neurology and neuroscience Flashcards

1
Q

what are the 4 main characteristics of the cerebral cortex?

A

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

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2
Q

what is the microscopic organisation of the cerebral cortex?

A

6 layers

(I closest to surface, VI deepest)

also columns

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3
Q

how are regions of the cortex classified?

A

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

often correlates with function

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4
Q

what are the functions of the frontal lobe?

A

regulate and initiate motor function

language

cognitive function - e.g planning

attention

memory

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5
Q

what are the functions of the parietal lobe?

A

sensation - touch, pain

sensory language aspects

spatial orientation and self perception

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6
Q

what are the functions of the occipital lobe?

A

visual input

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7
Q

what are the functions of the temporal lobe?

A

processing auditory information

emotions

forming memories

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8
Q

what are the functions of the limbic lobe?

A

learning

memory

emotion

motivation and reward

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9
Q

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

A

concerned with visceral sensations

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

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10
Q

what is grey matter (outside)?

A

neuronal cell bodies and glial cells

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11
Q

what is white matter(inside)?

A

Myelinated neuronal axons arranged in tracts

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

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12
Q

what are the 3 main types of white matter tract?

A

association, commissural and projection fibres

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13
Q

which cortical areas do association fibres connect?

A

connect areas within the same hemisphere

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14
Q

which cortical areas do commissural fibres connect?

A

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

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15
Q

which cortical areas do projection fibres connect?

A

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

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16
Q

what do short association fibres/U fibres connect?

A

adjacent cortical regions (usually same lobe)

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17
Q

what are the 4 types of long association fibres?

A

superior longitudinal fasciculus

arcuate fasciculus

inferior longitudinal fasciculus

uncinate fasciculus

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18
Q

what two lobes does the superior longitudinal fasciculus connect?

A

frontal and occipital

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19
Q

what two lobes does the arcuate fasciculus connect?

A

frontal and temporal

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20
Q

what two lobes does the inferior longitudinal fasciculus connect?

A

temporal and occipital

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21
Q

what two lobes does the uncinate fasciculus connect?

A

anterior frontal and temporal

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22
Q

what is the corpus callosum an example of?

A

commissural fibres (connects left and right hemispheres)

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23
Q

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

A

anterior commissure

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24
Q

how are projection fibres arranged?

A

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

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25
what is the function of afferent projection fibres?
bring information to brain from outside world via spinal cord and cortex sensory impulses
26
what is the function of efferent projection fibres?
take information out from the cortex down to brain stem, spinal cord and out motor impulses
27
what are the afferent and efferent projection fibres collectively known as?
corona radiata
28
what are the 3 differences between primary and secondary/association cortices?
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
29
what is the function of the primary motor cortex in the frontal lobe?
controls fine, discrete, precise voluntary movements provides descending signals to execute movements
30
what is the function of the supplementary cortex of the frontal lobe?
involved in planning movements (e.g. externally cued - the plan to move an arm to pick up an object, for example)
31
what is the function of the premotor cortex of the frontal lobe?
involved in planning complex movements (e.g. internally cued - the plan to co ordinate fibres to generate speech by making muscles contract, for example)
32
what is the function of the primary somatosensory cortex in the parietal lobe?
processes somatic sensations arising from receptors in the body (e.g. fine touch, vibration, two-point discrimination, proprioception, pain and temperature)
33
what is the function of the somatosensory association cortex in the parietal lobe?
interpret significance of sensory information, e.g. recognizing an object placed in the hand. Awareness of self and awareness of personal space
34
what is the function of the primary visual cortex in the parietal lobe?
processes visual stimuli - input from retina reaches here
35
what is the function of the visual association cortex in the parietal lobe?
gives meaning and interpretation of visual input
36
what is the function of the primary auditory cortex in the temporal lobe?
processes auditory stimuli
37
what is the function of the auditory association cortex in the temporal lobe?
gives meaning and interpretation of auditory input
38
what are the functions of the prefrontal cortex?
attention adjusting social behaviour planning personality expression decision making
39
where are Broca's and Wernicke's areas found?
left hemisphere only (association/secondary cortex)
40
what is the function of Broca's area?
production of language (motor region - i.e motor commands and movement to generate speech)
41
what is the function of Wernicke's area?
understanding of language (sensory region - i.e information about language is understood)
42
what may a frontal lobe lesion cause?
personality changes socially inappropriate behaviour
43
what may a parietal lobe lesion cause?
contralateral neglect lesion in right hemisphere causes lack of awareness of self and extrapersonal space on the left side
44
what are the 2 types of temporal lobe lesion?
lateral and medial
45
what may a temporal lobe lesion cause?
agnosia - inability to recognise things
46
what is the effect of a lesion to Broca's area?
expressive aphasia - poor production of speech, comprehension intact
47
what is the effect of a lesion to Wernicke's area?
receptive aphasia - poor comprehension of speech, production intact
48
what structure connects Broca's and Wernicke's areas?
arcuate fasciculus
49
what is the effect of a lesion on the primary visual cortex?
blindness in the corresponding part of the visual field
50
what is the effect of a lesion on the visual association cortex?
deficits in interpretation of visual information e.g. prosopagnosia: inability to recognise familiar faces or learn new faces (face blindness)
51
how can cortical function be assessed?
positron emission tomography (PET) functional magnetic resonance imaging (fMRI) electroencephalography/magnetoencephalography (EEG/MEG)
52
how does a positron emission tomography (PET) work?
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
53
how does functional magnetic resonance imaging (fMRI) work?
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
54
what is temporal resolution?
how quickly can it be ascertained that things are changing
55
what is spatial resolution?
how detailed a picture can be obtained at the level of individual cells vs groups of cells etc.
56
how does an EEG work?
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)
57
how does an MEG work?
measures magnetic signals produced by brain
58
where is an EEG often used and why?
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)
59
how are somatosensory evoked potentials used to assess cortical function?
stimulus to peripheral nerve series of waves that reflect sequential activation of neural structures along somatosensory pathways
60
when are somatosensory evoked potentials used to assess cortical function?
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
61
when are transcranial magnetic stimulations (TMS) used?
assess the functional integrity of neural circuits uses electromagnetic induction to stimulate neurons
62
how does a transcranial magnetic stimulation (TMS) work?
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
63
what conditions may transcranial magnetic stimulation (TMS) also be used to treat and why?
epilepsy tinnitus migraine depression all are associated with firing of cortical neurones - magnetic pulses can also modulate overactive brain regions by interfering with transmission
64
what is transcranial direct current stimulation (tDCS) and how does it work?
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
65
how can the structure of the brain be assessed?
diffusion tensor imaging (DTI) DTI with tractography
66
why is assessing brain structure important?
understanding connection between brain regions e.g if two linked regions are functioning individually but the pathway between them is damaged
67
how does diffusion tensor imaging (DTI) work?
based on diffusion of water molecules
68
what is diffusion tensor imaging (DTI) with tractography?
3D reconstruction to assess neural tracts
69
why is the brain vulnerable if blood supply is impaired?
high metabolic demands therefore extensive vascular supply needed for function (uses around 20% of all cardiac output, oxygen consumption, 2/3 of liver glucose)
70
what arteries supply the brain?
vertebral internal carotid
71
what is the path of the common carotid artery?
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)
72
what is the path of the internal carotid artery?
branches off from common carotid carries on with no branches, passes through base of skull (so-called carotid canal) and into cranial cavity
73
what is the path of the vertebral artery?
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
74
what is the arrangement of vessels at the base of the brain called?
circle of Willis, vessels are adjoined
75
what is the structure of the circle of Willis?
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
76
what is the advantage of the arrangement of the circle of Willis?
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
77
why is the advantage of the arrangement of the circle of Willis not always effective?
not universal compensation between posterior circulation and anterior circulation is often weak because posterior communicating arteries are very thin
78
how does blood exit the brain?
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
79
what is the structure of the dural sinuses?
dura mater is made up of two layers that are usually closely pressed together when these layers separate they form the venous sinuses
80
how does venous blood drain through the sinuses?
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
81
what are the 4 types of intercranial haemorrhage?
extradural subdural subarachnoid intracerebral
82
what causes extradural haemorrhage?
nearly always trauma main artery supplying dura is right behind pterion so trauma is likely to rupture this artery
83
what is the effect of an extradural haemorrhage?
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
84
why are subdural bleeds dangerous and how can the potential effects be prevented?
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
85
what causes subarachnoid haemorrhage?
circle of Willis has weaknesses in blood vessels called aneurysms (generally congenital) these may burst (especially if hypertensive) and produces subarachnoid bleed
86
people with which pre-existing condition are more at risk of intracerebral haemorrhage?
hypertension
87
what is an intracerebral haemorrhage?
bleed in substance of brain itself
88
what is the definition of a stroke/cerebrovascular accident?
rapidly developing focal disturbance of brain function of presumed vascular origin and of >24 hours duration
89
what are the two main types of stroke and how common are they?
thrombo-embolic (85%) haemorrhagic (15%)
90
what is the definition of a transient ischaemic attack (TIA)?
rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours
91
what is the definition of an infarction?
degenerative changes which occur in tissue following occlusion of an artery
92
what is the definition of cerebral ischaemia?
lack of sufficient blood supply to nervous tissue resulting in permanent damage if blood flow is not restored quickly
93
what could a transient ischaemic attack indicate?
risk of stroke further on
94
what is the difference between ischaemia and anoxia/hypoxia?
anoxia/hypoxia only refers to oxygen deficit in blood ischaemia refers to loss of all required metabolites in blood (e.g. glucose etc.)
95
what is thrombosis?
formation of a blood clot (thrombus)
96
what is an embolism?
plugging of small vessel by material carried from larger vessel e.g. thrombi from the heart or atherosclerotic debris from the internal carotid
97
what are the risk factors for stroke?
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)
98
what is the perfusion field of the middle cerebral artery?
much of the brain's lateral surface subcortical deep structures of the brain
99
what is the perfusion field of the anterior cerebral artery?
midline structures all the way back perfuses all the way back to parietal-occipital fissure
100
what is the perfusion field of the posterior cerebral artery?
occipital lobe inferior part of temporal lobe
101
why are perfusion fields important?
can judge where in the brain a stroke might have occurred
102
what symptoms indicate an anterior cerebral artery issue?
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)
103
what symptoms indicate a middle cerebral artery issue?
“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)
104
what symptoms indicate a posterior cerebral artery issue?
supply to occipital lobe is cut off so- homonymous hemianopia visual agnosia
105
what are the broad principles of motor control?
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)
106
what is functional segregation?
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
107
what are the 2 major descending tracts?
pyramidal extrapyramidal
108
what are the pathways of the pyramidal tracts?
pass through pyramids of medulla output neurones in motor cortex, project down to spinal cord or cranial nerve nuclei in brainstem
109
what are the 2 pyramidal tracts?
corticospinal corticobulbar`
110
what do the pyramidal tracts control?
voluntary movements of body and face
111
what are the pathways of the extrapyramidal tract?
do not pass through pyramids of medulla upper motor neurones in cortex, lower motor neurones in brainstem nuclei - project down to muscles
112
what do the extrapyramidal tracts control?
involuntary (automatic) movements for balance, posture and locomotion
113
what are the 4 extrapyramidal tracts?
vestibulospinal tectospinal reticulospinal ` rubrospinal
114
where is the primary motor cortex situated?
precentral gyrus, anterior to central sulcus
115
what does the primary motor cortex control?
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
116
where is the premotor area located?
anterior to primary motor cortex
117
what does the premotor area control?
involved in planning movements | regulates externally cued movements e.g. seeing an apple and reaching for it
118
where is the supplementary motor area located?
anterior and medial to primary motor cortex
119
what does the supplementary motor area control?
involved in planning complex movements (e.g. internally cued, speech) becomes active prior to voluntary movement
120
what is the pathway of the corticospinal tract?
upper motor neurones in primary motor cortex midbrain contains cerebral peduncle most fibres decussate, about 10% do not
121
what is the function of decussated fibres in the corticospinal tract?
make up lateral corticospinal tract responsible for limb muscle control
122
what is the function of non-decussated fibres in the corticospinal tract?
make up anterior corticospinal tract responsible for trunk muscle control
123
what is the main function of the corticobulbar tract?
principal motor pathway for voluntary movements of the face (and neck)
124
which nuclei control the function of extraocular muscles (corticobulbar tract)?
oculomotor trochlear abducens
125
which nuclei control the function of jaw muscles (muscles of mastication) (corticobulbar tract)?
trigeminal motor nucleus
126
which nuclei control the facial muscles (corticobulbar tract)?
facial
127
which nuclei control the tongue (corticobulbar tract)?
hypoglossal
128
what is the function of the vestibulospinal (extrapyramidal) tract?
stabilise head during body movements, or as head moves coordinate head movements with eye movements mediate postural adjustments
129
what is the function of the reticulospinal (extrapyramidal) tract?
(most primitive descending tract - from medulla and pons) changes in muscles tone associated with voluntary movement postural stability
130
what is the function of the tectospinal (extrapyramidal) tract?
(from superior colliculus of midbrain) orientation of the head and neck during eye movements
131
what is the function of the rubrospinal (extrapyramidal) tract?
(From red nucleus of midbrain - in humans mainly taken over by corticospinal tract) innervate lower motor neurons of flexors of the upper limb
132
what are the negative signs of an upper motor neurone lesion?
loss of voluntary motor function paresis: graded weakness of movements paralysis (plegia): complete loss of voluntary muscle activity
133
what are the positive signs of an upper motor neurone lesion?
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
134
what is apraxia?
disorder of skilled movement patients are not paretic but have lost information about how to perform skilled movements
135
disease of which areas (including stroke and dementia) can cause apraxia?
inferior parietal lobe frontal lobe (premotor cortex, supplementary motor area - SMA)
136
what are the effects of a lower motor neurone lesion?
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
137
what is motor neurone disease (MND)/amyotrophic lateral sclerosis (ALS)?
progressive neurodegenerative disorder of motor system - affects both upper and lower motor neurones
138
which muscles have trouble contracting in motor neurone disease (MND)?
tongue intercostal muscles - eventual death caused by lack of respiratory function upper and lower limb
139
what are the upper motor neurone signs of motor neurone disease?
spasticity (increased tone of limbs and tongue) brisk limbs and jaw reflexes Babinski’s sign loss of dexterity dysarthria (difficulty speaking) dysphagia (difficulty swallowing)
140
what are the lower motor neurone signs of motor neurone disease?
weakness muscle wasting tongue fasciculations and wasting nasal speech dysphagia
141
what are the structures that make up the basal ganglia?
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)
142
what are the functions of the basal ganglia?
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
143
what causes Parkinson's disease?
degeneration of dopaminergic neurons originating in the substantia nigra and projecting to the striatum
144
what are the symptoms of Parkinson's disease?
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
145
what causes Huntington's disease?
degeneration of GABAergic neurons in the striatum, caudate and then putamen chromosome 4, autosomal dominant CAG repeat
146
what are the symptoms of Huntington's disease?
``` 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
147
what is ballism?
sudden uncontrolled flinging of the extremities usually from stroke affecting the subthalamic nucleus symptoms occur contralaterally
148
what are the functions of the vestibulocerebellum?
regulation of gait, posture and equilibrium coordination of head movements with eye movements
149
what does damage (tumour) to the vestibulocerebellum cause?
syndrome similar to vestibular disease leads to gait ataxia, tendency to fall (even when patient sitting and eyes open)
150
what are the functions of the spinocerebellum?
coordination of speech adjustment of muscle tone coordination of limb movements
151
what does damage (degeneration and atrophy associated with chronic alcoholism) to the spinocerebellum cause?
affects mainly legs causes abnormal gait and stance (wide-based)
152
what are the functions of the cerebrocerebellum?
coordination of skilled movements cognitive function attention processing of language emotional control
153
what does damage to the cerebrocerebellum cause?
affects mainly arms/skilled coordinated movements (tremor) speech
154
what are the main signs of cerebellar dysfunction?
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
155
what is an alpha motor neuron?
lower motor neuron of brainstem and spinal cord occupy anterior/ventral horn of grey matter of spinal cord
156
what is the function of alpha motor neurons?
innervate extrafusal muscle fibres (fibres with contractile elements) of skeletal muscles (i.e. activation causes muscle contraction)
157
what is a motor neuron pool?
contains all alpha motor neurons innervating a single muscle
158
what are the intrafusal muscle fibres?
contain sensory organs which respond to stretch and tension within the muscle - convey information about sensitivity to bring about reflex activity
159
what is a motor unit?
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
160
what are the 3 types of motor unit?
slow (S, type I) fast, fatigue resistant (FR, type IIa) fast, fatigable (FF, type IIb)
161
what are the characteristics of a slow motor unit?
smallest diameter cell bodies small dendritic trees thinnest axons slowest conduction velocity
162
what are the characteristics of a fast motor unit (both fatigue resistant and fatigable?
larger diameter cell bodies larger dendritic trees thicker axons faster conduction velocity
163
how are the 3 different types of motor unit classified?
amount of tension generated speed of contraction fatigability
164
what is the difference between the response to single motor neuron action potential between the 3 types of motor unit?
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
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?
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)
166
where would a slow motor unit be found? why?
muscles used for postural stability no need to generate large amounts of force, but need to maintain maximal force for many hours
167
where would a fast motor unit be found? why?
gastrocnemius (calf) can generate a lot of force quite quickly
168
what are the two mechanisms by which the brain regulates the force that a single muscle can produce?
recruitment rate coding
169
how does recruitment work in regulating muscle force?
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
170
how does rate coding work to regulate muscle force?
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
171
what is a neurotrophic factor?
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)
172
how can it be determined that the motor neurone has some effect on the properties of the muscle fibres that it innervates?
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
173
what is the most common change from one type of neurone to another?
IIB to IIA (fast fatigue to fatigue resistant) most common following training
174
when is a change from a type I neurone to a type II neurone possible?
in cases of severe deconditioning or spinal cord injury microgravity during spaceflight results in shift from slow to fast muscle fibre types
175
what kind of change in motor units/muscle fibres occurs during the ageing process?
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)
176
what is a reflex?
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
177
how do reflexes differ from voluntary movements?
cannot be stopped once they are released
178
what is the path of the monosynaptic (stretch) reflex?
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
179
what is the Jendrassik manoeuvre?
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
180
why is the Jendrassik manoeuvre important?
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
181
what is the role of higher centres of the CNS in the stretch reflex?
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
182
what can cause an overactive or tonic stretch reflex?
brain damage causes rigidity and spasticity
183
what is the pathway of descending (supraspinal) control of reflexes?
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
184
what is hyper-reflexia?
overactive reflexes loss of descending inhibition (associated with loss of voluntary movement) associated with upper motor neuron lesions
185
what is clonus in hyper-reflexia?
involuntary and rhythmic muscle contraction loss of descending inhibition associated with upper motor neuron lesions
186
what is Babinski's sign (hyper-reflexia)?
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
187
what is hypo-reflexia?
below normal or absent reflexes associated with lower motor neuron disease
188
what are gamma motor neurones?
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
189
where is the ear located?
embedded in petrous portion of temporal bone (hardest in body)
190
what are the functions of the outer ear?
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
191
what does the outer ear consist of?
pinna external auditory canal`
192
what are the functions of the middle ear?
(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
193
what makes up the middle ear?
tympanic membrane to oval window ossicles - articulated with each other to allow transmission of sound to inner ear
194
what makes up the inner ear?
cochlea
195
what are the functions of the inner ear?
transduces vibration into nervous impulses simultaneously produces frequency and intensity analysis of the sound
196
what are the 3 compartments of the cochlea?
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)
197
what is the structure of the scala vestibuli and the scala tympani?
bone structures contain perilymph (high in sodium)
198
what is the structure of the scala media?
membranous structure contains endolymph (high in potassium) hearing organ/organ of Corti located here
199
where is the structure where the organ of Corti lies?
basilar membrane
200
how is the basilar membrane of the ear arranged?
tonotopically i.e. sensitive to different frequencies at different points along its length high frequencies near base, low frequencies near apex
201
what are the 2 types of hair cells in the organ of Corti?
inner hair cells (IHC) outer hair cells (OHC)
202
how are the inner and outer hair cells arranged in the organ of Corti?
IHC arranged on 1 column OHC arranged on 3 columns
203
how does the tectorial membrane interact with inner and outer hair cells in the organ of Corti?
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
204
what is the function of the inner hair cells (IHC) in the organ of Corti?
transduction of sound into nerve impulses carry 95% of afferent information of auditory nerve
205
what is the function of the outer hair cells (OHC) in the organ of Corti?
modulation of the sensitivity of the response carry 95% of efferent information of auditory nerve
206
how does transduction work in the auditory system?
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)
207
what is the structure of the auditory pathways?
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
208
how is hearing organised (central auditory pathways)?
tonotopically organised
209
what is frequency?
pitch (Hz) cycles per second, perceived tone
210
what is amplitude?
loudness (dB) sound pressure, subjective attribute correlated with physical strength
211
why is the decibel scale useful in measuring the amplitude of sounds?
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)
212
how does hearing change with age?
hearing acuity decreases with age, (particularly higher frequencies) medium and low frequencies could be affected with the progression of hearing loss
213
what are the aims of a hearing assessment?
determine: is there a hearing loss? - of what degree? - of what type?
214
what procedures are used in a hearing assessment?
tuning fork audiometry central processing assessment tympanometry otoacustic emission electrocochleography evoked potentials
215
how is a tuning fork used in a hearing assessment?
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:
216
how is pure tone audiometry (PTA) used in a hearing assessment?
science of measuring hearing acuity for variations in sound intensity and frequency audiometer: device used to produce sound of varying intensity and frequency
217
what is an audiogram?
graph plotting hearing thresholds to determine if there is hearing loss (normal threshold: 0 - 20 dB)
218
how is a central processing assessment used in a hearing assessment?
assessment of hearing abilities other than detection using verbal and non-verbal tests e.g. sound localization, filtered speech, speech in noise
219
how is tympanometry used in a hearing assessment?
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
220
how are otoacoustic emissions (OAEs) used in a hearing assessment?
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)
221
how are auditory evoked potentials used in a hearing assessment?
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. ```
222
what is the auditory brainstem response and how is it used in a hearing assessment?
electrical responses from the auditory pathway (often used in babies and children) alterations in latency of waves can point to location of the deficit
223
what would affect cortical potentials?
neurological conditions processing problems
224
what are the 2 types of hearing loss?
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)
225
how is the degree of hearing loss classified?
mild - profound
226
what are the causes of outer ear conductive hearing loss?
wax foreign body
227
what are the causes of middle ear conductive hearing loss?
otitis otosclerosis
228
what are the causes of inner ear sensorineural hearing loss?
presbycusis ototoxicity
229
what are the causes of nerve sensorineural hearing loss?
VIII tumour
230
what treatments are available for hearing loss?
treat cause hearing aids cochlear implants brainstem implants
231
how do hearing aids work in treating hearing loss?
amplify the sound, does not replace any structure
232
how do cochlear implants work in treating hearing loss?
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)
233
how do brainstem implants work in treating hearing loss?
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
234
what are the 3 main inputs of the vestibular system?
visual proprioceptive vestibular
235
what are the outputs of the vestibular system?
ocular reflex (maintain stable gaze) postural control (maintain stable posture) (unwanted output: nausea)
236
what are the inputs of the vestibular system?
visual (eye) rotation and gravity (inner and middle ear) pressure (feet)
237
how do the inputs generate the outputs in the vestibular system?
CNS integrates input information and generates the responses
238
where is the vestibular organ located?
posterior area of inner ear inner ear contains hair cells for hearing and balance
239
where are the utricle and saccule located?
vestibule joined by a conduit saccule is also joined to the cochlea
240
how are the semi-circular canals arranged?
three semi-circular canals on each ear (anterior, posterior, lateral) have an ampulla on one side, and they are connected to the utricle
241
what is the labyrinth in the skull?
superior projection of right bony labyrinth on base of skull
242
why is the location of the vestibular organ important?
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
243
what is the structure of vestibular hair cells?
have a kinocilium (the biggest cilium) and stereocilia
244
what is the function of the cilia on vestibular hair cells?
cilia allows the cells to depolarise the cell with movement of the endolymph generated by head movement
245
what are the the otolith organs?
utricle and saccule
246
where are the cells of the otolith organs located?
on the maculae placed horizontally in the utricle placed vertically in the saccule
247
what is the structure of the maculae?
contain the hair cells gelatinous matrix otoliths on top
248
what are otoliths?
carbonate crystals that help the deflection of the hairs
249
what is the structure of the semi-circular canals of the ear?
hair cells in the canals are located in ampulla rest of the canal only has endolymph (high potassium)
250
what is the structure of the ampulla?
has crista where hair cells are located cells surrounded by cupula (helps hair cell movement)
251
how are the semi-circular canals oriented?
defines 3 planes anterior and posterior form a 90° angle lateral is horizontal to other canals
252
where do vestibular nuclei have projections to?
spinal cord (postural control) nuclei of the extraocular muscles (eye movement) cerebellum (feedback) centres for cardiovascular + respiratory control
253
where do the primary afferents in the vestibular system end?
vestibular nuclei cerebellum
254
which vestibular nuclei are associated with the ventroposterior nucleus and vestibular cortex?
superior and lateral
255
which vestibular nuclei are associated with the vestibulospinal reflexes?
lateral, medial, inferior
256
what are the 3 reflexes produced by vestibular pathways?
vestibulo-ocular reflex (VOR) vestibulocerebellar reflexes vestibulospinal reflexes
257
where is the vestibular cortex located?
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))
258
what does the vestibular physiology look like?
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
259
what are the functions of the vestibular system?
to detect and inform about head movements to keep images fixed in the retina during head movements postural control
260
how do hair cells alter potential?
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
261
how do the otolith organs work?
linear acceleration and tilt cause otolith movement and therefore detection utricle - horizontal movement saccule - vertical movement
262
how do the semi-circular canals work?
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
263
how does the vestibulo-ocular reflex (VOR) work?
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
264
how does the vestibulo-spinal reflex (VSR) work?
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
265
how is the vestibular system assessed?
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
266
what is the main symptom of a balance disorder?
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
267
what are some peripheral vestibular disorders (labyrinth and/or VIII nerve)?
vestibular neuritis benign paroxysmal positional vertigo (BPPV) Meniere’s disease unilateral and bilateral vestibular hypofunction
268
what are some central vestibular disorders (CNS - brainstem/cerebellum)?
stroke MS tumour
269
what are 2 examples of an acute balance disorder?
vestibular neuritis ('labyrinthitis') stroke
270
what is an example of an intermittent balance disorder?
Benign Paroxysmal Positional Vertigo (BPPV)
271
what are 2 examples of a recurrent balance disorder?
Meniere's disease migraine
272
what are 2 examples of a progressive balance disorder?
schwannoma vestibular (VIIIth nerve) degenerative conditions (MS)
273
what are some non-vestibular causes of dizziness?
heart disorders presyncopal episodes orthostatic hypotension anaemia hypoglycaemia psychological gait disorders
274
what are the bases for a headache?
structural (not just brain, could be scalp, skull, meninges, spinal fluid, blood vessels, eyeballs, ear apparatus, veins etc.) pharmacological psychological
275
what are some things that may cause an acute single headache?
febrile illness, sinusitis first attack of migraine following a head injury subarachnoid haemorrhage meningitis tumour drugs toxins stroke thunderclap (sudden onset), low pressure
276
what are some things that may cause a dull headache, increasing in severity?
(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
277
what are some things that may cause a dull headache, unchanged over months?
chronic tension headache depressive, atypical facial pain
278
what are some things that may cause a triggered headache?
coughing, straining, exertion coitus food and drink
279
what are some things that may cause a recurrent headache?
migraine cluster headache episodic tension headache trigeminal or post-herpetic neuralgia
280
what are the red flags associated with onset of a headache?
"thunderclap" headache (like patient has been struck by thunder or lightning suddenly) acute subacute
281
what are the red flags associated with meningism?
photophobia phonophobia stiff neck vomiting
282
what are red flag systemic symptoms that may occur in conjunction with a headache?
fever rash weight loss
283
what are red flag neurological symptoms/focal signs that may occur in conjunction with a headache?
visual loss confusion seizures hemiparesis double vision (focal sign) 3rd nerve palsy (focal sign - droopy eyelid) Horner syndrome (focal sign) papilloedema
284
what are some red flags for a headache in general?
orthostatic (better lying down strictly unilateral
285
what are the signs of a subarachnoid silhouette?
sudden generalised headache - "blow to the head" meningism - stiff neck and photophobia
286
what causes a subarachnoid haemorrhage?
most caused by a ruptured aneurysm a few from arteriovenous malformations some are unexplained
287
how are subarachnoid haemorrhages treated?
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
288
how are aneurysms treated?
filled with platinum coils used to be clipped or wrapped
289
how are aneurysms treated?
filled with platinum coils used to be clipped or wrapped
290
what is an acute intracerebral bleed?
fatal haemorrhage due to coning | mechanism of coning - raised intracranial pressure (ICP)
291
what is papilloedema?
optic disc swelling due to raised intracranial pressure
292
how likely is a carotid and vertebral artery dissection to lead to stroke?
20% of ischaemic strokes under 45 years old mean age 40 - carotid > vertebral
293
how is a carotid and vertebral artery dissection diagnosed?
headache and neck pain MRI/MRA Doppler angiography (test if traumatic vs. spontaneous)
294
how is a carotid and vertebral artery dissection treated?
aspirin or anticoagulation
295
what are the symptoms of temporal arteritis?
(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
296
how is temporal arteritis treated?
high dose steroids aspirin
297
what is cerebral venous thrombosis?
thrombosis in dural venous sinus or cerebral vein
298
what can cause cerebral venous thrombosis?
non-territorial ischaemia “venous infarcts” haemorrhage thrombophilia pregnancy dehydration Behcets
299
what causes headaches in cerebral venous thrombosis?
raised ICP
300
what can cause viral meningitis?
coxsackie ECHO mumps EBV
301
what can cause bacterial meningitis?
Meningococci Pneumococci Haemophilus tuberculous
302
what can cause fungal meningitis?
Cryptococci
303
what can cause granulomatous meningitis?
sarcoid Lyme Brucella Behcet's syphilis
304
what are the types of meningitis?
viral bacterial fungal tuberculous granulomatous carcinomatous
305
what are the presenting symptoms of meningitis?
malaise headache fever neck stiffness photophobia confusion alteration of consciousness
306
what is herpes simplex encephalitis?
classic haemorrhagic changes in temporal lobes
307
how is meningitis treated?
(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
308
what does bacterial meningitis look like?
cerebral oedema effacement of ventricles and sulci inflamed meninges
309
what are the symptoms of sinusitis?
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
310
brain tumour
glioblastoma multiforme
311
what demographic often suffers from pseudotumour cerebri?
young obese women
312
what are the symptoms of a pseudotumour cerebri?
headache visual obscurations diplopia tinnitus papilloedema with or without visual field loss
313
what drugs are used in pseudotumour cerebri?
hormones steroids antibiotics vitamin E
314
what treatments are needed for pseudotumour cerebri?
weight loss diuretics optic nerve sheath decompression lumboperitoneal shunt stenting of stenosed venous sinuses
315
what does raised intracranial pressure look like on an MRI?
cerebral oedema effacement of ventricles and sulci no mass lesion
316
what can cause a low pressure headache?
CSF leak due to tear in dura traumatic (post-lumbar puncture) or spontaneous
317
how can a low pressure headache be identified on an MRI?
meningeal enhancement
318
how is a low pressure headache treated?
rehydration caffeine blood patch
319
what is a Chiari malformation?
brain sits low within skull
320
how does a Chiari malformation cause triggered headaches?
cerebellar tonsils descending through foramen magnum descend further when patient coughs - tugs on the meninges causing cough headache
321
what are the signs of obstructive sleep apnoea?
often characteristic body habitus history of loud snoring and apnoeic spells hypoxia, CO2 retention non-refreshing sleep depression impotence poor performance at work
322
how is obstructive sleep apnoea treated?
require sleep study nocturnal NI surgery
323
what is trigeminal neuralgia?
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.
324
what causes trigeminal neuralgia?
neurovascular conflict at the point of entry of the nerve into the pons
325
how is trigeminal neuralgia treated?
carbamazepine lamotrigine gabapentin posterior fossa decompression
326
what are the symptoms of atypical facial pain?
(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)
327
how is atypical facial pain treated?
unresponsive to conventional analgesics, opiates and nerve blocks mainstay of management tricyclics
328
how likely is a post traumatic headache?
depends on nature of injury - high in victims of car accidents - low in perpetrators of car accidents - low in sports injuries
329
what are the mechanisms that may cause post traumatic headache?
neck injury scalp injury vasodilation - autonomic damage depression - often delayed
330
how is a post traumatic headache managed?
explain, prevent analgesic abuse non-steroidal anti-inflammatories - ibuprofen, naproxen tricyclic antidepressants - Amitriptyline will take 3-4 years
331
what causes cervical spondylosis?
narrowing of joint space due to worn disk commonest cause of new headache in older patients
332
what are the characteristics of a headache caused by cervical spondylosis?
usually bilateral occipital pain can radiate forwards to the frontal region steady pain no nausea or vomiting worsened by moving the neck
333
how is a headache caused by cervical spondylosis treated?
rest, deep heat, massage anti-inflammatory analgesics (NB over-manipulation may be harmful)
334
what are the 3 types of tears?
basal reflex emotional
335
where is the lacrimal gland located?
within orbit latero-superior to globe
336
what are basal tears?
lacrimal gland produces tears at a constant level (even in the absence of irritation or stimulation)
337
what are reflex tears?
refers to increased tear production in response to ocular irritation
338
what makes up the tear reflex pathway?
afferent pathway (cornea, cranial nerve V1, ophthalmic trigeminal) CNS efferent (parasympathetic nerve) lacrimal gland
339
how is the cornea innervated?
sensory nerve fibres via ophthalmic branch of trigeminal nerve
340
how are tears produced?
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
341
what are the functions of the tear film?
maintains smooth cornea-air surface source of oxygen and nutrient supply to the anterior segment (normal cornea has no blood vessels) bactericide
342
why is a smooth cornea-air surface important?
maintaining clear vision removing surface debris during blinking
343
what are the 3 layers of the tear film?
lipid layer (superficial) aqueous layer (forms bulk of film) mucinous (deep)
344
how is the lipid layer of the tear film formed?
secreted by Meibomian Glands (situated along the eyelid margins)
345
what is the function of the lipid layer of the tear film?
responsible for protecting the tear film from rapid evaporation
346
what are the functions of the aqueous layer of the tear film?
delivers oxygen and nutrient to surrounding tissue contains factors against potentially harmful bacteria (bactericide)
347
what is the function of the mucinous layer of the tear film?
ensures that tear film sticks to the eye surface maintains surface wetting
348
how does the mucinous layer of the tear film carry out its function?
mucin molecules act by binding water molecules to hydrophobic corneal epithelial cell surface
349
what is the conjunctiva?
thin, transparent tissue that covers eye's outer surface nourished by tiny blood vessels that are nearly invisible to the naked eye
350
what area does the conjunctiva cover?
begins at outer edge of cornea covers visible part of eye lines inside of eyelids
351
what are the 3 layers of the coat of the eye?
outermost - sclera (white of the eye) choroid innermost - retina (neurosensory tissue)
352
what is the function of the sclera?
protecting the eye maintaining the shape of the eye
353
what is the function of the choroid?
providing circulation to the eye shielding out unwanted scattered light
354
what is the function of the retina?
converting light into neurological impulses | to be transmitted to the brain via the optic nerve
355
what are the structural properties of the sclera?
hard fibrous opaque high water content
356
what are the structural properties of the choroid?
pigmented vascular - layers of blood vessels that nourish the back of the eye
357
what is the cornea?
transparent, dome-shaped window covering the front of the eye
358
what is the function of the cornea?
powerful refracting surface (providing 2/3 of eye's focusing power) gives us a clear window to look through
359
what are the 5 layers of the cornea?
epithelium Bowman’s membrane stroma Descemet’s membrane endothelium
360
what feature of the stroma of the cornea contributes towards transparency?
its regularity
361
what is the function of the endothelium of the cornea?
pumps fluid out of cornea, prevents corneal oedema | cornea has low water content
362
what is the uvea?
vascular coat of eyeball lies between the sclera and retina
363
what are the 3 parts that make up the uvea?
iris ciliary body choroid (intimately connected - disease of one part also affects the other portions though not necessarily to the same degree)
364
what is the function of the iris?
controls light levels inside the eye similar to the aperture on a camera 
365
how does the iris control pupil size?
embedded with tiny muscles dilate and constrict pupil size 
366
what is the structure of the lens?
outer acellular capsule regular inner elongated cell fibres – transparency
367
how does the lens change with age?
may lose its transparency with age results in an opaque lens (cataract)
368
what is the function of the lens of the eye?
refractive Power 1/3 of the eye focusing power - higher refractive index than aqueous fluid and vitreous accommodation elasticity
369
what is the function of the optic nerve?
transmits electrical impulses from the retina to the brain
370
how is the optic nerve arranged?
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
371
where is the macula located?
roughly in the centre of the retina temporal to the optic nerve
372
what is the function of the macula?
small and highly sensitive part of the retina responsible for detailed central vision allows us to perform tasks such as reading
373
what is the fovea?
centre of macula most sensitive part of the retina
374
what is the arrangement of cells on the fovea?
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
375
why is the high concentration of cones on the fovea important?
allow perception in detail
376
what are the 2 types of visual function?
central peripheral
377
what is central vision responsible for?
detailed day vision colour vision – fovea has the highest concentration of cone photoreceptors (reading, facial recognition)
378
what problems will people with loss of central vision have?
poor visual acuity (loss of foveal vision) problems with reading and recognising faces
379
what is peripheral vision responsible for?
shape movement night vision navigation vision
380
what problems will people with loss of peripheral vision have?
extensive loss of visual field – unable to navigate in environment, patient may need white stick even with perfect visual acuity problems navigating the world
381
how is central vision assessed?
visual acuity assessment
382
how is peripheral vision assessed?
visual field assessment
383
what are the 2 layers of the retina?
retinal pigment epithelium (in front of choroid) neuroretina (inner, thicker layer)
384
what are the functions of the retinal pigment epithelium?
transports nutrient from the choroid to the photo-receptor cells removes metabolic waste from the retina
385
what are the 3 layers of the neuroretina?
outer, middle, inner
386
what cells are present on the outer layer of the neuroretina?
photoreceptors (1st order neuron)
387
what is the the function of the outer layer of the neuroretina?
detection of light
388
what cells are present on the middle layer of the neuroretina?
bipolar cells (2nd order neuron)
389
what is the the function of the middle layer of the neuroretina?
local signal processing to improve contrast sensitivity, regulate sensitivity
390
what cells are present on the inner layer of the neuroretina?
retinal ganglion cells (3rd order neuron) axon runs along optic nerve into brain
391
what is the the function of the inner layer of the neuroretina?
transmission of signal from the eye to the brain
392
what are the 2 classes of photoreceptor?
rods and cones
393
what are rods responsible for?
night vision (scotopic vision) peripheral vision recognises motion more photoreceptors, more pigment - higher spatial and temporal summation
394
what are cones responsible for?
daylight fine vision and colour vision (photopic vision)
395
how do rods and cones differ in terms of sensitivity to light?
rods 100x more sensitive than cones
396
how do rods and cones differ in terms of response to light?
rods have slower response than cones
397
how do rods and cones differ in terms of their outer segment?
rods have longer outer segment (therefore more photosensitive pigment) than cones
398
where are photopigments synthesised?
inner photo-receptor segment of rods and cones then transported to outer segment
399
how is the outer segment of rods and cones arranged?
stacks of discs
400
how are photopigments regenerated?
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
401
where are rod photoreceptors distributed?
widely distributed all over the retina, highest density just outside the macula density tails off towards the periphery completely absent within the macula
402
where are cone photoreceptors distributed?
only within macula
403
where is the peak of rod vison light sensitivity?
498nm wavelength | rods used for night vision and spatial recognition, not really sensitive to any particular colour
404
what are the 3 cone photopigment sub-types?
S-cones M-cones L- cones
405
what wavelengths are S-cones sensitive to?
short wavelength (blue) peak sensitivity: 430nm
406
what wavelengths are M-cones sensitive to?
medium wavelength (green) peak sensitivity: 540nm
407
what wavelengths are L-cones sensitive to?
long wavelength (red) peak sensitivity: 570nm
408
how is yellow light experienced?
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
409
what is deuteranomaly/Daltonism (most common form of colour vision deficiency) caused by?
shifting of the M-cone sensitivity peak towards that of the L-cone curve causes red-green confusion
410
what 2 things can cause colour vision deficits?
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
411
what is dichromatism?
only two cone photo-pigment sub-types are present
412
what is monochromatism?
complete absence of colour vision
413
what is blue cone monochromatism?
presence of only blue L-cones normal daylight visual acuity
414
what is rod monochromatism?
a total absence of all cone photo-receptors no functional day vision
415
what is achromatopsia?
full colour blindness (occurs in very small percentage of the population)
416
what is the Ishihara test?
colour blindness test
417
what is the basis of refraction?
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)
418
what is the index of refraction?
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
419
what are the 2 types of lens?
convex (takes light rays and brings them to a point) concave (takes light rays and spreads them outward)
420
when might a convex lens be used practically?
camera focus image on film
421
what is emmetropia?
adequate correlation between axial length and refractive power (functioning eye) parallel light rays fall on the retina (no accommodation)
422
what is ametropia?
mismatch between axial length and refractive power parallel light rays don’t fall on the retina (no accommodation)
423
what are some ametropic errors?
near-sightedness (myopia) farsightedness (hyperopia) astigmatism presbyopia
424
how does the path of light lead to myopia?
parallel rays converge at a focal point anterior to the retina
425
what causes myopia?
excessive long globe (axial myopia) - more common excessive refractive power (refractive myopia)
426
what is the etiology of myopia and hyperopia?
unclear genetic factor
427
what are the symptoms of myopia?
blurred distance vision squint in an attempt to improve uncorrected visual acuity when gazing into the distance headache
428
how is myopia treated?
correction with diverging lenses (negative lenses) correction with contact lens correction by removing the lens to reduce refractive power of the eye
429
how does the path of light lead to hyperopia?
parallel rays converge at a focal point posterior to the retina
430
what causes hyperopia?
excessive short globe (axial hyperopia) -more common insufficient refractive power (refractive hyperopia)
431
what are the symptoms of hyperopia?
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
432
how is hyperopia treated?
correction with converging (positive lenses) correction with positive lens + cataract extraction correction with contact lens correction with intraocular lens
433
how does the path of light lead to astigmatism?
parallel rays come to focus in 2 focal lines rather than a single focal point
434
what causes astigmatism?
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)
435
what is the etiology of astigmatism?
heredity
436
what are the symptoms of astigmatism?
asthenopic symptoms - headache - eyepain blurred vision distortion of vision head tilting and turning
437
how is regular astigmatism treated?
cylinder lenses with or without spherical lenses (convex or concave), Sx
438
how is irregular astigmatism treated?
rigid cylinder lenses surgery
439
what is the near response triad?
adaptation for near vision
440
what 3 things form the near response triad? what is their function?
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
441
what is presbyopia?
naturally occurring loss of accommodation (focus for near objects), distant vision intact onset from age 40 years
442
how is presbyopia treated?
convex lenses in near vision - reading glasses - bifocal glasses - trifocal glasses - progressive power glasses
443
what are the 2 types of spectacle lens?
monofocal lenses - spherical lenses - cylindrical lenses multifocal lenses
444
what is the difference between contact lenses and spectacle lenses?
higher quality of optical image and less influence on the size of retinal image than spectacle lenses
445
when are contact lenses used?
cosmetic athletic activities occupational irregular corneal astigmatism high anisometropia corneal disease
446
what are the disadvantages of contact lenses?
careful daily cleaning and disinfection expense complications - infectious keratitis - giant papillary conjunctivitis - corneal vascularization - severe chronic conjunctivitis
447
what are intraocular lenses?
replacement of cataract crystalline lens
448
what are the advantages of intraocular lenses?
give best optical correction for aphakia avoid significant magnification and distortion caused by spectacle lenses
449
what are the types of keratorefractive surgery?
RK AK PRK LASIK ICR thermokeratoplasty
450
what are the types of intraocular surgery?
clear lens extraction (with or without IOL) phakic IOL
451
how is surgical correction carried out?
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
452
what is the process of clear lens extraction and addition of an intraocular lens?
cataract extraction implantation of artificial lens
453
what occurs as a result of clear lens extraction and addition of an intraocular lens?
loss of accommodation (patient needs reading glasses)
454
what is the function of the visual pathway?
transmits signal from eye to the visual cortex
455
what are the visual pathway landmarks?
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
456
what are first order neurons within the visual pathway?
photoreceptors
457
what are second order neurons within the visual pathway?
phototreceptors synapse on retinal bipolar cells
458
what are third order neurons within the visual pathway?
retinal ganglion cells
459
what feature of retinal ganglion nerve fibres allows better signal transmission of visual information out of the eye to the brain?
myelination after entering optic nerve
460
what is decussation in the visual pathway?
half of the retina ganglion nerve fibres cross to the opposite side at the optic chiasm
461
what are fourth order neurons within the visual pathway?
retinal ganglion Fibres terminate at the lateral geniculate ganglion (thalamus) and synapse upon the fourth order neurons, or optic radiation
462
what will a lesion anterior to the optic chiasma affect?
visual field in one eye
463
what will a lesion posterior to the optic chiasma affect?
visual field simultaneously in both eyes because of fibre crossing at chiasma
464
where do the crossed fibres at the optic chiasma predominantly originate from?
nasal retina
465
which half of the visual field are the crossed fibres at the optic chiasma responsible for?
temporal
466
where do the uncrossed fibres at the optic chiasma predominantly originate from?
temporal retina
467
which half of the visual field are the uncrossed fibres at the optic chiasma responsible for?
nasal
468
what will a lesion at the optic chiasma affect?
damages crossed ganglion fibres from nasal retina in both eyes temporal field deficit in both eyes – bitemporal hemianopia
469
what will a right sided lesion (optic tract, optic radiation or visual cortex) posterior to the optic chiasma affect?
left homonymous hemianopia (both eyes)
470
what will a left sided lesion (optic tract, optic radiation or visual cortex) posterior to the optic chiasma affect?
right homonymous hemianopia (both eyes)
471
what is a bitemporal hemianopia generally caused by?
enlargement of benign pituitary gland tumour pressing on optic chiasma from above
472
what is a homonymous hemianopia generally caused by?
stroke cerebrovascular accidents in the brain
473
when does contralateral homonymous hemianopia with macular sparing occur?
damage to the primary visual cortex due to stroke
474
why does contralateral homonymous hemianopia with macular sparing occur?
area within primary visual cortex representing macula is well protected - receives blood supply from both right and left posterior cerebral arteries
475
what is the function of the pupil?
regulates light input to the eye
476
what is pupillary constriction mediated by?
parasympathetic nerve within cranial nerve III
477
what happens to the pupil in light conditions?
iris circular muscles contract, decreased pupil size (less light entering eye)
478
what happens to the pupil in dark conditions?
iris radial muscles contract, pupil dilation (more light entering eye)
479
why does the pupil contract in light conditions?
decreases spherical aberrations and glare increases depth of field – near response triad reduces bleaching of photo-pigments
480
what is the afferent pathway of the pupillary reflex?
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
481
what is the efferent pathway of the pupillary reflex?
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
482
what does the pathway of the pupillary reflex mean?
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
483
what will a right afferent defect (e.g. damaged right optic nerve) in the pupillary reflex pathway cause?
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
484
what will a right efferent defect (e.g. damaged right 3rd nerve) in the pupillary reflex pathway cause?
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
485
what is the relative afferent pupillary defect?
damage to afferent pathway is usually incomplete, or relative some degree of of pupillary constriction remains (albeit weaker response when damaged side is stimulated)
486
how can a relative afferent pupillary defect be demonstrated?
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
487
why is eye movement necessary?
acquiring and tracking visual stimuli
488
what is eye movement facilitated by?
six extraocular muscles innervated by the three cranial nerves (III, IV and VI)
489
what is duction (eye movements)?
eye movement in one eye
490
what is version (eye movements)?
simultaneous movement of both eyes in the same direction dextroversion: both eyes looking right levoversion: both eyes looking left
491
what is vergence (eye movements)?
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
492
what is saccade?
short fast burst eye movement (up to 900 degrees per second)
493
what are the different types of saccade?
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)
494
what is smooth pursuit?
slow sustained eye movement (up to 60 degrees per second) involuntary movement, driven by motion of moving target across retina
495
which extraocular muscles allow straight movement?
superior, inferior, lateral, medial rectus
496
where do the extraocular muscles come from?
all except inferior oblique come from a cone in the back of the orbit inferior oblique comes in nasally
497
how does the superior rectus move the eye?
upwards
498
how does the inferior rectus move the eye?
downwards
499
how does the lateral rectus move the eye?
towards the outside of the head (towards temple)
500
how does the medial rectus move the eye?
towards the middle of the head (towards the nose)
501
how is the superior oblique arranged?
attached high on temporal side of eye passes under superior rectus travels through the trochlea
502
how does the superior oblique move the eye?
diagonal pattern (down and out)
503
how is the inferior oblique arranged?
attached low on nasal side of eye. passes over inferior rectus
504
how does the inferior oblique move the eye?
diagonal pattern (up and out)
505
what does the superior branch of the third cranial nerve innervate?
superior rectus – elevates eye levator palpebrae superioris
506
what does the inferior branch of the third cranial nerve (oculomotor) innervate?
inferior rectus - depresses eye medial rectus – adducts eye inferior oblique – elevates eye parasympathetic nerve – constricts pupil
507
what does the fourth cranial nerve (trochlear) innervate?
superior oblique – depresses eye
508
what does the sixth cranial nerve (abducens) innervate?
lateral rectus - abducts eye
509
how is eye movement tested?
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
510
how can upwards, downwards, inwards, outwards and rotating movements of the eye be described?
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
511
what does third nerve (oculomotor) palsy cause?
unopposed action of lateral rectus and superior oblique (causes eye to stay down and out) ptosis (eyelid drooping) - levator palpabrae superioris loses innervation
512
what does sixth nerve (abducens) palsy cause?
lateral rectus loses innervation affected eye cannot abduct, deviates inwards double vision worsens on gazing to side of affected eye
513
what is nystagmus?
oscillatory movement of the eye (physiological or pathological)
514
what is optokinetic nystagmus?
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
515
why is optokinetic nystagmus useful?
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
516
what are the features of a migraine disorder?
tendency to repeated attacks triggers easily hung-over visual vertigo motion sickness
517
what are the 3 forms of attack of a migraine disorder?
pain focal symptoms both pain and focal symptoms
518
what are the 5 phases of a migraine?
prodrome aura headache resolution recovery (about 48 hours in total)
519
what happens in the prodrome phase of a migraine?
changes in mood changes in urination and fluid retention food craving yawning
520
what happens in the aura phase of a migraine?
visual, sensory (numbness/paraesthesia) weakness speech arrest
521
what happens in the headache phase of a migraine?
head and body pain nausea photophobia
522
what happens in the resolution phase of a migraine?
rest and sleep
523
what happens in the recovery phase of a migraine?
mood disturbed food intolerance feeling hungover
524
how do positive and negative symptoms together during the aura phase of a migraine present?
scintillations blindspot
525
what things are seen by the patient during the aura phase of a migraine?
expanding 'C's' elemental visual disturbance
526
how is an acute migraine attack treated?
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
527
what are the lifestyle issues caused by migraines?
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
528
how can environmental issues that trigger migraines be controlled?
(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
529
what are the prophylactic methods of controlling migraines?
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)
530
how is erenumab used as a prophylactic for migraines?
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)
531
what is a tension type headache?
tight muscles around head and neck bilaterally, as though head is in a vice
532
how is a tension type headache treated?
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
533
what is a cluster headache?
severe unilateral pain lasting 15-180 minutes untreated classified as a trigeminal autonomic cephalgia
534
what is needed for a headache to be classed as a cluster headache? what are the symptoms?
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
535
how is an acute cluster headache treated?
inhaled oxygen (oxygen inhibits neuronal activation in trigeminocervical complex) S/C or nasal sumatriptan
536
what drugs are used to prevent a cluster headache?
verapamil prednisolone lithium valproate gabapentin topiramate pizotifen
537
what is the difference in distribution between migraines and cluster headaches?
migraine - 33% men, 67% women cluster headache - 90% men, 10% women
538
what is the difference in duration between migraines and cluster headaches?
migraine - 3-12 hours cluster headache - 45min – 3 hours
539
what is the difference in frequency between migraines and cluster headaches?
migraine - 1-8 attacks monthly cluster headache - 1-3 attacks daily (often at night)
540
what is the difference in remission between migraines and cluster headaches?
migraine - long remissions unusual cluster headache - long remissions common
541
what is the difference in nausea between migraines and cluster headaches?
migraine - nausea, vomiting frequent cluster headache - nausea rare
542
what is the difference in pain between migraines and cluster headaches?
migraine - pulsating hemicranial pain cluster headache - steady, exceptionally severe, well localised pain, unilateral in each cluster
543
what is the difference in symptoms between migraines and cluster headaches?
migraine - visual or sensory auras seen cluster headache - eye waters, nose blocked, ptosis etc
544
what is the difference in activity between migraines and cluster headaches?
migraine - patients lie in the dark cluster headache - patients pace about
545
what is the commonest cause of dementia?
Alzheimer's disease
546
what characterisis dementia?
fatal neurodegenerative disorder progressive social, cognitive and functional impairment
547
what is the best treatment possible for dementia at present?
acetylcholinesterase inhibitors modest symptomatic benefit in early stages (1-2 years)
548
what are newer methods that allow diagnosis of dementia in life?
PET imaging, structural imaging CSF and plasma markers
549
what is the difference between young onset and later onset dementia?
cut off age of 65 yrs
550
what usually causes familial Alzheimer's disease?
APP (amyloid precursor protein) or presenilin mutations
551
what is the difference in the types of dementia between young onset and late onset sufferers?
'rarer' forms (vascular, frontotemporal, Lewy body, other) account for a greater percentage (70%) than Alzheimer's in young onset
552
what are some potentially reversible factors that may lead to depression?
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)
553
why can it be difficult to diagnose dementia in the clinic?
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
554
what are some pathologies of the brain associated with dementia?
neuronal tau Aβ TDP-43 α-synuclein parenchymal ischaemic changes vessel wall pathology - e.g. cerebral amyloid angiopathy
555
what is the clinical process of dealing with dementia?
referral (from GP, psychiatrist, psychologist, geriatrician) history - includes clinical interview examination investigations diagnosis - Alzheimer's - vascular - Lewy body - frontotemporal - depression - delirium - none management
556
what is the checklist to interview patients with suspected dementia?
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
557
why is it important to ask a potential dementia sufferer's friends and family about their behaviour and mental state?
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
558
why is asking about memory important in a potential dementia sufferer?
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
559
why is asking about language important in a potential dementia sufferer?
not just speaking skills, also word finding difficulties second language English? any deterioration? naming things in first language?
560
why is asking about numerical skills important in a potential dementia sufferer?
ability to calculate, manage finances alone etc. more vulnerable to exploitation, especially if no access to attorney or other support
561
why is asking about executive skills and visuospatial skills important in a potential dementia sufferer?
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
562
why is asking about altered visual perception, route finding and landmark identification important in a potential dementia sufferer?
people may often wander unfamiliar routes difficult to follow as dementia progresses
563
why is asking about personality and social conduct important in a potential dementia sufferer?
must know how personality traits etc. were before symptoms started - gauge progression
564
why is asking about sexual behaviour important in a potential dementia sufferer?
disinhibition as Alzheimer's progresses, frontotemporal dementia - more disinhibited behavioural phenotype patients exhibit sexual behaviour that they may not have done before dementia
565
why is asking about eating habits important in a potential dementia sufferer?
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)
566
why is asking about mood important in a potential dementia sufferer?
treating depression if present - may restore some cognitive deficits
567
why is asking about delusions and hallucinations important in a potential dementia sufferer?
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
568
why is it important to ask about the chronology of each potential aspect of dementia?
if they are improving, it may not be a dementia process potentially reversible causes sudden or marked deterioration (subtle deterioration - Alzheimer's, stepwise - vascular)
569
what examinations are done in dementia testing?
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
570
what investigations are done in dementia testing?
neuropsychological tests (MMSE, Addenbrooke's Cognitive Exam - more memory focussed bloods MRI (bilateral medial temporal volume loss, hippocampal volume loss) PET
571
what blood tests are done in investigating dementia?
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)
572
how does a PET scan work?
inject patient with contrast agent travels to brain, lights up amyloid corresponds with beta amyloid antibody immunohistochemistry
573
how is dementia managed?
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
574
how can you differentiate between the different types of dementia to make a diagnosis?
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
575
what is the head-turning sign?
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.)
576
what is episodic memory and what does it depend on?
memory for particular episodes in life depends on medial temporal lobes, including hippocampus and entorhinal cortex
577
what does the pathology of dementia depend on?
amyloid tau
578
what is Lewy body dementia generally caused by?
aggregation of alpha synuclein
579
how can the different types of dementia be differentiated on an MRI?
preserved hippocampal volume in Lewy body (as compared to Alzheimer's) typically asymmetrical bilateral perisylvian atrophy in FTD
580
how can frontotemporal dementia be assessed with genetic testing?
pathological expansion of C9orf72 gene
581
what is meningitis?
inflammation of meninges caused by viral or bacterial infection
582
what is encephalitis?
inflammation of the brain caused by infection or autoimmune mechanisms
583
what is cerebral vasculitis?
inflammation of blood vessel walls (sometimes called angiitis)
584
what is the blood brain barrier?
brain tissue protected from contents of bloodstream
585
what is the basis of the blood brain barrier?
dense vascularisation of brain tissue neurons are always close to capillaries - therefore capillaries very dense capillaries form blood brain barrier
586
what do the capillaries forming the blood brain barrier look like?
extensive tight junctions at the endothelial cell-cell contacts
587
how does the structure of the capillaries forming the blood brain barrier allow it to carry out its function?
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
588
what other structures help maintain the structure of the blood brain barrier and the vessel wall?
basal lamina other glial cells (particularly astrocytes)
589
how can the blood brain barrier be broken down?
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
590
what can a breakdown of the blood brain barrier cause?
infection
591
what are the symptoms of encephalitis?
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
592
what are the most common causes of encephalitis?
viral infection usually: - Herpes Simplex  - measles - Varicella (chickenpox) - rubella
593
what are some non-viral causes of encephalitis?
mosquito, tick and other insect bites bacterial and fungal infections trauma autoimmune
594
what treatments are used for encephalitis?
(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
595
what is multiple sclerosis?
auto immune demyelinating disease of CNS intermittent - relapses linked to inflammatory activity progression linked to neurodegeneration - deficits increase over time, fewer remissions
596
what is the cellular pathology of multiple sclerosis?
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
597
why do the symptoms of multiple sclerosis vary?
MS is a random disorder - can affect white matter anywhere in CNS amount and location of the damage vary
598
what is perivascular cuffing?
perivascular accumulation of leukocytes seen in infectious, inflammatory, or autoimmune diseases
599
what does perivascular cuffing look like in multiple sclerosis?
immune cells (usually CD3 T cells, CD20 B cells) cross blood brain barrier, form cuff around vessels causes demyelination, inflammation
600
what is meningitis?
irritation, inflammation and swelling of meninges
601
what are the most common causes of meningitis?
usually bacterial - meningococcal – (most common cause of bacterial meningitis in UK) - pneumococcal - haemophilus influenzae type b (Hib)  - streptococccal (main cause in newborns)
602
what are some non-bacterial causes of meningitis?
viral -  very rarely life-threatening fungal
603
what is an infection of the spinal cord known as?
meningitis (meninges cover spinal cord as well as brain)