learning outcomes Flashcards
(489 cards)
1
Q
the fibrous layer of the eye contains
A
contains the cornea and sclera.
2
Q
function of the cornea and sclera
A
The cornea is transparent and allows light to enter, the sclera provides attachment for the muscles moving the eye.
3
Q
vascular layer of the eye contains
A
contains the ciliary body, iris and choroid.
4
Q
function of the ciliary body, iris and choroid
A
The ciliary body suspends the lens and produces aqueous humor, the iris which controls the entry of light through the diameter and the choroid which supplies blood to the outer layers of the retina.
5
Q
the sensory layer contains and function
A
with the retina which contains the light sensitive rods and cones which enable sight.
6
Q
anterior segment contains
A
a watery fluid called aqueous humour
7
Q
posterior segment contains
A
transparent gel called vitreous humour
8
Q
structure and function of the conjunctiva
A
the conjunctiva is the mucous membrane on the inside with a thin vascular membrane. its function is to generate moisture for the eye
9
Q
the structure of eyelids
A
The hard plate known as the tarsal plate that help keeps its shape and contains the meibomian glands, and oily secretory glands for tear film. There is a muscle levator palpebrae superioris and orbicularis oculi
10
Q
structure and innervation of the lacrimal system
A
The lacrimal gland is situated in the orbit laterally innervated parasympathetically by the facial nerve, its duct opens into the conjunctival sac via the punctae. Through the lacrimal duct it then empties into the inferior meatus of the nasal cavity.
11
Q
the posterior chamber is behind the
A
iris
12
Q
the function of vitreous humour
A
maintains posterior segment pressure
13
Q
posterior segment is behind the
A
lens
14
Q
function of the aqueous humour
A
fluid that maintains the intraocular pressure
15
Q
anterior chamber is in front of the
A
iris
16
Q
anterior segment is in front of the
A
lens
17
Q
6 extraocular muscles
A
there are 6 extrinsic ocular muscle that move the eye such as the medial, lateral, inferior, and superior rectus and 2 oblique such as the superior and inferior.
18
Q
bones of the orbit
A
frontal bone, sphenoid, lacrimal, ethmoid, maxillary, zygomatic, palatine
19
Q
fissures of the eye
A
There is the optic foramen, superior orbital fissure and inferior orbital fissure.
20
Q
intrinsic eye muscles and inner
A
The intrinsic eye muscles are the ciliaris muscle and constrictor pupillae innervated by the parasympathetic 3 cranial nerve. Dilator pupillae which is innervated by the sympathetic plexus around blood vessels.
21
Q
histological features of the cornea
A
there is the surface epithelium with stratified squamous non-keratinised. The basement membrane is called the bowman’s membrane. Then there is the avascular stroma, which is regularly arranged collagen. Then there is the descemet’s layer which is the basement membrane of the endothelium.
22
Q
tear film function and physiology
A
tear film washes the cornea, maintains moisture. Contains lysozymes and provides a smooth layer for refraction. It consists of three layers a mucinous layer, aqueous, and oily. The aqueous layer evaporates and once it the mucinous and oily layers come into contact the tear film disintegrates and stimulates a blink.
23
Q
cornea transparency physiology
A
the Cornea is avascular which aids in transparency, the main form of transparency is from the stroma and the parallel collagen fibres.
24
Q
aqueous humour outflow
A
the aqueous humour is produced in the ciliary body, flows into the anterior segment in front of the lens, towards the angle of the anterior chamber through the trabecular meshwork, into the schlemm’s canal then into venous drainage.
25
Describe how the functional anatomy of the eye serves to project a sharp image onto the retina
light waves bend at the cornea and at the lens through refraction the image is projected onto the retina. As object moves close, the lens thickens to allows for a clear image to still be formed.
26
accommodation means
refers to the ability of the eye to allow focus to change.
27
ciliary muscles of our eyes to accommodate
ciliary muscles can contract, causing the ciliary body to bulge which results in the suspensory ligaments relaxing and the lens becoming thicker as it is no longer stretched
28
pupils and their function in accommodation
pupils can constrict to limit the entry of light through the sphincter pupillae via parasympathetic innervation to enable close focus.
29
medial rectus and its role in accommodation
the medial rectus muscle of our eyes stimulated by the third cranial nerve can allow our eyes to converge to enable close work to be performed.
30
myopic refers to
myopic refers to the eyeball being too long, the image is formed in front of the retina so far off objects cannot be seen. The bending power of the cornea and lens is too much.
31
myopic symptoms
Symptoms include headaches, divergent squint, and easy loss of interest.
32
treatment of myopia
biconcave
33
hyperopia refers to
hyperopia is farsightedness meaning close objects are hazy. The eyeball is too short or the cornea/lens is too flat resulting in the image being formed behind the retina. The individual uses their accommodative power to thicken the lens for distant objects and thus cannot see close objects
34
symptoms of hyperopia
Symptoms of eye strain, convergent squint
35
treatment of hyperopia
biconvex
36
astigmatism refers to and requires
when close and distant objects appear hazy as the surface of the cornea has different curvatures. It requires cylindrical glasses to cancel out the incorrect medians called toric glasses.
37
presbyopia refers to
is old age long sightedness in which ciliary muscles contractions don’t stimulate the ciliary body and ligaments as well. Close objects become difficult to see and thus require biconvex reading glasses.
38
photo transduction mechanism
light particle enters the eye and goes to a rod cell. it hits a integral transmembrane helical protein complex called rhodopsin on the many lamellae, stimulating a chromophore retinal derived from vitamin A to alter shape from a cis to a trans. This chromophore can no longer fit into opsin and causes rhodopsin to split resulting in bleaching. This then stimulates a cascade event that culminates in sodium channels closing and less sodium entering the cell which stimulates hyperpolarisation of the rod cell and a rush of calcium ions to the bipolar cell synapse. Vitamin A is then essential for regeneration of this process in the pigment epithelial cell.
39
constrictor papillae innervation
parasympathetic 3rd cranial nerve
40
dilator papillae innervation
sympathetic fibres from blood vessels
41
optic neural pathway
fibres pass through optic nerve to optic chiasma in which the nasal fibres cross to the opposite side. Optic tract contains fibres from the lateral temporal half of the ipsilateral eye and crossed over nasal fibres from the contralateral eye. Fibres from optic tract finally synapse at the lateral geniculate body of the thalamus, then optic radiation passes to reach the primary visual cortex.
42
lateral rectus abducts causing
; SR elevates, IR depresses
43
medial rectus adducts causing
SR intorsion, IR extorsion
44
superior rectus function
elevates, adducts, intorsion
45
inferior rectus functions
depresses, adducts, extorsion
46
superior oblique functions
intorsion, depression and abduction
47
inferior oblique functions
extorsion, elevation, abduction
48
esotropia refers to
convergent squint
49
exotropia refers to
divergent squint
50
amblyopia refers to
brain supressing eye leading to poor image
51
diplopia refers to
double vision
52
visual field explained from the left eye
In the eyes the temporal side of the left eye will take in light from the right visual field and in the nasal side from the left visual field.
53
primary visual cortex in terms of visual fields
the right side of the primary visual cortex in the occipital will process only from the right visual field, and the left PVC of the occipital will process only the light from the left visual field.
54
visual field explained from the right eye
n a right eye the temporal side will take light in from the left visual field and the nasal will take in light from the right visual field.
55
damage to the right optic nerve will cause
right eye blindness
56
damage to the optic chiasma will cause
bitemporal hemianopia
57
left optic tract damage will cause
contralateral homonymous hemianopia
58
if optic radiation damaged then
contralateral homonymous hemianopia
59
damage to the left optic nerve will cause
left eye blindness
60
pupillary light reflex afferent fibres
impulses from light travel from the retina along the optic nerve to the chiasma and to the optic tract. The activation of the pupillary reflex arise from the midbrain to the nucleus of the oculomotor nerve known as the Edinger-Westphal nucleus
61
efferent limb of pupillary light reflex
pupillary reflex arise from the midbrain to the nucleus of the oculomotor nerve known as the Edinger-Westphal nucleus for parasympathetic innervation to stimulate the pupillary reflex fibres on both sides. this travels along the preganglionic fibre via the oculomotor nerve to synapse in the ciliary ganglion then travel along the short ciliary nerves to constrictor pupillae.
62
why does disruption to sympathetic innervation produces horner's syndrome
Horner’s syndrome symptoms are anisocoria due to sympathetic innervation damage, ptosis, anhidrosis and miosis. Sympathetic innervation arises from the thoracolumbar outflow from the sympathetic chain to the cervical ganglion and that post ganglionic fibres travel along the blood vessels. Something like a tumour compression such as Pancoast will cause Horner’s syndrome
63
if pupillary reflex is absent during oculomotor nerve palsy you have to assume
cerebral artery aneurysm
64
explain a cataract formation
since the lens is a avascular structure produced by parallel collagen fibres, damage in the from of UV rays result in damage, and more collagen fibres being produced causing an increase in density and thus becoming gradually more opaque.
65
aetiology of conjunctivitis
; viral or bacterial infection
66
features of conjunctivitis
red, watery eyes, discharge. Vision unaffected unless corneal spread.
67
management of conjunctivitis
antibiotic eye drops
68
corneal ulcer aetiology
viral/bacterial or from trauma and degeneration
69
features of corneal ulcer
opacification of the cornea
70
management of corneal ulcer
keratoplasty
71
non inflammatory corneal dystrophy aetiology
; genetic, accumulation of lipids
72
features of non inflammatory corneal dystrophy
bilateral, opacification commonly in first to fourth decade
73
management of non-inflammatory corneal dystrophy
keratoplasty
74
cataracts aetiology
UV rays and damage to lens
75
features of cataracts
opacification of lens
76
management of cataracts
cataract surgery
77
aetiology of glaucoma primary open angle
raised intra ocular pressure due to drainage through trabecular meshwork blockage
78
features of glaucoma primary open angle
asymptomatic, bilateral, altered field of vision, gradual
79
treatment of glaucoma primary open angle
eyedrops such as beta blockers, carbonic anhydrase inhibitors, prostaglandin analogues and trabeculoplasty or trabeculectomy.
80
glaucoma closed angle features
sudden onset, painful, blurry vision, headaches, red eye, opaque cornea
81
glaucoma closed angle aetiology
; intra ocular pressure severely raised due to peripheral iris blocking the angle preventing aqueous humour from draining
82
management of glaucoma closed angle
; steroid eye drops, IV carbonic anhydrase inhibitors, analgesics, antiemetics, constrictor eye drops pilocarpine and iridotomy to bypass blockage
83
uveitis aetiology
illness, autoimmune, infectious disease TB, or systemic disease
84
features of uveitis
red, painful, visual loss, floaters in vision, blurred vision
85
describe the main components of nervous system (general)
central nervous system with the brain and spinal cord
the peripheral nervous system with the cranial and spinal nerves, which further sub divides into the sensory afferent division and motor efferent division, the motor efferent division divides into the somatic motor and autonomic with the sympathetic and parasympathetic divisions.
86
describe neurones
there are neurons which are excitable cells that carry nerve impulses. They have multiple dendrites and one axon and transmit impulses from cell body to the synaptic terminal typically. They have a high metabolic rate, long living and amitotic. They may be myelinated and conduct via saltatory conduction.
87
different types of neurones
There are interneurons for motor transmission, bipolar found in the olfactory mucosa or retinal fibres and pseudo-unipolar sensory neurons.
88
schwann cells are for
in the peripheral nervous system there are satellite cells for surrounding cell bodies, and schwann cells for myelination.
89
ependymal cells are for
lining ventricles
90
astrocytes are for
form the blood-brain barrier, surrounding synapses and potassium buffering,
91
oligodendrocytes are for
myelination and microglia for phagocytosis.
92
compare grey matter and white matter
grey matter is collections of cell bodies such as ganglion or nuclei in the brain and in the spinal cord. White matter is axons, white due to the myelination and forms tracts for specific signals.
93
CSF purpose
CSF maintains intracranial pressure and protecting the brain to some degree from crushing itself
94
CSF presence and circulation and production
weight between the pia and arachnoid and its also present within the ventricles, being produced by a choroid plexus in each ventricle, it then circulate around the brain being eventually reabsorbed by the arachnoid villi into the sagittal sinus a venous channel in the brain
95
blood brain barrier description
it’s a protective mechanism to prevent harmful amino acids and ions transferring from the blood to the brain consisting of tight junctions between endothelium, a thick basal lamina and the foot processes of astrocytes.
96
drug therapy and the brain barrier
There are a few circumventricular organs such as the hypothalamus, and posterior pituitary that enables the delivery of lipid soluble drugs or certain vectors.
97
describe the lateral ventricle
lateral ‘C’ ventricles in the cerebral hemisphere
98
3rd ventricle is within
diencephalon
99
lateral and 3rd ventricle are connected by the
interventricular foramen
100
4rth and 3rd ventricles are connected by
the cerebral aqueduct in the midbrain
101
the 4rth ventricles is within
diamond shaped in the hindbrain
102
describe the meninges
the dura mater is a tough fibrous layer with fold then there is the arachnoid mater and the subarachnoid space which contains the cerebrospinal fluid and the pia mater which is vascularised and dips into the folds of the brain.
103
sensory cells in the bony canals are called
ampulla
104
the ampulla contains
flexible jelly like cupula organs that respond to endolymph movement.
105
movement is detected by in the ampulla
The embedded cilia synapse with the vestibular nerve and detect rotational acceleration, the movement of the ampulla then the delayed movement of the endolymph due to its inertia generates drag.
106
hyperpolarisation of the kinocilium are generated by
movement away from the kinocilium
107
depolarisation of the kinocilium is generated by
movement towards the kinocilium
108
sensory receptors within the utricle and saccule are called
the maculae
109
the maculae are
sensory receptors within the utricle and saccule
110
the ampulla Is
sensory cells within the base of the bony canals
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the utricle detects
the horizontal plane
112
the saccule detects the
vertical plane
113
cilia detecting movement in the macula
The cilia protrude into a mass called the otolith membrane which is embedded also with CaCO3 crystals called otoliths which move in response to gravity. Tilted the head stimulates the crystals greater then the endolymph and distorts the membrane moving the cilia, tilting backwards causes the kinocilium to depolarise and tilting forward causes hyperpolarisation
114
otoliths are
CaCO3 crystals
115
projections from the vestibular nuclei lead to the
descending motor pathways
116
what is vestibular nystagmus
saccadic eye movements that rotate the eye against body rotation to maintain focus on original intention, eye movement is restricted and when at its range it will flick back to a neutral position and this will repeat as long as rotation occurs.
117
how can vestibular nystagmus test vestibular function
post rotary nystagmus in experiments involves rotation in a barany chair the rotation to the left generates left nystagmus, then deceleration generates right nystagmus due to the endolymph overcoming the initial inertia and drag and pushing the cupula in an opposite direction.
118
COW caloric stimulation
Cold Opposite, Warm Same COWS).
119
caloric stimulation explanation
caloric stimulation, when washing the ear with hot or cold water it can generate conventional current altering the flow of endolymph, either towards the affected side if >37C or away if cold <37
120
labyrinthitis acute infection may cause
nausea, pallor, vertigo, dizziness, vomiting and sweating
121
Meniere's disease may cause
vertigo, nausea, nystagmus and tinnitus due to an overproduction of endolymph increasing the pressure
122
nystagmus at rest may be pathologically caused by
brain stem lesions
123
tonic labyrinthine reflexes
there are tonic labyrinthine reflexes which is the relationship between the head and the body which depends on the maculae and neck proprioceptors.
124
dynamic righting reflexes
there is the dynamic righting reflex which allows for rapid positional movement to aid in balance, it’s a long reflex depending on extension of all limbs to prevent falling when tripping.
125
vestibo-ocular reflexes
which follows afferent fibres from the semi circular canals to the extraocular nuclei to influence eye movement and the visual system aids in posture control.
126
vestibo-ocular static reflex
static reflex which is the ability of the eyes to compensate for head movement to maintain focus on an image and dynamic vestibular nystagmus which is saccadic eye movements that enable the eye to work against rotation of the body and head to that the gaze is preserved.
127
the medulla landmarks
it contains the fourth ventricle and is a continuation of the spinal cord through the foramen magnum. It contains the pyramids and their decussation, olives laterally, and connects to the cerebellum by the inferior cerebellar peduncle. It is associated with the cranial nerves 9-12.
128
pons landmarks
pons; it has the fourth ventricle posterior to it, and on the surface has the middle cerebellar peduncle and the cranial nerves 5-8.
129
midbrain landmarks
; it contains the cerebral aqueduct as well as the cerebral peduncle, superior cerebellar peduncle, the superior and inferior colliculus and the origins of the oculomotor nerve anteriorly and the trochlear nerve posteriorly
130
cerebellum landmarks
there is a right and left hemisphere separated by a vermis. Each hemisphere has an a small anterior lobe, large posterior lobe and tiny flocculonodular lobe as well as a small posterior section called the cerebellar tonsil. The surface is marked by sulci and folia and through three peduncles connects to the brainstem.
131
cerebellum function
its function is to receive motor information from the pyramidal tracts, ipsilateral peripheral proprioceptors and from the vestibular nuclei regarding balance and posture. It then coordinates force and direction of muscle for contraction to fine tune motor activity and posture and sends this to the cerebral cortex via the superior cerebellar peduncle.
132
diencephalon located
diencephalon lies deep within the cerebral hemispheres around the third ventricle
133
thalamus location
within the diencephalon. which is a dense collection of grey matter just lateral to the third ventricle and operates as a sensory relay station.
134
hypothalamus location
part of the diencephalon. There is the hypothalamus separated by the hypothalamic sulcus for controlling homeostasis and visceral organs, from the hypothalamus is the pituitary stalk.
135
internal carotids route
Two internal carotid arteries enter the skull through the foramen lacerum
136
vertebral artery route
then two vertebral arteries arise from the subclavian artery through the foramen magnum.
137
circle of Willis consists of
the circle of Willis is made up of the vertebral arteries joining to form the basilar artery, which then leads into the posterior cerebral artery, then the posterior communicating artery, then the internal carotid feeds in forming the ophthalmic artery, the middle cerebral artery and the anterior cerebral arteries which are joined by a anterior communicating artery.
138
ventrobasilar system supplies
brainstem and cerebellum
139
clinical significance of circle of willis
all branches are end arteries
140
anterior cerebral artery supplies
medial aspects but the occipital
141
middle cerebral artery supplies the
lateral aspects
142
the posterior cerebral artery supplies the
inferior cerebrum and occipital lobe
143
venous drainage of the brain is through
venous sinuses between 2 layers of dura mater such as the inferior sagittal sinus, superior sagittal sinus, the cavernous sinus, transverse sinus, and the petrosal superior and inferior sinuses all eventually feeding into the jugular veins.
144
frontal and parietal lobes are separated by
central sulcus
145
temporal lobe is separated from the frontal lobe by a
lateral sulcus
146
parietal lobe consists of
superior and inferior lobule
147
the occipital lobe is divided by
calcarine fissure
148
the corpus callosum and limbic lobe is separated from the cerebrum
cingulate sulcus
149
within the lateral fold of the temporal lobes is the
insula
150
frontal lobe is for
motor function and intellect
151
parietal lobe is for
somatosensory
152
temporal lobe is for
hearing and smell
153
occipital lobe for
vision
154
the frontal lobe contains
area 4 the precentral gyrus which the is primary motor cortex for somatotopic representation of the contralateral half of the body.
the inferior frontal gyrus known as Broca’s area of motor speech are 44,45.
then there is the prefrontal cortex which is involved in cognitive functions.
155
are 4/precentral gyrus is for
primary motor cortex
156
inferior frontal gyrus is for
broca's area of motor speech 44,45
157
area's 3,1,2 Is the
primary sensory area receives somatotopic representation of general sensation from contralateral half of the body.
158
post central gyrus contains
areas 3,1,2 known as the primary sensory area which receives somatotopic representation of general sensation from contralateral half of the body.
159
superior parietal lobe function
processes general sensory data and conscious sensation of contralateral half of the body making it an association area
160
inferior parietal lobule is for
interface between the somatosensory cortex and visual/auditory areas, in the dominant sphere it contributes to language function.
161
temporal lobe contains
the superior temporal gyrus which is the primary auditory cortex areas 41, 42.
Then there is the Wernicke’s area, the auditory association area in the dominant sphere crucial for spoken word understanding.
the inferior surface receives fibres form the olfactory tract for conscious appreciation of smell.
162
superior temporal gyrus is the
which is the primary auditory cortex areas 41, 42.
163
areas 41, 42 are the
superior temporal gyrus in the primary auditory cortex
164
Wernicke's are is for
the auditory association area in the dominant sphere crucial for spoken word understanding.
165
the auditory association area in the dominant sphere crucial for spoken word understanding is called
Wernicke's area
166
inferior surface of the temporal lobe is for
receiving fibres from the olfactory tract
167
occipital lobe contains
responsible for vision, on the medial surface either side of the calcarine sulcus is the primary vision cortex 17. Areas 18, 19 is responsible for interpretation of visual images.
168
the calcarine sulcus is the
primary vision cortex 17
169
primary vision cortex 17 is located in the occipital lobe at the
calcarine sulcus
170
areas 18, 19 Is for
interpretation of visual images
171
interpretation of the visual images occurs in the
area 18, 19 of the occipital lobes
172
association area is for
integration and processing of information
173
premotor cortex function is
planning, control and execution of voluntary movements
174
primary motor cortex is for
sending signals to generate movements
175
language centres of the forebrain
Broca’s area (44,45) is the motor speech area, Wernicke’s area if auditory association area for recognition of spoken word in the dominant hemisphere, the auditory cortex (41,42) and motor control of mouth and lips in the precentral gyrus are also essential
176
what fibres connect the two hemispheres through the corpus callosum is
commissural fibres
177
the parts of the cortex is connected through
association fibres
178
connections between the cerebral cortex and subcortical centres pass through the corona radiata and internal capsule fibres
projection fibres
179
projection fibres
Then finally is the projection fibres which run between the cerebral cortex and various subcortical centres though the corona radiata and internal capsule.
180
basal ganglia consist of
deep grey matter
181
basal ganglia are the
There is the caudate, globus pallidus and the putamen which form the lentiform nucleus and the substantia nigra.
182
the caudate and putamen receive information from and this then goes to
the motor cortex, premotor cortex and thalamus, it then sends this to the output regions which are the globus pallidus and substantia nigra and then projects this to the thalamus
183
the purpose of the basal ganglia are
The purpose of this system is regulate movement through initiating or terminating movement making it extrapyramidal system.
184
gross anatomy of the spinal cord
on a cross section there is a dorsal and ventral side. On the dorsal side there is the dorsal root ganglion and the dorsal root feeding into a dorsal horn. on the ventral side is the ventral root, both roots arising from a spinal nerve into the ventral horn. The horns consist of grey matter and surrounded by white matter which form tracts.
185
ascending corticospinal tract carries
the corticospinal tract carries motor impulses from the motor cortex to the skeletal muscle. The pathway starts in area 4 the motor cortex, passing through the internal capsule and along the cerebral peduncle, before travelling along the pons pyramids and then decussating to the contralateral corticospinal tract where is will then leave through the ventral horn to the root, then into the spinal nerve to the muscle.
186
the ascending posterior dorsal column
the posterior dorsal column carries touch, vibration, tactile localisation and proprioception. The signal travels from the dorsal root ganglion to the dorsal horn and along the tract, synapsing in the gracile and cuneate nucleii in the medulla and decussating across into the contralateral half of the medial lemniscus of the pons before synapsing again in the VPL nucleus of the thalamus which sends the signal to the post central gyrus of the parietal lobe.
187
the lateral spinothalamic tract
the lateral spinothalamic tract is responsible for pain and temperature. The sensory neuron enters through the dorsal root ganglion, synapsing at its spinal segment, crossing over contralaterally to the tract before heading to the VPL of the thalamus, synapsing again before heading to the post central gyrus of the parietal lobe.
188
posterior dorsal column carries
touch, vibration, tactile localisation and proprioception.
189
the corticospinal tract carries
motor impulses from the motor cortex to the skeletal muscle.
190
lateral spinothalamic tract carries
pain and temperature
191
corticospinal tract decussates in the
pons pyramids
192
posterior dorsal column decussates
medial lemniscus of the pons
193
lateral spinothalamic tract decussates
at its spinal segment
194
what is lower motor neurone disease
affects the ventral horn of the spinal cord resulting in neurone death and muscle atrophy. It is a progressive incurable disease.
195
lower motor neurones mediates
reflexes and muscle tone, they link upper motor neurones to the muscle and mediate control.
196
upper motor neurones mediates
carry the information from the brain down the spinal cord.
197
upper motor neurone lesion
cause spasticity paralysis and hyperreflexia,
198
lower motor neurone lesion causes
LMN caused flaccidity paralysis and areflexia.
199
stretch reflex explained
tendon stretched then leads to intrafusal muscle fibre stimulation, which results in sensory neurone activation. This signal travels along a monosynaptic arc, whilst a polysynaptic reflex arc to an inhibitory interneuron to the antagonist muscle. The agonist muscle contract and the antagonist muscle receive reciprocal inhibitory innervation.
200
flexor reflex arc explain
involves a pain stimulus, sensory neurone activation, a polysynaptic arc with flexion and withdrawal unilaterally, and contralateral extensor response.
201
left upper motor neuron lesion within the internal capsule for the corticospinal tract yields
right sided paralysis, hyper reflexia, and increased tone.
202
left upper motor neurone lesion at upper cervical spinal cord results in
left sided paralysis, hyper flexia and increased tone.
203
left lower motor neurone lesion results in
left sided paralysis, absent reflexes and flaccidity.
204
in the posterior dorsal column lesions above the decussation result
in contralateral sensory loss,
205
in the posterior dorsal column lesions below the decussation result
the decussation is ipsilateral sensory loss for fine touch, tactile localisation, vibration and proprioception.
206
stage 1 sleep
slow wave, slow eye movements. Easily roused. High amplitude and low frequency theta waves associated with sleep or stress
207
stage 2 sleep
cessation of eye movements, frequency reduced with sleep spindle clusters of high frequency bursts
208
stage 3 sleep
; increasing amplitude, slow delta waves associated with deep sleep. Presence of spindle activity declining.
209
stage 4 sleep
; exclusively delta waves associated with deep sleep.
210
REM sleep
rapid eye movements, paradoxical sleep associated with alpha and beta waves. High frequency and low fast asynchronous amplitude waves.
211
typical night pattern of sleep
it cycles from awake, eyes closed in alpha waves, progressing to the short-lasting stage one REM, then to the transition states of stage 2 and 3, before entering a deep sleep stage. This cycle repeats again but REM gradually increases and deep sleep stages will only occur once more before being replaced by REM.
212
describe the characteristic of deep slow wave sleep
deep slow wave sleep allows for dreams, deep restful sleep and decreased vascular tone and blood pressure, and reduced respiratory and basal metabolic rate.
213
without sleep there is
is impaired cognitive function, physical performance, fatigue, and irritability as well as increased risk of psychosis.
214
sleep is important for
for neuronal plasticity, learning and memory, cognition, clearance of waste from the CNs, conservation of energy and immune function.
215
dreams occur in
REM sleep
216
REM sleep description/physiology
eyes have burst of rapid activity whilst skeletal muscle is inhibited by the pons. This stage depends on cholinergic pathwats within the reticular formation projecting to the thalamus, hypothalamus and cortex. Heart rate and brain metabolism irregularly increases and brain waves resemble beta waves. We are difficult to arouse in this stage and it appears to be of some clinical importance.
217
falling asleep process physiological process
sleep centres in within the mid-pons take over when the active excitatory cells for wakefulness become fatigued resulting in inhibition of the cortex and this inhibitory process is likely serotonergic as well as being supported by sleep inducing peptides in the CSF. There is also support from suprachiasmatic nuclei in the hypothalamus for generating a circadian rhythm that induces the release of melatonin from the pineal gland for stimulating sleepiness.
218
waking process physiology
On the contrary wakefulness is stimulated by a hypothalamus neurotransmitter orexin which stimulate excitatory neurons in the ascending reticular activating system are released from inhibition by sleep centres in the reticular formation generating a feedback loop.
219
insomnia description
chronically unable to have quality sleep to maintain normal behaviour.
220
night terrors occur during
delta sleep
221
somnambulism refers to
sleepwalking during non REM sleep
222
narcolepsy description
individual enters REM sleep suddenly and is linked to dysfunctional orexin release from the hypothalamus.
223
role of suprachiasmatic nucleus in circadian rhythm
suprachiasmatic nucleus of the hypothalamus above the optic chiasma have an inherent 24hr cycle imbued by external cues such as light via the optic nerve. If destroyed there is likely the loss of melatonin signalling and orexin signalling in the hypothalamus.
224
describe the different components of voluntary motor system
voluntary brain control of muscles or reflexive control is via the common pathway which is alpha motor neurones in the spinal cord, particularly for reflexes it’s at a segmental level. the cerebral cortex, basal ganglia and cerebellum influence the brainstem nuclei to integrate and control reflexes through descending tracts such as the vestibulospinal and reticulospinal.
225
basal ganglia function in voluntary movement
initiates movement stimulating the cortex in regard to planning and initiating movement
226
the brainstem in the voluntary movement
brainstem centers for basic movements and posture which are influenced by the cerebellum in regards to sensory information about coordination of movement.
227
sensory inputs stimulate for voluntary movement
, sensory inputs stimulate local circuit neurons to integrate information and travel then along the common path for both system the alpha motor neurone which ultimately influences skeletal muscle.
228
how can descending inputs interact with segmental reflexes
descending input from the brainstem and direct cortical input travels along the corticospinal pyramidal tract. Descending voluntary excitation of alpha motor neurones can override the inhibition from the golgi tendon organs to maintain contraction if the cause is deemed worthy. This is the same for stretch reflex. The descending inputs are the result of the motor cortex planning, initiating and directing voluntary movements and the brainstem controlling basic movements and posture control.
229
how are muscles mapped in the spinal cord
there is a spatial map of body musculature that is mediolaterally mapped. Proximal muscles to medial motor neurones and distal to lateral motor neurones. This then travels along the axis of the spinal cord generating a 3D image essentially of functional motor neurones.
230
inverse stretch reflex is mediated by and physiology
mediated by golgi tendon organs monitoring muscle tension, contraction pulls the tendon and an impulse is sent along a 1b sensory neurone stimulating activation of inhibitory interneurons to the agonist muscle, and excitatory interneurons to the antagonist muscle, as well as informing the somatosensory cortex via the dorsal columns. This is a polysynaptic and protective process.
231
readiness potential refers to
Readiness potential refers to the increase in electrical cortical activity prior to voluntary movement in which the duration of the manifestation reflects the complexity.
232
readiness potential influence with the basal ganglia
The basal ganglia then process this to initiate the voluntary movement
233
readiness potential within the cerebellum
the cerebellum processes this and modulates timing, coordination and automatic voluntary movements, known as reflexes
234
Parkinson's disease explanation
Parkinson’s disease results in hypokinesia which is slowness characterised by rigidity and tremors. It is due to atrophy of neurones in the substantia nigra and their dopaminergic inputs to the striatum.
235
huntington's disease explanation
Huntington’s unlike Parkinson’s disease reflects hyperkinesia. Often characterised by spontaneous movements. It is due to atrophy of caudate, putamen and globus pallidus, preventing the inhibitory effects of the basal ganglia.
236
cerebellum for motor learning
gathers previous experiences to modulate motor processes with calculations to compare intention with action and then compensates to ensure success. Information from the somatosensory cortex, layer 5, and areas 4 and 6 are all projected to the cerebellum via the cortico-ponto-cerebellar projection. This connects the cortex, pontine nuclei and cerebellum. The cerebellum then feeds back to the cortex via the ventrolateral thalamus. Essentially this process is a feedback loop of voluntary movement.
237
lesions to the cerebellum cause
uncoordinated movements, ataxia, failure to touch the nose with the eyes shut, similar to the effects of alcohol.
238
presentation of multiple sclerosis
gradual onset over days
stabilises day to weeks
optic neuritis presents with subacute visual loss, painful eye movement, colour vision loss and relative afferent pupillary defect.
brainstem relapsed involve internuclear ophthalmoplegia, cranial nerve involvement, vertigo, nystagmus, ataxia and upper motor neurone signs in the limbs and sensory involvement.
myelitis often involves a hyperaesthesia, weakness, and bladder/bowel involvement.
gradual resolution to complete or partial recovery, often has relapses however.
239
MS relapse
a relapse results in optic neuritis, sensory symptoms, limb weakness. With vertigo, diplopia, vertigo and ataxia. Often with spinal cord bilateral symptoms and signs of bladder involvement. As well as limb weakness and sphincter disturbance.
240
MS clinically isolated syndrome
syndrome will be just a on off episode or is may be episodes of demyelination disseminated in space and time.
241
progressive phase MS
phase involves an accumulation of symptoms and signs with fatigue, sensory, stiffness, spasms, slurred speech, swallowing, bladder and bowel, diplopia, oscillopsia, and cognitive dementia.
242
progressive MS
. Primary progressive presents in their 50’s to 60’s with no relapses, poor prognosis and bladder/spinal symptoms.
243
MS Pathology
multiple sclerosis is a central nervous disease affecting the central nervous system, particularly the white matter through demyelination. This is through an auto-immune disease as T cells cross the blood brain barrier and inflame the myelin sheath.
244
MS diagnosis
diagnosis often depends on stage but signs involve sensory, cerebellar, hyperreflexia, plantar extensor, afferent pupillary defect, weakness, nystagmus and spasticity.
For a formal diagnosis it requires evidence of demyelination over a period of time and space. Often may be clinical through macdonald criteria or MRI. On an MRI you are looking for lesions. Other investigations involve lumbar puncture, visual/somatosensory responses, bloods and CXR.
245
general treatment for MS
involves general health, diet, vaccines, treatment of relapse
246
MS relapse treatment
looking for infection, treat with oral prednisolone, rehabilitation and SYMPTOMATIC TREATMENT
247
disease modifying treatment
treatment are intramuscular or subcutaneous injections of beta interferons or glatiramer acetate. Oral treatment includes teriflunomide and dimethyl fumarate. Second line treatments are natalizumab, fingolimod, and alemtuzumab.
248
symptomatic treatment is
anti-spasmodic medication, physiotherapy, for the dysesthesia amitriptyline or gabapentin, for urinary symptoms anticholinergics or catheters, constipation use laxatives and sexual dysfunction sildenafil is recommended. Cognitive behavioural therapy for depression, aids for the tremors, vision carbamazepine, SALT for speech/swallowing. Treat the patient’s symptoms not the general.
249
sensory transduction
the ability of sensory receptors to transduce adequate stimulus into a local detrimental depolarising generator potential, if significant enough the generator potential will overcome the threshold and reach the trigger zone activating action potentials. The frequency of which will be translated to reflect the intensity of stimulus. The receptive field encodes the location of the stimulus.
250
the major pathway by which information from the body about pain and temperature reaches consciousness
transported by A delta small myelinated and C unmyelinated fibres to synapse in the dorsal horn, then decussate in the segmental level to then project through the contralateral spinothalamic tract to the reticular formation, thalamus and ending in the somatosensory cortex of the post central gyrus S1.
251
pain and temperature are transported fibres by
small myelinated A delta and C unmyelinated
252
Describe the major pathway by which information from the body about touch and limb position reaches consciousness
touch is transported by A beta large myelinated fibres which project up through ipsilateral dorsal columns, synapsing in the cuneate and gracile nuclei. The 2nd order fibres decussate in the brain stem and project to the reticular formation, thalamus and ending into the somatosensory cortex S1 in the post central gyrus.
253
nociceptors are activated by
low pH by ASIC receptors, TRPV for heat, or through noxious stimuli channel activated by bradykinin which is stimulated by prostaglandins via G protein cascade. This results in depolarisation.
254
Pain pathway
This then travels along A delta and C fibres via the dorsal root ganglion, synapsing in the dorsal horn then decussating across at the segmental level to travel along the spinothalamic tract to the reticular formation, thalamus and finally terminating in the somatosensory cortex of the post central gyrus S1.
255
Explain why pain originating from the viscera can often result in sensation being referred to a somatic structure from the same dermatomes
this is due to convergence. The system enables to reduce the number of necessary neurones but results in specific ascending pathways where two touch receptors may synapse to the same second order neurone. There are also nonspecific ascending pathways in which a touch receptor and temperature receptor may synapse at the same second order neurone. This is often seen as resulting in referred pain.
256
explain convergence in neurone pathways
this is due to convergence. The system enables to reduce the number of necessary neurones but results in specific ascending pathways where two touch receptors may synapse to the same second order neurone.
257
non-specific ascending pathways in pain neurone pathways
pathways in which a touch receptor and temperature receptor may synapse at the same second order neurone. This is often seen as resulting in referred pain.
258
gate control hypothesis for pain modulation
Segmental control arises from faster fibres for touch and pressure, A alpha and A beta which activate inhibitory interneurons which release opioid peptides called endorphins that “close the gate”
259
Describe how pain can be controlled by descending pathway in the CNS
descending controls from the peri-aqueductal grey matter PAG and the nucleus Raphe Magnus NRM stimulate the same inhibitory interneurons that release endorphins closing the gate.
260
non-steroidal anti-inflammatory drugs pharmacological process
they inhibit cyclo-oxygenase which normally converts arachidonic acid to prostaglandins. Thus, preventing the sensation of nociceptors to bradykinin.
261
local anaesthetics process pharmacological process
blocks sodium action potentials and therefore all axonal transmission
262
trans cutaneous electric nerve stimulation pharmacological process
electrically stimulating the skin to stimulate A beta neurones to stimulate inhibitory interneurons to close the gate.
263
opiates pharmacological process
reduce the sensitivity of nociceptors. They block transmitter release in the dorsal horn and activate descending inhibitory pathways.
264
limbic system relevance in memory
emotional significance for memory
265
cingulate gyrus and amygdala association for in memory
emotion
266
hypothalamus is associated with
autonomic nervous system
267
immediate memory
experiences held for seconds, visual decaying fastest then auditory slowest.
268
what decays faster auditory or visual memory?
visual
269
short term memory
seconds to hours as a working memory associated with reverberating circuits.
270
intermediate long term memory
hours to weeks associated with chemical adaptation at the presynaptic terminal. Often associated with increased calcium entry stimulating greater neurotransmitter release.
271
long term memory
ifelong, associated with structural changes in the synaptic connections.
There is also an increased amplitude in graded membrane potential in the post synaptic cell called long term potential allowing a well-established pattern associated with a memory.
272
long term memory types
. Long term memory can be declarative, abstract recall of rules, events and language requiring the hippocampus or procedural acquired through repetition “motor memory”, it is independent of the hippocampus and based in the cerebellum.
273
reverberating circuit significance in memory
reverberating circuit is the idea a memory is initially electrical, circulating around neurones that needs to be continually excited. It’s essentially the first step to consolidating memory from short term to long term. This activity is through the papez circuit which is the hippocampus, mamillary bodies, anterior thalamus and cingulate gyrus.
274
retrograde amnesia explain
cannot access old memories. Cannot remember leading up to the injury. Long term memories are unaffected, often presents with anterograde amnesia, however if the thalamus is damaged and hippocampus spared then it is only retrograde amnesia as its essential for accessing memories.
275
antergrade amnesia explain
cannot form new memories. Cannot recall events after an injury, often associated with injury to the hippocampus.
276
short term memory into long term memory
continually activating a reverberating circuit will provide time for the memory to be deemed significant, allowing for consolidation. This requires converting an electrical memory into a chemical, and structural change. This is through selective strengthening of the synaptic connections. Memory is eventually stored in various parts of the cortex with visual in the visual cortex
277
importance for sleep for memory processing
consolidation requires attention. Subjects deprived of REM sleep show impairment of memory consolidation for complex cognitive tasks, dreaming may enable consolidation and reinforce weaker circuits
278
Acute angle closure Glaucoma symptoms
very painful, redness, blurred vision, nausea and vomiting, hazy cornea, fixed mid-dilated pupil and hard eyeball
279
scleritis symptoms
; very painful, redness, nodules, very tender
280
acute anterior uveitis symptoms
pain, watering, photophobia, blurred vision, floaters, red, cells in anterior chamber, hypopyon, small irregular pupil, prior history.
281
corneal abrasion symptoms
; pain, watering, blurred vision, epithelial defects
282
allergic conjunctivitis symptoms
itchy, red, discharge, acute, lid swelling, conjunctival swelling
283
infective conjunctivitis symptoms
gritty, red, discharge
284
symptoms and signs of cellulitis
symptoms and signs include painful, redness, blurred vision, malaise, proptosis, reduced eye movement.
285
management of cellulitis
involves admittance to hospital, Ct scan and drainage of pus.
286
FFA – Fluorescein angiography - method
rapid fundal photography following injection of fluorescein dye to examine flow of the vessels, pigment epithelium detail and retinal circulation and assessment of retinal vessel integrity.
287
OCT- optical coherence tomography method
use of infrared light to capture 3D images from optical scattering media.
288
ERG Electroretinography method
is an eye test for detecting the function of the retina. It picks up the electrical signals from photoreceptors. It uses an electrode on the cornea to measure electrical response.
289
EOG electrooculography
recording eye movements and position by measuring the difference in electrical potential between two electrodes on either side of the eye. There is a dark phase and a light phase. If its ratio is less than 1.8 it indicates a malfunction of the structure form which the potential originates.
290
VEP – visual evoked potential
visual evoked potential is a test using a visual stimulus such as a alternating checkerboard on a computer screen, responses are recorded using electrodes on the back of the head and presented as an EEG reading. It highlights the receiving and interpreting of visual signals.
291
non-arteritic painless anterior ischaemic optic neuropathy description
infarct within the short posterior ciliary arteries resulting In compartment syndrome from the oedema resulting In retinal ganglion cell death
292
signs of non-arteritic painless anterior ischaemic optic neuropathy;
Normal signs of decreased visual acuity, dyschromatopisa acquired loss of colour vision), and a swollen optic nerve.
293
non-arteritic painless anterior ischaemic optic neuropathy; symptoms
acute, painless unilateral vision loss commonly described as blurring/cloudiness.
294
Central retinal artery occlusion; description
obstruction of the retinal vascular lumen by embolus, thrombosis or inflammation, damage or spasm, associated with giant cell arteritis. Ischaemia of the inner retina occurs and oedema, this resolves by choroidal circulation with mild recovery.
295
central retinal artery occlusion signs
include normal fundus, relative afferent pupillary defect, retinal whitening and cherry red spot. Chronic signs include pale optic disc, thin retinal tissue, attenuated vessels and altered retinal pigment
296
symptoms of central retinal artery occlusion
acute painless vision loss
297
central vein occlusion description
gradual loss or sudden loss of vision due to a blocked vein and fluid leakage into the retina, swelling altering vision and nerve cell death.
298
symptoms of central retinal vein occlusion
Symptoms are floaters/dark spots in vision, in severe cases pain and pressure. Normally unilateral.
299
cataracts explanation
gradual opacification of the lens with symptoms of loss of vision, dazzle and glare
300
glaucoma explanation
raised intraocular pressure with optic neuropathy associated with visual field changes.
301
diabetic retinopathy explanation
high blood sugar blocks of the small blood vessels for supplying the retina, new vessels develop but will be weaker and leak blood into the eye.
302
signs of diabetic retinopathy
signs of microaneurysms, retinal exudate and neovascularisation.
303
symptoms of diabetic retinopathy
loss of central vision, inability to see colours and black spots in vision.
304
central retinal artery occlusion retinal appearance
retina pale except in the macular area in which the choroidal circulation causes a cherry red spot to form resulting in sudden, painless and complete loss of vision in one eye.
305
central retinal vein occlusion retinal appearance
gives the appearance of a stormy sunset with engorged veins, and haemorrhages alongside them.
306
optic neuritis pathology
Develops as a result of demyelination of the optic nerve resulting in visual loss. It’s often associated with multiple sclerosis. Due to the autoimmune processes of systemic T cell targeting of myelin.
307
ischaemic optic neuropathy pathology
often develops due to giant cell arteritis or atherosclerosis in non-arteritis. The acute ischaemia then causes nerve oedema, causing swelling to the optic disk and retina dysfunction.
308
optic neuritis signs
associated with multiple sclerosis, commonly affects young adults in one eye
309
optic neuritis symptoms
vision loss, reduced colour vision, pain on eye movement
310
ischaemic optic neuropathy signs
unilateral, reduced visual acuity, afferent pupillary defect. Splinter haemorrhage optic disk and swollen. Pale if arteritis or non-arteritis then hyperaemic, defect often in the inferior and central visual fields.
311
symptoms of ischaemic optic neuropathy
vision loss, painless, rapid. Malaise, muscle aches and pains, headaches, jaw claudication
312
retinitis pigmentosa pathology
progressive inherited disease that results in retinal degeneration.
313
symptoms retinitis pigmentosa
Often symptoms include peripheral and night vision. Then as it progresses colour perception, visual acuity and central vision are diminished
314
signs of age related macular degeneration
symptoms of progressive distortion of central vision. It has signs of distortion on an amsler chart, drusen and pigmental changes
315
pathology of age related macular degeneration DRY
It may be dry due to atrophy, or wet due to choroidal angiogenesis. either way it results in damage to the macula, made noticeable by pigment changes in the retina. Late stage dry AMD is due to the gradual breakdown of light sensitive cells in the macula and supporting tissue
316
Wet Age related macular degeneration pathology
is due to abnormal vessel growth leaking fluid into the macula causing it to swell and degrade. It may be rapid or long term.
317
symptoms of muscle disorders
weakness of skeletal muscle, shortness of breath, poor swallow, cardiomyopathy, cramp, pain, stiffness and myoglobinuria.
318
signs of muscle disorders
wasting, hypertrophy, reduced tone and reflex and no sensory signs purely motor weakness.
319
congenital classifications of muscle disease
structural muscular dystrophy, contractile congenital myopathies, coupling channelopathies, and energy with enzyme and mitochondria dysfunction
320
acquired diseases of muscles classifications
metabolic, endocrine, inflammatory and iatrogenic
321
investigations of muscle diseases
creatine kinase, EMG, muscle biopsy of structure, biochemistry, and inflammation. As well as genetic testing.
322
myasthenia gravis presentation
fatigable weakness of limbs, eyelids, muscles of mastication resulting in difficulty or fatigue in talking, breathing and diplopia
323
investigations of myasthenia gravis
investigations involve an AChR ab, anti MuSK ab, neurophysiology of repetitive stimulation and jitter, and a CT scan of the chest to check for a thymoma.
324
treatment for myasthenia gravis
involves acetylcholinesterase inhibitor, and immunosuppression through prednisolone, and steroid saving agent. Immunoglobulins/plasma exchange and a thymectomy.
325
causes of peripheral neuropathy
lesion of an individual nerve through compression or vasculitis or through a general peripheral neuropathy.
326
general neuropathy causes
General neuropathy causes are though hereditary, metabolic particularly alcohol or diabetes, toxic drugs, infection, malignancy as a paraneoplastic syndrome or inflammation causing demyelination as acute Gullian Barre syndrome or chronic polyneuropathy.
327
nerve root symptoms
nerve root symptoms include myotomal wasting and weakness, reflex changes, and dermatomal sensory change.
328
generalised peripheral neuropathy symptoms
include sensory and motor symptoms stating distally and moving proximally.
329
individual nerve symptoms pathology
There is individual nerve symptoms of specific sensory changes, and wasting/weakness of innervated muscle
330
LMN
muscle fasciculation, wasting and weakness, reduced tone, reflexes, flexor planter
331
UMN
increased tone, brisk reflexes, no wasting, and pyramidal pattern of weakness, extensor plantar
332
clinical presentation of motor neurone disease
muscle fasciculations, wasting and weakness associated with lower motor neurones lesions, and upper motor neurones signs of increased tone and brisk reflexes. No sensory involvement and cognitive decline in 10%. Starts with limb, progressing to bulbar and then respiratory
333
treatment of motor neurone disease
Treatment is supportive through PEG feed, non-invasive ventilation, physio, OT, SALT, care. Riluzole, and anticipatory care/palliation.
334
investigations of motor neurone disease
signs and EMG
335
spinal cord stroke symptoms
back pain, visceral referred pain, weakness, vascular risk factors. Onset over several hours or sudden, paraesthesia, and urinary symptoms with urinary retention and incontinence.
336
symptoms prior to a migraine
Prior to an attack there is fatigue, mood swings, cognitive changes, muscle pains and food cravings
337
early migraine headaches are characterized
characterized by dull headaches, nasal congestion and muscle pain.
338
advanced migraines are characterised
Advanced headaches are unilateral throbbing with nausea, photophobia, osmophobia, and phonophobia.
339
Aura is a
transient cortical dysfunction affecting visual, sensory, motor or speech in a slow wave.
340
postdrome migraine characteristics
fatigue, cognitive changes and muscle pain
341
percentage of migraines that originate from medication
60%
342
chronic migraine is a migraine that lasts longer than
15 days taking a symptomatic drugs
343
causes of a medication migraine
Triptans, ergots, opioids (>10 per month), analgesics, or caffeine overuse
344
cluster head description and symptoms
mainly orbital and temporal, 15 minute to 3 hours of pain with a rapid onset and cessation. Extremely excruciating with prominent autonomic symptoms and typical aura. It occurs in clusters with 1 to 8 in a day over a bout of time.
345
paroxysmal hemicrania symptoms ad description
can occur up to 1 to 40 times a day for 2-3 minutes resulting in restlessness unlike migraines, precipitated by bending or rotating the head and normally chronic.
346
SUNCT description/ symptoms
SUNCT lasts only 240 seconds characterised by stabbing or pulsatile pain, with frequency of 3-200 a day accompanied by conjunctival injection and lacrimation
347
tension headache description
headaches are rarely disabling, with a bilateral tightening but with no associated features.
348
migraine treatment
abortive use of aspirin, Triptans, limit to 10 days a month. Prophylactic use of propranolol, anti-epileptics, tricyclic anti-depressants, venlafaxine.
349
cluster headache treatment
abortive use of nasal spray, oxygen and subcutaneous injection of sumatriptan as it needs to be rapid. Abortive for a bout requires depomedrone injection, or oral prednisone. Preventative; verapamil high dose, or lithium.
350
paroxysmal hemicrania prophylaxis
indomethacin
351
SUNCT/SUNA prophylaxis
gabapentin or carbamazepine
352
trigeminal neuralgia treatment
carbamazepine or surgical intervention with glycerol ganglion injection, decompression surgery or stereotactic radiosurgery.
353
red flags for headaches
```
thunderclap
persisting
>50
immunosuppression
cancer
neuro symptoms
fever
neck stiffness
exertional
morning headaches
standing up trigger
jaw claudication
visual
```
354
thunderclap presentation
high intensity within a minute
355
raised ICP presentation
worse in morning, worse lying flat, focal symptoms, cognitive/ personality changes, seizures and visual obscuration and pulsatile tinnitus.
356
intracranial hypotension presentation
worse standing upright
357
giant cell arteritis presentation
diffuse, persistent, systematic unwellness, scalp tenderness, jaw claudication and visual disturbance with prominent temporal arteries.
358
trigeminal neuralgia features
maxillary or mandibular sensory area with unilateral stabbing pain with similar SUNCT triggers and frequency but with no autonomic features
359
treatment for trigeminal neuralgia
treatment; prophylaxis with carbamazepine or surgical intervention with a glycerol ganglion injection, stereotactic radiosurgery or decompression surgery.
360
thunderclap management
hospital assessment, CT, angiography an LP in case of subarachnoid haemorrhage.
361
meningitis features
headache and fever, nausea, vomiting, photo/phonophobia, stiff neck
362
raised ICP features
progressive headache that’s worse lying down or in the morning, focal symptoms and signs, cognitive changes, seizures, visual obscuration’s and pulsatile tinnitus.
363
intracranial hypotension treatment
MRI, bed rest, fluids, analgesia, caffeine, epidural blood patch.
364
giant cell arteritis features
diffuse, persistent, severe, systemic unwellness, scalp tenderness, jaw claudication, visual disturbance and prominent temporal arteries
365
treatment of giant cell arteritis
elevated ESR >50, raised CRP then high dose prednisolone and biopsy.
366
pain fibres
Alpha delta fibres and C fibres
367
the second order neurone pain pathway
spinothalamic tract, decussating at that segmental level along the lateral side of the tract in rexed lamina 2 & 5. It is then transmitted to the brain via the ventroposterior thalamic nuclei within the medial thalamus. Next the signal is sent to the limbic system and cortex via the pain matrix as pain is perceived in the somatosensory cortex.
368
descending pathway of pain
The medial part of the pain matrix feedback information and forward it to the brainstem PAG for emotional and affective components and control of pain. Finally, the descending pathway if from the brain to the dorsal horn via a noradrenergic periaqueductal grey matter and usually decreases the pain.
369
allodynia
inflammatory markers from an injury that decreases the threshold for a response causing hyperalgesia
370
hyperalgesia
increased perception of noxious stimuli
371
secondary hyperalgesia
increased perception of noxious stimuli in uninjured tissue
372
wind up modulation of pain pathways
to the activated homo synaptic synapses that depend on progressive increase of neurones to increases the response, growing over the course of the stimuli and terminating with the stimuli.
373
classical sensitization of pain pathways
new (hetero) synapses in the dorsal horn will start transmitting once the threshold has ben met and begins immediately, outlasting the initial stimuli and maintain at low levels of stimuli if they are ongoing and it is this process responsible for secondary hyperalgesia.
374
neuropathic pain
often chronic pain, initiated by a primary lesion or dysfunction in somatosensory nervous system. May be referred pain due to the neurological territory and responds poorly to analgesics.
375
differentials of blackouts
syncope, first seizure, hypoxic seizure, concussive seizure, cardiac arrhythmia, non-epileptic attack.
376
features of partial seizures
characterised according to aura, motor features, autonomic features and degree of awareness, may even into a generalised convulsive seizure. Occurs at any age, focal abnormality on EEG and MRI may show the cause.
377
history of the epilepsy
what were they doing at the time, any warning, what they were doing the night before, how did they feel, incontinence, tongue biting.
378
investigation of epilepsy
blood sugar, ECG, consider alcohol and drugs, CT head. Video telemetry may be recommended and a EEG, with stimulation.
379
first line therapy for epilepsy
first line; sodium valproate
levetiracetam for primary general
carbamazepine for partial and secondary
380
treatment of status epilepticus
requires midazolam, lorazepam and diazepam. Second line is phenytoin or valproate and third line being anaesthesia
381
after 1 seizure normal patient must wait before driving
6 month s
382
patients with seizures must wait
1 year free on medication
383
features for viral encephalitis
flu like prodrome, progressive headache, +/- meningism, gradually progressive cerebral dysfunction with confusion, abnormal behaviour, memory disturbance, depressed consciousness, seizures, focal symptoms and signs.
384
autoimmune encephalitis causes
anti VGKC
| anti NMDA
385
investigations for encephalitis
blood cultures, CT +/- MRI, lumbar puncture (unless signs of a lesion, or raised intracranial pressure), EEG
386
microbiology for encephalitis
herpes simplex virus, enteroviruses, arbovirus,
387
Anti-VGKC epilepsy symptoms
seizures, amnesia, altered mental state
388
Anti-NMDA symptoms
prodrome, psychiatric features, seizures and altered mental states, progresses to movement disorder and coma.
389
cerebral abscess features
; fever, headache, focal symptoms, papilledema, depressed consciousness, +/- meningism.
390
cerebral abscess of microbiology
spread from adjacent infection, blood borne infection or from neurosurgical procedure. Often polymicrobial, often streptococci and anaerobes such as bacteriodes or prevotella
391
treatment for cerebral abscess
; surgical drainage, high doses of penicillin or ceftriaxone for streps or metronidazole for anaerobes.
392
meningitis clinical features
; neck stiffness, altered mental state, fever. Short history or progressive headache, photophobia, nausea, vomiting, cerebral dysfunction, cranial nerve palsy, and petechial skin rash.
393
microbiology of meningitis
bacterial meningococcal meningitis or streptococcus pneumonia, or viral from enteroviruses
394
investigations of meningitis
blood cultures, CSF lumbar puncture (unless lesion or raised intracranial pressure)
395
lyme disease features
features; vector borne, multi system rheumatological, neurological, ophthalmological, cardiac.
Local infection with erythema migrans with flu symptoms, fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness. Stage 2 multi system, Peripheral nervous system affected more. Stage 3 subacute encephalopathy and encephalomyelitis.
396
investigations for lyme disease
serology, CSF lymphocytosis, MRI brain/spine, nerve conduction studies
397
treatment for lyme disease
I.V. ceftriaxone, oral doxycycline
398
microbiology for lyme disease
borrelia burgdorferi
399
neurosyphilis investigations
treponema antibody tests, CSF lymphocytes
400
microbiology of neurosyphilis
treponema pallidum
401
treatment of neurosyphilis
high dose penicillin
402
a prion is
transmissible proteinaceous particle
403
CJD affect on nervous system
rapid onset dementia, myoclonus, neurological decline, cerebellar ataxia, cortical blindness and seizures, extrapyramidal with tremors, rigidity, bradykinesias, dystonia, pyramidal with weakness, spasticity and hyper-reflexes and pyramidal with weakness, spasticity and hyper reflexes
404
rabies immunisation
to those at risk, post exposure given passive immunisation and active immunisation.
405
tetanus immunisation
toxoid immunisation and passive immunisation for those at high risk.
botulism given anti toxin
406
longstanding ischaemia pathological appearance
results in localised brain death due to death of neurones from oxygen starvation. The wedge shaped is a result of the arterial perfusion territory, it then becomes soft and then cystic. Foamy macrophages move in to repair the damage resulting in fibrosis and there is yellowing of tissue.
407
watershed zones reason for in ischaemia
prolonged period of hypotension with oxygenated blood results in watershed zones (areas between cerebral artery territories) being poorly perfused. Often symmetrical
408
pathological appearance of cardiac arrest ischaemia
cardiac arrest, brain deprived of oxygen results in large grey matter areas thinning, necrosis and laminar lines.
409
primary brain tumours
neuroepithelial tissue and can be pituitary adenomas, gliomas and meningioma
410
secondary brain tumours
metastatic spread
411
glioma description
Glioma’s arise from astrocytes, therefore are aggressive, and spread through the white matter and CSF pathways but unlikely to spread systematically.
412
meningioma description
slow growing, extra axial benign tumours arising from the arachnoid. Often along the falx, convexity or sphenoid bone.
413
pituitary tumours often causes
often cause visual disturbance and hormone imbalances
414
CSF production
400-450cc
415
CSF function
CSF; bathes brain and spinal cord from the subarachnoid space. Main function is to act as a shock absorber, removes some waste products and provides some immunological support.
416
foramina of the 4rth ventricle
foramen of magendie (medial 1 ) and foramen of Luschka (lateral 2)
417
flow of CSF
choroid plexus to flow is from lateral, foramina of munro, 3rd, aqueduct of sylvius, 4rth, foramen of magendie and foramen of Luschka2 then into the subarachnoid space, to the granulations and uptake by the villi into the dural venous sinuses.
418
hydrocephalus is the
blockage of CSF
419
obstructive hydrocephalus is
blockage of ventricle outflow
420
communicating obstructive hydrocephalus
level of arachnoid granulations
421
features of hydrocephalus
features; asymptomatic, increased ICP, headaches worse in the morning or on coughing, papilledema, visual disturbances, gait abnormality, loss of up gaze or abducens palsy, impaired consciousness.
422
treatment of hydrocephalus
carbonic anhydrase inhibitor, extraventricular drain in emergencies, CSF diversion through 3rd ventriculostomy for non- communicating or shunt insertion.
423
indications for a lumbar puncture
; CSF for analysis for blood, protein, viral, bacterial infections, measurement of pressure, and diagnostic tests as well as therapeutic for raised pressure.
424
normal pressure hydrocephalus features
reversible dementia, gait disturbance (magnetic), urinary incontinence, over age of 60
425
idiopathic hydrocephalus features
raised ICP without cause, headaches an visual disturbances, often young obese females
426
management post lumbar puncture
bed rest for 2-4 hours, warn for low pressure headaches. Stop if patient becomes unconscious or develops neurological deficit.
427
normal CSF stats
normal CSF should be clear, colourless, pH of 7.33 to 7.35, WBC 0-5, 0 RBC’s, Protein of 300 mg/l and glucose around 40-80mg/dl. Total volume should be 150ml.
428
meningitis CSF
cloudy, lots of polymorphs, protein >1g and low glucose.
429
CSF blood
trauma
430
yellow CSF
breakdown of blood products
431
stroke epidemiology
2nd - 3rd leading cause of death
432
ACA occlusion symptoms
contralateral paralysis of foot and leg with sensory loss. Impairment of gait and stance.
433
MCA occlusion symptoms
contralateral paralysis of arm, face leg, sensory loss and homonymous hemianopia. Gaze paralysis to opposite side, aphasia if on dominant side, unilateral neglect and agnosia for half of external space in non-dominant stroke.
434
lacunar stroke symptoms
can be pure motor, pure sensory, dysarthria and ataxic hemiparesis.
435
PCA circulation symptoms
; coma, vertigo, vomiting, nerve palsies, ataxia, hemiparesis, hemisensory loss, crossed sensori-motor deficits visual field deficits
436
stroke acute treatment
thrombectomy has the highest rate of preventing death. Then it is a IV TPA within 3 hours, then stroke units and IV TPA within 3-5 hours. Aspirin has the lowest number needed to prevent 1 death or dependency.
437
secondary prevention for a stroke
a carotid endarterectomy for internal carotid stenosis. However there are anti hypertensives, anti-platelets, lipid lowering agents, warfarin for AF all reduce risk.
438
stroke investigation
investigations; routine blood tests, CT for infarct, haemorrhage then MRI, ECG, echocardiogram, carotid doppler, cerebral angiogram, hyper coagulability screen.
439
TPA contraindications
It cannot be used if blood is present, recent surgery or bleeding episodes, coagulation problems, BP >185 or diastolic >110, or if glucose is less than <2.8 or >22mmol/L.
440
depressed respiration
drug overdose, metabolic disturbance
441
increased respiration
hypoxia, hypercapnia, acidosis
442
fluctuating respiration
brainstem lesion
443
investigations for a coma
blood sample for biochemistry, haematology, blood gas, toxicology, glucose. Establish baseline pressure, pulse, temperature.
temperature, skin, breath, abdomen, meningism, fundal examination, respiration, heart rate, blood pressure, CVs.
444
coma without focal or lateralising signs or without meningism - investigations
toxicology, blood sugar and electrolytes, hepatic and renal function, acid-base and arterial blood gases, blood pressure and carbon monoxide poisoning.
445
coma without focal or lateralising signs but with meningism; - investigations
; CT scan, lumbar puncture
446
coma with focal brainstem or lateralising cerebral signs - investigations
CT/MRI with metabolic screens, lumbar puncture or EEG if necessary
447
prognosis of coma
15% of patient in non-traumatic coma >6 hours make a recovery.
448
management of coma
maintenance of vital functions, skin care and avoidance of pressure sores, management of bladder and bowel function, control of seizures, prophylaxis of DVT and peptic ulcers, prevention of contractures.
449
coma definition
state of unarousable psychological unresponsiveness with not psychological response to stimulus or needs”
450
consciousness requires
an intact ascending reticular activating system for alertness, and a functioning cerebral cortex for interpretation of consciousness. Therefore, consciousness is arousal and awareness of environment
451
persistent vegetative state definition
brain stem recovery but with no cortical function. There is arousal but no awareness of the state.
452
coma without focal or lateralising signs or without meningism causes
ischaemia, metabolic, intoxication, systemic infection, hyperthermia or hypothermia, epilepsy are all possible causes.
453
coma without focal or lateralising signs but with meningism
subarachnoid haemorrhage, meningitis, encephalitis
454
coma with focal brainstem or lateralising cerebral signs
tumour, haemorrhage, infraction or abscesses in the cerebrum
455
locked in syndrome definition
head injuries such as diffuse axonal injury, contusion, intracerebral haematoma, extracerebral haematoma (sub/extradural).
456
management of increases intracranial pressure
surgery to relieve pressure via a haematoma, or ventricular shunt. Osmotic agents such as mannitol, analgesics, maintain PO2 whilst reducing PCO2 and reduce metabolism through temperature reduction and barbiturates.
457
subdural CT appearance haemorrhage
convex ellipse
458
extradural CT haemorrhage appearance
concave, convex lens
459
test for CN2
– visual acuity, pupillary reactions, fundoscopy, colour vision, visual fields
460
tests for CN 3,5,6
ptosis, pupil size, pupillary reaction, eye movements.
461
CN 5 tests
sensation, power of mastication, corneal reflex, jaw reflex.
462
CN 7 tests
expression, corneal reflex, taste
463
CN 8 tests
Rhinne’s and Weber tests, Dix Hallpike test and Untenberger’s test
464
9,10CN tests
movement of palate, gag reflex, quality of speech, quality of cough
465
CN 11 tests
shoulder shrugging and head turning
466
CN 12 tests
appearance, movement and power of tongue
467
pupillary light reaction afferent and efferent
2 afferent, efferent 3
468
corneal reflex afferent and efferent
afferent 5, efferent 7
469
jaw jerk reflex afferent and efferent
afferent and efferent 5
470
gag reflex afferent and efferent
afferent 9, efferent 10 #
471
causes for dilated pupils
third nerve palsy results in dilated pupils. As well as youth, dim lighting, mydriatic eye drops, amphetamine or cocaine, brain death, anxiety.
472
constricted pupil reasons
pathway results in a constricted pupil. Other causes include old age, bright lights, miotic eye drops, opiate overdose, horner’s syndrome.
473
trigeminal neuralgia features
paroxysmal attacks of lancinating pain, middle aged and older, caused by a vascular loop compression.
474
ball's palsy features
unilateral facial weakness, LMN, pain behind ear, risk of corneal damage due to eye closure disruption.
475
vestibular neuronitis features
sudden onset, disabling vertigo, vomiting, gradual recovery, may be viral.
476
pseudobulbar palsy features
difficulty swallowing and disorder articulation/slurring occurs in bulbar and pseudobulbar palsy.
pseudobulbar palsy is a UMN lesion of both internal capsules resulting in dysarthria, dysphonia, dysphagia, spastic mobile tongue, brisk jaw reflex, brisk gag reflex.
477
bulbar reflex feature
bulbar reflex is a bilateral LMN lesion affecting 9-12th cranial nerves resulting in a wasted fasciculation tongue, dysarthria, dysphonia, and dysphagia.
478
cranial nerve midbrain nuclei
3 + 4
479
pons CN nuclei
5+6+7
480
pontomedullary junction CN nuclei
8
481
medulla CN nuclei
9 +10+11+12
482
dementia clinical syndrome
progressive impairment of multiple domains of cognitive function in alert patient leading to loss of acquired skills and interference in occupational and social roles.
483
Parkinson's syndrome
dopamine loss within the basal ganglia resulting in bradykinesia, rigidity, tremor, postural instability.
484
dementia diagnosis + inv
history, family history, progression, risk factors and deficits. Investigations involve routine bloods, CT/MRI others include CSF, EEG, functional imaging and genetics. Cognitive function may be measured with the MMSE on montreal screening tests.
485
Parkinson's diagnosis
bradykinesia with tremor, rigidity, postural instability and slowly progressive. Responsive to dopamine replacement treatment. May use a dopamine transporter SPECT to diagnose
486
alzheimer's treatment
cholinesterase inhibitors with donepezil, or NMDA antagonist.
487
Parkinson's treatment
dopamine replacement treatment through dopamine agonists, MOA-B inhibitor, COMT inhibitor. Followed on by Levodopa increased half life, continuous infusions, functional neurosurgery (deep brain stimulation) and allied health care professionals.
488
features of temporo-parietal features
early memory disturbance, language and visuospatial problems, personality preserved until later.
489
frontotemporal dementia features
early change in personality, behaviour, change in eating habits, early dysphasia, memory and visuospatial relatively preserved
