 534

what is needed for a headache to be classed as a cluster headache? what are the symptoms?

Answer 534

at least one of the following, ipsilaterally:

• conjunctival redness and/or lacrimation
• nasal congestion and/or rhinorrhoea
• eyelid oedema

forehead and facial sweating

miosis and/or ptosis

sense of restlessness or agitation

frequency between one on alternate days to 8 per day.

not associated with a brain lesion on MRI

Question 535

how is an acute cluster headache treated?

Answer 535

inhaled oxygen (oxygen inhibits neuronal activation in trigeminocervical complex)

S/C or nasal sumatriptan

Question 536

what drugs are used to prevent a cluster headache?

Answer 536

verapamil

prednisolone

lithium

valproate

gabapentin

topiramate

pizotifen

Question 537

what is the difference in distribution between migraines and cluster headaches?

Answer 537

migraine - 33% men, 67% women

cluster headache - 90% men, 10% women

Question 538

what is the difference in duration between migraines and cluster headaches?

Answer 538

migraine - 3-12 hours

cluster headache - 45min – 3 hours

Question 539

what is the difference in frequency between migraines and cluster headaches?

Answer 539

migraine - 1-8 attacks monthly

cluster headache - 1-3 attacks daily (often at night)

Question 540

what is the difference in remission between migraines and cluster headaches?

Answer 540

migraine - long remissions unusual

cluster headache - long remissions common

Question 541

what is the difference in nausea between migraines and cluster headaches?

Answer 541

migraine - nausea, vomiting frequent

cluster headache - nausea rare

Question 542

what is the difference in pain between migraines and cluster headaches?

Answer 542

migraine - pulsating hemicranial pain

cluster headache - steady, exceptionally severe, well localised pain, unilateral in each cluster

Question 543

what is the difference in symptoms between migraines and cluster headaches?

Answer 543

migraine - visual or sensory auras seen

cluster headache - eye waters, nose blocked, ptosis etc

Question 544

what is the difference in activity between migraines and cluster headaches?

Answer 544

migraine - patients lie in the dark

cluster headache - patients pace about

Question 545

what is the commonest cause of dementia?

Answer 545

Alzheimer’s disease

Question 546

what characterisis dementia?

Answer 546

fatal neurodegenerative disorder

progressive social, cognitive and functional impairment

Question 547

what is the best treatment possible for dementia at present?

Answer 547

acetylcholinesterase inhibitors

modest symptomatic benefit in early stages (1-2 years)

Question 548

what are newer methods that allow diagnosis of dementia in life?

Answer 548

PET imaging, structural imaging

CSF and plasma markers

Question 549

what is the difference between young onset and later onset dementia?

Answer 549

cut off age of 65 yrs

Question 550

what usually causes familial Alzheimer’s disease?

Answer 550

APP (amyloid precursor protein) or presenilin mutations

Question 551

what is the difference in the types of dementia between young onset and late onset sufferers?

Answer 551

‘rarer’ forms (vascular, frontotemporal, Lewy body, other) account for a greater percentage (70%) than Alzheimer’s in young onset

Question 552

what are some potentially reversible factors that may lead to depression?

Answer 552

depression - cognitive issues can be reversed

alcohol related brain damage - subtle hippocampal vulnerability to more serious things

endocrine (hypothyroidism, Cushing’s, Addison’s)

B1/B12/B6 deficiency - can be supplemented

benign tumours

normal pressure hydrocephalus

infections (HIV/syphilis, Whipple’s disease)

limbic encephalitis (paraneoplastic/autoimmune)

inflammatory (vasculitis, MS, sarcoid)

Question 553

why can it be difficult to diagnose dementia in the clinic?

Answer 553

disease follows heterogenous course

old age - disease presentation is of multiple comorbidities, lots of mixed/uncertain pictures
e.g. patients with Alzheimer’s or sporadic late-onset Alzheimer’s also have hypertension, may also have diabetes, may have had a heart attack or vascular damage over their life

clinical history is paramount to see patient’s function and how they change

Question 554

what are some pathologies of the brain associated with dementia?

Answer 554

neuronal tau

Aβ

TDP-43

α-synuclein

parenchymal ischaemic changes

vessel wall pathology - e.g. cerebral amyloid angiopathy

Question 555

what is the clinical process of dealing with dementia?

Answer 555

referral (from GP, psychiatrist, psychologist, geriatrician)

history - includes clinical interview

examination

investigations

diagnosis

• Alzheimer’s
• vascular
• Lewy body
• frontotemporal
• depression
• delirium
• none

management

Question 556

what is the checklist to interview patients with suspected dementia?

Answer 556

memory

language

numerical skills

executive skills

visuospatial skills

neglect phenomena - part of progression

visual perception

route finding, landmark identification

personality and social conduct

sexual behaviour

eating

mood

motivation/apathy

anxiety, agitation - common in all dementias

delusions, hallucinations

activities in daily life

Question 557

why is it important to ask a potential dementia sufferer’s friends and family about their behaviour and mental state?

Answer 557

key feature of dementia - as it progresses, patient loses insight into the symptoms they inhibit

patients will not be able to volunteer information, person that sees them frequently is more aware of the difficulties

Question 558

why is asking about memory important in a potential dementia sufferer?

Answer 558

usually impaired, especially short term

what did you do today? what did you eat for lunch? can ask about recent events if they follow them

Question 559

why is asking about language important in a potential dementia sufferer?

Answer 559

not just speaking skills, also word finding difficulties

second language English? any deterioration? naming things in first language?

Question 560

why is asking about numerical skills important in a potential dementia sufferer?

Answer 560

ability to calculate, manage finances alone etc.

more vulnerable to exploitation, especially if no access to attorney or other support

Question 561

why is asking about executive skills and visuospatial skills important in a potential dementia sufferer?

Answer 561

narrow down dementia diagnosis (subtypes)

find out deficits caused
- e.g. visuospatial deficits in a rare form of Alzheimer’s called posterior cortical atrophy often present with road accidents - people back into other cars, don’t realise their visuospatial deficit

Question 562

why is asking about altered visual perception, route finding and landmark identification important in a potential dementia sufferer?

Answer 562

people may often wander

unfamiliar routes difficult to follow as dementia progresses

Question 563

why is asking about personality and social conduct important in a potential dementia sufferer?

Answer 563

must know how personality traits etc. were before symptoms started - gauge progression

Question 564

why is asking about sexual behaviour important in a potential dementia sufferer?

Answer 564

disinhibition

as Alzheimer’s progresses, frontotemporal dementia - more disinhibited behavioural phenotype

patients exhibit sexual behaviour that they may not have done before dementia

Question 565

why is asking about eating habits important in a potential dementia sufferer?

Answer 565

people may forget they have had meals etc.

if biological cognitive phenotype of depression, might be altering eating habits due to this and not dementia

(also applies to taking other medications)

Question 566

why is asking about mood important in a potential dementia sufferer?

Answer 566

treating depression if present - may restore some cognitive deficits

Question 567

why is asking about delusions and hallucinations important in a potential dementia sufferer?

Answer 567

patient often does not want to be challenged, very strongly held belief

delusions of theft common

type of hallucination (auditory, visual, somatic) important to distinguish type of dementia

• visual hallucinations, Lilliputian hallucinations - common in Lewy body dementia
• people, animals present can be distressing with alcohol related brain damage, alcohol dependence or withdrawal

Question 568

why is it important to ask about the chronology of each potential aspect of dementia?

Answer 568

if they are improving, it may not be a dementia process

potentially reversible causes

sudden or marked deterioration (subtle deterioration - Alzheimer’s, stepwise - vascular)

Question 569

what examinations are done in dementia testing?

Answer 569

neurological examination
- cranial nerve tests, upper and lower limb tests, focus tests, frontal lobe function)

mental state
- appearance, behaviour, speech, mood, thought form, perception, cognition, insight

Question 570

what investigations are done in dementia testing?

Answer 570

neuropsychological tests (MMSE, Addenbrooke’s Cognitive Exam - more memory focussed

bloods

MRI (bilateral medial temporal volume loss, hippocampal volume loss)

PET

Question 571

what blood tests are done in investigating dementia?

Answer 571

full blood count

inflammatory markers (anything that could affect cognition)

thyroid function

biochemistry, renal function

glucose

B12, folate

clotting (vitamin deficiency)

syphilis serology

HIV

Caeruloplasmin (other causes of dementia, rare)

Question 572

how does a PET scan work?

Answer 572

inject patient with contrast agent

travels to brain, lights up amyloid

corresponds with beta amyloid antibody immunohistochemistry

Question 573

how is dementia managed?

Answer 573

acetylcholinesterase inhibitors

watch and wait if unsure - ideally need to see successive deterioration over 6 months - 1 year

treat behavioural, psychological symptoms
- anti-depressants, anti-psychotics depending on patient’s distress

occupational therapy/social services

specialist therapy

Question 574

how can you differentiate between the different types of dementia to make a diagnosis?

Answer 574

rule out delirium (transience in consciousness, usually caused by infection) and depression

Alzheimer’s

• subtle, insidious amnestic/non-amnestic presentation
• amnestic visuospatial presentations (posterior cortical atrophy)

vascular

• related to cerebrovascular diseases with classic step-wise deterioration
• may have had multiple infarcts

Lewy body
- cognitive impairment before/within 1 year of Parkinsonian symptoms, visual hallucinations and fluctuating cognition
- high risk of falls
may have REM sleep disorder

frontotemporal dementia

• behaviour variant FTD
• may have REM sleep disorder
• semantic dementia
• non-fluent aphasia

rapidly progressing dementia

Question 575

what is the head-turning sign?

Answer 575

ask a potential dementia sufferer a direct question, they don’t have the answer or they are not sure

turn to person next to them (caregiver, friend etc.)

Question 576

what is episodic memory and what does it depend on?

Answer 576

memory for particular episodes in life

depends on medial temporal lobes, including hippocampus and entorhinal cortex

Question 577

what does the pathology of dementia depend on?

Answer 577

amyloid

tau

Question 578

what is Lewy body dementia generally caused by?

Answer 578

aggregation of alpha synuclein

Question 579

how can the different types of dementia be differentiated on an MRI?

Answer 579

preserved hippocampal volume in Lewy body (as compared to Alzheimer’s)

typically asymmetrical bilateral perisylvian atrophy in FTD

Question 580

how can frontotemporal dementia be assessed with genetic testing?

Answer 580

pathological expansion of C9orf72 gene

Question 581

what is meningitis?

Answer 581

inflammation of meninges caused by viral or bacterial infection

Question 582

what is encephalitis?

Answer 582

inflammation of the brain caused by infection or autoimmune mechanisms

Question 583

what is cerebral vasculitis?

Answer 583

inflammation of blood vessel walls (sometimes called angiitis)

Question 584

what is the blood brain barrier?

Answer 584

brain tissue protected from contents of bloodstream

Question 585

what is the basis of the blood brain barrier?

Answer 585

dense vascularisation of brain tissue

neurons are always close to capillaries - therefore capillaries very dense

capillaries form blood brain barrier

Question 586

what do the capillaries forming the blood brain barrier look like?

Answer 586

extensive tight junctions at the endothelial cell-cell contacts

Question 587

how does the structure of the capillaries forming the blood brain barrier allow it to carry out its function?

Answer 587

tight junctions between the endothelial cells lining the vessel

reduces any passive movement of solutes and fluid across capillary wall into the tissue

this allows blood brain barrier to control the exchange of these substances using specific membrane transporters to transport into and out of the CNS (influx and efflux transporters)

blood-borne infectious agents have reduced entry into CNS tissue - protection

Question 588

what other structures help maintain the structure of the blood brain barrier and the vessel wall?

Answer 588

basal lamina

other glial cells (particularly astrocytes)

Question 589

how can the blood brain barrier be broken down?

Answer 589

the endothelial cell lining the vessels can become disrupted

causes opening of the blood brain barrier here - contents of the blood (e.g. fibrinogen) can move into the parenchyma

fibrinogen moving into tissue causes glial cells to react

astrocytes retract, break down the blood brain barrier

basement membrane change - collagen disrupted, may build up

sclerosis of these vessels

Question 590

what can a breakdown of the blood brain barrier cause?

Answer 590

infection

Question 591

what are the symptoms of encephalitis?

Answer 591

initial:
- flu-like, with pyrexia and headache

within hours, days or weeks:

• confusion or disorientation
• seizures or fits
• changes in personality and behaviour
• difficulty speaking
• weakness or loss of movement
• loss of consciousness

Question 592

what are the most common causes of encephalitis?

Answer 592

viral infection

usually:

• Herpes Simplex
• measles
• Varicella (chickenpox)
• rubella

Question 593

what are some non-viral causes of encephalitis?

Answer 593

mosquito, tick and other insect bites

bacterial and fungal infections

trauma

autoimmune

Question 594

what treatments are used for encephalitis?

Answer 594

(depends on underlying cause)

antivirals (e.g. acyclovir) for viral infection

steroids - reduce inflammation

antibiotics/antifungals

analgesics

anti-convulsants (if risk of seizure)

ventilation if breathing is severely impaired

Question 595

what is multiple sclerosis?

Answer 595

auto immune demyelinating disease of CNS

intermittent - relapses linked to inflammatory activity

progression linked to neurodegeneration - deficits increase over time, fewer remissions

Question 596

what is the cellular pathology of multiple sclerosis?

Answer 596

inflammation - linked to relapses

demyelination

axonal loss - the longer you have the disease, the more the axon loss, the more the residual deficits

neurodegeneration causes progression

Question 597

why do the symptoms of multiple sclerosis vary?

Answer 597

MS is a random disorder - can affect white matter anywhere in CNS

amount and location of the damage vary

Question 598

what is perivascular cuffing?

Answer 598

perivascular accumulation of leukocytes seen in infectious, inflammatory, or autoimmune diseases

Question 599

what does perivascular cuffing look like in multiple sclerosis?

Answer 599

immune cells (usually CD3 T cells, CD20 B cells) cross blood brain barrier, form cuff around vessels

causes demyelination, inflammation

Question 600

what is meningitis?

Answer 600

irritation, inflammation and swelling of meninges

Question 601

what are the most common causes of meningitis?

Answer 601

usually bacterial

• meningococcal – (most common cause of bacterial meningitis in UK)
• pneumococcal
• haemophilus influenzae type b (Hib)
• streptococccal (main cause in newborns)

Question 602

what are some non-bacterial causes of meningitis?

Answer 602

viral - very rarely life-threatening

fungal

Question 603

what is an infection of the spinal cord known as?

Answer 603

meningitis (meninges cover spinal cord as well as brain)