Neuro Flashcards
(278 cards)
1
Q
How many neuones in somatic vs autonomic pathways
A
2 vs 3
2
Q
What are the emergent properties of the brain?
A
Properties the whole system has but individual components do not. e.g. consciousness, sensory awareness, thought process, sensory attention
3
Q
What is a Brodmann area?
A
Area of cortex classificed on histological appearence and subsequently function
4
Q
Explain rostral caudal in CNS
A
Different for brain stem and cerebrum
5
Q
Explain evolution of brain - out to in
A
Neocotex - complex function
Paleocortex - memory and emotion e.g. cingulate gyrus, archicortex e.g. brainstem, olfaction
6
Q
What structure separates the anterior lateral ventricles?
A
Septum pellucidum
7
Q
What is the fornix
A
Band of nerve fibres within the limbic system which connects the hippocampus, mammillary bodies and the anterior nuclei of the thalamus
8
Q
Where is the calcarine sulcus?
A
Sagital view- occipital lobe
9
Q
Where is the lateral fissure/ sulcus
A
Between temporal and frontal/ parietal lobes
10
Q
What is the insula?
A
Infolding of brian deep
Responsible for consciousness, emotion and homeostasis
11
Q
What is the corona radiata
A
Neural traffic from cerebral cortex
12
Q
What is the caudate nucleus
A
Part of basal ganglia.
Involved in voluntary movement.
Loops around the putamen/ globus palidus, lateral to thalamus and medial to insula
13
Q
What is the lenticular nucleus
A
Lens shaped, formed from the putamen and globus pallidus (medial).
14
Q
What is the corpus striatum?
A
striatum plus globus pallidus/ caudate + lenticular
15
Q
What is the (neo)striatum?
A
Caudate nucleus and the putamen.
Responsible for reward, motivation, motor and action planning
16
Q
What composes the basal ganglia
A
Corpus striatum, substantia nigra and subthalamic nucleus
17
Q
What are the cerebellar peduncles
A
Fibres from cerebellum to brain stem. L and R sup, mid and inf (6)
18
Q
Briefly explain drainage on the brain
A
Centrally via the superior and inferior sagittal sinuses. Into confluence with occipital.
Transverse sinuses to sigmoid to IJV
19
Q
What is the conus medullaris
A
Tapering end of spinal cord T12-L1
20
Q
What is the filum terminale
A
Delicate strand of fibrous tissue from apex of conus medullaris - continuation of pia. Travels within a dural sac before adhering to the dural and then fusing to the coccyx
21
Q
What are the denticulate ligaments?
A
Ligaments either side of the spinal cord which attach to the arachnoid and dura maters to provide support (between them) extension of Pia.
22
Q
Describe lumbar puncture
A
L3/4 by finding the PSIS and going medially- feel above and below for largest space
23
Q
Safe Lumbar puncture in kids?
A
L5/S1
24
Q
Where is the substantia gelatinosa and what is found there?
A
Rexed lamina 2. Part of spinothalamic trunk. C fibres pain gate control theory of pain. Fibres from Lissauer’s synapse here. 2nd order neuones then deccusate in the anterior white commissure.
25
Where is the substantia nigra and what is found there?
Parts of rexed lamina III-V form. Pain and temperature from spinthalamic. Fibres from Lissauer's synapse here. 2nd order neuones then deccusate in the anterior white commissure.
26
Difference between ataxia and apraxia
```
Apraxia = inability to perform complex movements despite having the capability to bring about movement
Ataxia = a loss of full control of body movements
```
27
Aphasia vs aphonia vs dysarthria
aphasia = speech and language disorder
aphone = pysical inability to produce sound e.g. bilateral recurrent laryngeal nerve damage
Disarthria - disruption of articulation of speech e.g. movement of tongue
28
What is paraplegia
Loss of sensory and motor functions of lower limbs
29
What is Chorea
Involuntary jerky movements of hips shoulders face e.g. Huntington's
30
Describe features of spasticity
hypertonia, hyperreflexia and paralysis
31
What is a neuropore
End of neral tube as it fuses away from cervical region
32
How can spina bifida be detected before birth?
alpha-fetoprotein in blood test or amniocentesis
| USS
33
Types of spina bifidal
Occulta - just vertebrae affected often asymptomatic
meningocoele - meningeal involvement
Myelomeningocoele - neural tissue outside the body
34
Symtoms of spina bifida
Anywhere along length of cord by normally lumbosacral.
Weakness in lower limbs.
Blader control
Orthopaedic problems
Pressure sores
Hydrocephalus
Neurological development - behaviour, problem solving and memory
35
Neural tube defect cranially
Anencephaly
Rachischisis - failure of neural fold elevations = motor and sensory deficits, chronic infections, and disturbances in bladder function or anencephaly
36
How can hydrocephalus be treated? What happens if no treatment?
Peritoneal/ jugular shunt
causing convulsion, tunnel vision, and mental disability.
headaches, vomiting, nausea, papilledema, sleepiness or coma
37
Describe the dilations/ development of brain
3 cranial dilations in neural nube.
Prosencephalon becomes telencephalon (cerebrum) and diencephalon (thalamus).
Mesencephalon becomes mesencephalon (midbrain).
Rhombencephalon becomes metencephalon (pons) and myelencephalon (medulla oblongata)
38
Location of ventricles in respect to enbryology
Lateral in tele
third in Di
Aqueduct in mes
Forth in Met/ myel
39
Describe the flexures of the CNS
Cervical at spinal cord/ medulla juntion
| Cephalic at midbrain
40
Describe the growth of the neural tube into CNS structures
Thickening around central canal = neuroepitheal layer
Mantal around that into dorsal/ alar (sensory) and ventral/ basal plates being motor. Around that is marginal layer which is white matter
41
Descrbe neural crest cells in CNS developemtn
```
Migrate
Undergo epithial to mesenchyme tranisition.
Include:
Cranial nerve ganglia
Spinal/ dorsal root ganglia
Sympathetic ganglia
Schwanne cells
Leptomeninges
```
42
How can alcohol affect developing CNS?
Neural crest cell migration
43
What is Hirschsprung's disease
Aganglion megacolon - failure of migration
44
Describe the functions of astrocytes
Provides structural support
Provides blood brain barrier
Removes (uptakes) neurotransmittors
Provides nutrient to neurones e.g. glucose-lactate shuttle as no glycogen store
Maintains ionic environment e.g. buffers K
45
Describe the functions of microglia
Phagocytose foreign material and debris - becomes activated. Can APC and activate t cells although inflam is limited as CNS is immune privileged (not to raise ICP). Immune privileged means they can tolerate antigens without an inflam response.
46
Describe components of the BBB
Tight endothelial cell junctions, basement membrane and astrocyte foot processes.
47
Types of neurotranmittors
Amino acids e.g. GABA, glycine, glutamate. Biogenic amine e.g. dopamine, na, 5HT, histamine. Peptides e.g. dynorphin, somatostatin, CCK. Others e.g. purines
48
Describe Glutamate as a neurotransmittor
70% of all synapses. Excitatory.
| Ionotropic or metabotropic
49
Explain ionotropic glutamate receptors
AMPA -fast K Na
Kainate- K Na
NMDA - slow K Na Ca (glycine also agonises) Causes depoalrisation EPSP
50
Explain metabotropic glutamate receptors
G protein coupled, linked to IP3/ Ca/ cAMP. known as mGluRs. Can upregulate AMPA
51
Upregulation of Glutamate receptors? Signidicance?
From NMDA and mGluRs upreg AMPA.
| Long term potentiation. Ca through NMDA is important however too much can lead to excitotoxicity
52
Decribe GABA and glycine and their receptors
Inhibitory (IPSP).
Binding to receptors with integral Cl- causes hyperpolarisation.
GABA can also bind to modulatory GPCRs.
GABA is main ihibitory. Barbiturates and Benzos work here.
Glycine mostly in the spinal cord and brainstem - inhibitory interneurones in reflex pathways
53
General action of biogenic amines and Ach
Mostly neuromodulators confined to specific pathways.
54
Describe Ach neurotransmission effects and clin sig
Autonomic functions
Mostly excitatory
Often present on pre synaptic terminal to enhance the release of other transmitters.
Also nicotinic and muscurinic in CNS.
Neurones originate in basal forefrain and brainstem spread diffusely to cortex and hippocampus (hence learning and memory).
Within the corpus striatum.
Degen in Alzheimers
55
Dopamine pathways
Nigrostriatal = motor control (parkinsons)
Mesolimbic (psychotic treatment in schitzo D2) and mesocortical = mood, arousal and reward
tuberoinfundiblar = prolactin release and endocrine function
56
Describe Na pathways
Brainstem = neurone bodies.Most from locus coeruleus in pons.
Release of Na throughou cortex, hyothalamus, amygdala and cerebellum.
Inactive during sleep and increases with arousal.
Deficiency linked with depression
57
Describe 5HT pathways
```
Similar to NA.
From Raphe nuclei also in pons.
Functions:
Sleep
Wakefullness
Mood
Vomiting centre
```
58
Origin of superior cerebellar artery
Basilar artery just posterior to superior cerebellar artery
59
Origin of inferior cerebellar artery
Lateral off vertebral artery
60
Origin of anterior spinal artery
Anastomosis between vertebral arteries
61
Origin of pontine arteries
Basillar artery
62
Origin of opthalmic arteries
ICA just before it becomes middle
63
Describe blood supply to the spinal cord
Ant and 2 post in SAS. From anastomostes with segmental medulary arteries.
Radicular and intercostal arteries from abdominal aorta. Disruption of artery of Adamkiewicz can cause infarction e.g. AAA surgery
64
Supply of anterior posterior and middle cerebral arteries
Medially - mostly anterior (almost all of cingulate gyrus and corpus callosum) the posterior for occipital lobe.
Middle = lateral surface (not feet of precentral gyrus.
Middle and posterir share temporal lobe
65
How does CSF cushion brain?
Isotonic
66
Causes of subarachnoid
Berry aneurysm
67
How does CSF get removed and where?
Arachnoid granulations at superior sagittal sinus
68
CSF from forth to subarachnoid space via?
foramen magendie
69
What drives flow of CSF
Pressure and chorid epithelia villi
70
What causes a communicating hydrocephalus
Factors external to ventricular system e.g. scarring of meninges at arachnoid granulations
71
How is CSF different from blood?
Lower conc of glucose, Ca, protein, K but higher Na, Mg and Cl. Very low immune cells
72
State the foramen of the cranial nerves as they leave the skull base
```
1 Cribiform plate
2 Optic canal
3 Superior orbital fissure
4 Superior orbital fissure
5i Superior orbital fissure
5ii Foramen rotundum
5iii Foramen ovale (post sphenoid) and foramen spinosum just lateral to in
6 Superior orbital fissure
7 Facial canal (internal acoustic meatus then stylomastoid foramen)
8 Internal acoustic meatus
9 Jugular foramen
10 Jugular foramen
11 Jugular foramen
12 Hypoglossal canal
```
73
Describe sensory neuones
Free nerve endings in temp
Encapsulated for pressure
Specialised cell cuch as pacinian corpuscle for pressure and vibration
74
What is a quality
Subset of a modality e.g. salt, sweet, sour
75
Types of receptors found in muscle
Proprioceptors in muscle spindle = length
| Golgi tendon organ = tension
76
Are receptors specific to one modality
Generally yes but punch in the eye
77
How are stronger stimuli recognised?
More AP frequency
| Neibouring cells activated
78
Whats the difference between tonic and phasic receptors
Tonic - slowly adapting, continually firign
| Phasic - raidly adapting, respond maximally and briefly to a stimulus
79
How is sensory acuity achieved? What is it?
```
Precision by which a stimulus can be located
Laterally inhibiting interneurones
2 point discrimination
Synaptic convergence (decrease) and divergence (increase
```
80
What is two point discrimination and what factors influence it?
Minimum distance required to percieve two simultaneously applied skin indentations.
Dependant on size of receptive field and density of sensory receptors.
81
How is the percieved loaction of a stimulation based on?
Crude thalamic localisation. Proetion into cortex.
Somatosensory cortex sharply localises the stimulus. Somatotropic representation.
Relays to other cortical and sub-cortical areas to chose how to respond
82
What is perception?
Ability to sense stimuli and discriminate between different types
83
What is the result of a lesion of the sensory cortex?
Epleptic events, loss of two point discrim, astereognosis (3D) touch
84
L and R of the spinal cord are divided by what?
Dorsal median sulcus and the ventral median fissure
85
What fibres do the dorsal columns carry
Light touch and proprioception
86
Describe the fasciculi of the dorsal column
Gracile = medial (thinner) above T6
| Cuneate lateral below T6
87
Describe the two corticospinal tracts' modalities
Lateral = limb
Ventral = axial
motor descending
88
Describe the spinothalamic tracts' modalities
```
Lateral = pain and temp
Anterior = crude touch
```
89
Describe the Medial lemniscus pathway
=Dorsal column.
1st ganglion = dorsal root ganglion.
Secondary neurones in the cuneate and gracile nuclei in the medulla.
Decussate to become the internal arcuate fibres to become the medial lemniscus pathway in the Pons and midbrain.
Terminate in Ventral posterolateral nucleus in the thalamus 3rd.
THese terminate in the post centra gyrus (proproception in the sensory-motor cerebral cortex).
90
Describe the spinothalamic tract pathway
Lissauer's fasciculus for 1-3 levels. 1st cell body = dorsal root.
Terminate in dorsal horn in Sub gel or nucleus proprius
Deccussate in same level.
Ascends to thalamus at the ventra posteriolateral nucleus.
Tertiary to post central gyrus via internal capsule.
Ascend somatotropically Caudal = dorsolateral.
91
What is Syringomyelia?
cyst (syrinx) in spinal cord from rugby/ spinal injury e.g. high tackles. Causes pain, paralysis, weakness, loss of temp sensation.
Filled with CSF into spinal cord
92
Describe Brown- Sequard syndrome
Hemisection of the spinal cord. Loss of ipselateral dorsal column = ipsilateral proprioception and fine touch.
Couterlateral = temp and pain.
(spinothalamic)
Causes include tumour, trauma, ischemia, infection and inflammation
93
B12 deficiency neuro?
| Also B6 -pyroxidine
Dorsal root column degeneration
94
Effect of syphillis on spinal cord?
Tabes dorsalis.
| Demyelination of dorsal column
95
What is Freidrich's ataxia?
Heridatary.
Sclerosis and degeneration of dorsal root ganglion, spinocerebellar tracts, lateral corticospinal tracts, and posterior columns.
5-15
96
Describe Shingles pathology
Reactivation. Dormant in dorsal root ganglion. Infects PNS neurones.
Increased sensitivity and rash.
Postherapeutic neuralgia = chronic pain
97
Explain conscious and unconscious proprioception pathways
```
Concious = Dorsal column spinal tract.
Unconscious = Dorsal and ventra spinocerebellar tracts and the Cuneo-cerebellar tract.
```
98
Describe the Spinocerebellar tracts
1st order from muscles terminate in Clarke's nucleus/ column. Cell body in dorsal root ganglion.
2nd order trvel in lateral funiculus 3.
Dorsal remains ipsilateral.
Anterior decussates in the cord but the recrosses in the cerebellum and is ipsilateral
99
Direct of fall in cerebellar damage
= ipsilateral fall and coordination
| Vermis damage = fall backwards
100
Define a motorneuone
A somatic efferent that displaces limbs and sets muscle tone.
Upper and lower motor neuone
101
Upper motor neurone lesion signs.
```
Hyper reflexia
Hyper tonia
Hypokinesia (regidity)
Spastic Paralysis
Chorea if extrapyradimal
Pyradimal = Babinski
```
102
Lower motor neurone lesion signs
```
Paralysis
Flaccid weakness
Hypotonia or atone
Hyporeflexia or areflexia
Atrophy
Fasciculations
```
103
Origin of LMN?
Rexed laminae VIII and IX. Cranial nerve motor nucleus = CNVII not in spinal cord?
104
What is a motor unit?
A-motorneurone and all the mucle fibres it supplies = minimal functional unit.
105
What is a strecthc relfex
An involuntary, unlearned, repeatable, automatic reaction to a specific stimulus that does not require the brain intact.
106
Name the 5 components to a strectch relex
```
A stretch receptor (e.g. golgi organ or muscle spindle)
Afferent fibre
Integration cetre
An efferent fibre
An effector
```
107
What is a myotatic reflex?
Monosynaptic stretch reflex. Sets motor tone
108
Muscle tone in utero and new born?
Low in utero and supressed in new born and returns within months
109
Muscle tone during sleep and exceptions?
Increased inhibition during sleep apart from resp, extraocular muscles and sphincters.
110
What do gamma motor neuones do?
Adjust sensitivity of muscle spindles, allow a motorneurones to continue to discharge
111
Signs of an extra pyradimal lesion e.g. cerebellum or basal ganglia
Tardive dyskinesia, parkinsonism (tremor, rigidity, dyskinesia), akathisia (muscle restlessness), dytonia e.g. spasms
Corticospinal = fine movements.
Extra pyradimal = way they are carried out
112
Two pyradimal tracts?
Corticobulbar and corticospinal tract
113
Describe the cortico-bulbar tract
Fibres from Motor cortex/ pre centra gyrus to nuclei of motor cranial nerves - 5, 7, 9,10,12 (not Occulomotor).
114
Descrube the corticospinal tract
Pre central gyrus (primary motor cortex).
Through internal capsule to brain stem.
Travels in anterior medulla in medullary pyramids.
Limb motor fibres deccasate at bottom of medulla and become lateral corticospinal tract.
Synapse directly in ipsilateral anterior horn (VIII, IX).
Ant = axial, no decussation in anterior white commissure then synapse in ant horn also.
115
Describe the non-cortical/ extrapyradimal descending tracts
```
Rubero = voluntary skeletal contraction e.g. hand.
Reticulospinal = Autonomic control, posture and locomotion, modulation pain
Tectospinal = automatic reactions to visual and auditory stimuli (cervical)
Vestibularspinal = Posture maintainance, damage = loss of righting reflex, ataxia of gait and postural instability
```
116
Decorticate appearence
Flexors- Cs = spinal tract or cerebral. Relative strength of flexors and extensors
117
Decerebrate appearence
Extensors Es = pons or midbrain e.g. reticulospinal
118
Why do you get fasciculations?
Upregulation of Ach receptors. Ach remnants in the blood.
119
What is spinal shock?
Damage to descending tracts.
Areflexia and flaccid.
Gradually turns to UMN signs.
120
Explain the functional zones of the cerebellum
Vestibulocerebellum (archicerebellum): balance and ocular relfexes
Spinocerebellum (Paleocerebellum)- error correction (recieves proprioceptive and visual imputs
Cerebrocerebellum (neocerebellum) - motor planning, memory and coordination
121
Signs of Cerebellar dysfunction
```
Dysdiadochokinesia, Dysmetria (past pointing)
Ataxia
Nystagmus
Intention tremor
Scanning dysarthia (monotone)
Hypotonia
```
No atrophy or weakness
122
Positive Romberg test and uses?
Causes of gate-
ataxia = sensory
Suggests cerebellar damage
123
Causes of Cerebellar dysfunction?
Tumour, stroke, genetic e.g. friedreich's ataxia
124
Briefly explain the direct, indirect and hypodirect pathways throught the basal ganglia
Direct = Cerebral cortex - striatum, inhibits GPi/ SNr, activates thalamus. - more movement. (Dopamine from SNc increases).
Indirect - striatum inhibits GPe, inhibits STN, activates GPi/ SNr, inhibits thalamus- acts to dampen direct and give finer control. (Dopamine inhibits)
Hypodirect - Cerebral cortex activates STN - activates GPi/ SNreticulata, inhibits thalamus. = breaks
125
Explain pathophysiology of parkinsons
Progressive degeneration of dopaminergic neurones of the substantia nigra/ nigrostriatal pathway.
Less contol of movements
126
Describe signs and symotoms of Parkinson's
Tremor at rest reduced by movement and increased by distraction 'pill roll'
Hypertonia - lead pipe/ cog wheel rigidity
Bradykinesia
PD gait - small shuffle, pedestal turn, tremor only in upper body
127
Define pain
An unpleasant and emotional experience involving actual or potential tissue damage.
Has autonomic, somatic, endocrine and emotional responses
128
What is nociception and some things that can affect it
The perception of physical pain
| Modified by experience, expectation, immediate context, culture
129
Threshold and tolerance to pain.
Threshold is all the same
| Tolerance is our variable reaction to a painful stimulum. Increases with age, placebo effect, ongoing pain ect.
130
Difference between direct and indirect lateral STT
Fasts vs Slow
Intensity loation, quality (somatotopic) vs affective e.g. arousal, emotion
no synapse vs synapse in BS
Corical target vs hypothalamus, RF, Limbic, autonomic centres
131
Describe the stages of nociception
Transduction - activation of nociceptors
Transmission - replay of action pertentials along nociceptive fibres to CNS
Modulation - By other peripheral nerves or CNS
Perception - Interpretation
132
Difference in stimulation of Adelta and C fibres
```
Ad = mechanical
C = mechanical, thermal, chemical (polymodal)
```
133
Perception of Ad, C and visceral fibres?
Ad = stabbing sharp, ow, well localised, first pain, lower threshold, withdrawral reflex
C = Dull throbbing 'ooh', poorly localised, second pain, higher threshold, tissue damage occuring.
Visceral fibres share somatic nociceptive fibres
134
Rexed lamina of Ad, C and cisceral fibres
```
Ad = I, V
C = Substantia gel (i, II) and V.
Visceral = V
```
135
Describe transduction of pain
Lesion = K, prostaglandins, 5HT, bradykinin which activate.
AP fired and substance P released from nerve endings.
P increases cap permeability and contributes to inflam.
P (and CGRP - calcitonin gene replated peptide) causes rast cells to release histamine (further nociceptive activation).
136
Actionn of drugs on transduction
NSAIDS -prostaglandin
| Steroids - IL
137
How can transmission be blocked
Local anaesthetic e.g. lignocaine, inhibits VGSC
138
What is analgesia and what can cause it?
Inability to perceive pain when tissue damage is occurring. Hypnosis, morphine, TENS (transcutaneous electrical nerve stimulation), natural childbirth techniques and placbos
139
Describe pain modulation in spinal cord
Exogenous methods e.g. analgesics.
Gate control theory
Endogenousour opioid peptide analgesics (and others) from centtral and decending spinal systems.
Mediated by the periaqueductal grey matter (PAG) in midbrain via feedback from thalamus, cortex, hypothalamus.
Act on nucleus raphe magnus
140
Why does rubbing help?
Stimulates cutaneous inhibition which increases descending inhibition
141
Describe perception of pain
```
Thalamus and the cortex
Varies hugely
Thalamocortical projection = info about pain.
Emotional via limbic
Stress via hypo
```
142
What is chronic pain
Pain >3 months. Unknown cause/ underlying problem or pain disorder.
143
Describe the gate control theory of pain
Between SG (via interneuones) around the synapse of C/A fibres in dorsal horn
144
What is hyperalgesia
Increased pain at a normal threshold stimulation.
| Results from peripheral and central sensitisation
145
What is allodynia
Pain from stimuli not normally painfull.
| Also from an area not stimulated (not referred)
146
Signs of pain
Brow lowers, lids tighten, nose wrinkles, lips tighten
147
Describe 'winding up'
Tissue injury causes nerve damage and pain
Repeated C stimulus
Excess Glutamate and NMDA.
Upregulation so these neurones become hyperexcitable (lower threshold) and hyperalgesia.
Can lead to receptive field expansion or allodynia.
Pain decreases after stimulus but does not reach zero before another (same stimulus).
Changes in somatosensory mapping
148
Types of chronic pain
Nocicpetive, Neuropathic (central and peripheral), Visceral (organ disease inflam), mixed e.g. cancer, lower back, FMS (fibromyalgia)
149
Explain nocicpetive chronic pain e.g. RA
```
Wind up
Inflam
Synovia damage
C and A delta
Hyperalgesia
```
150
Explain neuropathic pain
Neuronal origin
Not explained by a single location/ disease.
Central e.g. thalamic lesion presenting as somatic sensation, not responsive to opioids.
May be burning, shooting, pins and needles.
Causes usual decreased in thrshold, increased fields, prolonged stimulus (hyperpathia).
Spontaneous activity.
Includes hantom limb pain
151
Describe complex regional pain syndrome types
Type 1 - no lesion but after illness e.g. RSD (reflex sympathetic dystrophy)
Type 2 - identifiable nerve lesion e.g. causalgia - burning in limb caused by peripheral nerve lesion
152
What is RSD/ CRPS symptoms
Reflex sympathetic dystrophy
Sensory - severe, continuous burning pain, hyperalgesia,
Vasomotor -
Sudomotor/oedema
Motor/ trophic - decreased range of motion, dysfunction, trophic (skin) changes
153
Stages of CRPS
1 - acute
II dystrophic - thickening of skin, muscle wasting, oedema
III atrophic - limitation of movement, contractures, waxy skin
154
Opiod receptor info
GPCRs, close VOCC, open K, inhibit cAMP and neurotransmittior release
155
Opioids and their receptors
Endomorphins = MOP
Dynorphins = KOP
Enkephalns =DOP
156
Give common weak opiods
Codeine
157
Give strong opiod examples
Morphine, Fentanyl
158
Who analgesic ladder
1 non opiod +/- adjuvant
2 weak opiod adjuvant
3 strong oioid adjuvant,
Non = Paracetamol, NSAID
159
Definition of adjuvants and examples
A pharmacological agent fiven to increase or aid a drug's effect. Not analgesics in their own right.
AEDs and Steroids e.g. prednisolone
160
Central pain and opiods?
May be opiod insensitive so antidepressants, AEDs, local anaesthetics and opiod mixtures are given
161
Describe the development of the ear
Otic placodes arise laterally
Grow and invaginate
Pinch off to become auditory vesicle
Changes shape to form membranous labyrinth: Utricle and saccule/
Utricle becomes semi lunar canals and saccule become choclear. Ossicles from 1st and 2nd arches.
Pouch and cleft forms meatus.
Mandible grows and the ears ascend to be in line with eyes
162
Define placode
Thickened ectoderm patches on developing head
163
Congenital causes of middle ear deafness?
Problems with 1/2 branches
164
Causes of inner ear deafness
Tetratogenic agents and infection e.g. rubella
165
Describe development of the eyes to shreks ear
Lens placode invaginates and pinches off. Shreks ear. Choroid fissure in the middle.
166
Whats inside the choroid fissure and its fate
Hyaloid artery- degenerates distally to become the central artery of the retina
167
Fate of the optic cup?
Retina (pigment and sesnory/ neural) in to layers which fuse, iris and ciliary body (from the rim)
168
Where do muscles of the eye come from?
Preoptic myotomes from the surrounding region
169
How does coloboma arise?
Failure of fusion of the edges of the optic stalk around choroid fissure inferio-medially
170
Future pathology associated with the optic cup?
Retinal tear = separation of the layers
171
What is the iris?
A contractile diaphragm with a central aperture
172
Features of rubella?
Microcephaly, PDA, cataracts
173
Where does the optic tract start and terminate?
Starts at the optic chiasm and terminates at the lateral genicular nucleus
174
Temporal lobe optic rediation lesion = what?
Superior visual field defect (ST elevation) so an inferior retinal field problem.
175
Where is Meyers loop?
Temporal optic radiation
176
Describe differences in rods and cones
Not in fovea vs fovea
Photosensitive vs high acuity
Dark adapted vs day vision
Converge on bipolar cells vs blue, red and green.
177
Describe the three main functional classes of neurones
Photoreceptors
Interneurones
Ganglion cells
178
Describe interneurones
Bipolar, horizontal and amacrine.
| Combine photoreceptor signils
179
Describe Magnocellular ganglion cell pathways
No sensitive to colour
Sesnsitive to luminescence contrast and fast motion. Magnum = fig e.g. foramne magnum - looks at big picture? Via the dorsal stream to the posterior parietal cortex
180
dESCRIBE pARVOCELLULAR GANGLIIONIC CELLS
bETTER AT COLOUR CONTRAST, NOT LUMINANCE AND FINE DETAIL HOWEVER LESS SENSITIVE TO MOTION.
Goes via the ventral stream to the inferior temporal cortex
181
Describe the primary visual cortex
Separated by the calcarine fissure
Occipital lobe
Each quarter of VF is represented, larger area for macula/ fovea.
Interpretation by cortex e.g. comparison of things so some may seem bigger.
182
Explain the development of cones
Take ages to mature.
Can be seen via Optical coherence tomography (OCT) - images the retina.
Can see development of the outer nuclear layer still at 5 years. Fovea only has an outer nuclear layer
183
Sign of fovea hyperplasia?
Nystagmus
184
What is ambyopia?
Diminished vision in one eye and a result of disuse in childhood.
185
Causes of ambyopia
Strabismus - inability to focus both eyes on one object = lazy eye
Anisometropia = refractive difference in botheyes
Deprivation e.g. congenital cataracts, ptosis, media opacies
186
Types of anisometropia
```
Emmetropia = normal
Myopia = infront of retina
Hyperopia = behind retina
```
187
Types of Stabismus
Esotropia = In
Exotropia = out
Left hypertropia = up
hypotropia = down
188
Treatment of ambyopia
Glasses/ patch when yound due to brain plasticity but poor comliance
189
What is glaucoma
High intraocular pressure, damage to optic nerve, peripheral field defect which is often unnoticed and gradual
190
Sympathetic innervation of eye pathway
Hypothalamus to T1, To Superior cervical ganlion under SCA to dilator pupillae
191
Abduction and adduction movements
SR and IR are opposite
SR and SO are inverse.
SO abduct = intorsion
192
Appearance of VI nerve palsy
Esotropia
193
IV nerve palsy
Hypertrophia
194
III
Exotropia and hypotropic
| Also ptosis and mydriasis
195
Describe the properties of sound
Compressive wave, frequencey and amplitude
196
Level of conversation and painful sound
60dB vs 120dB
197
Describe the travelling wave theory
Basillar membrane resonates and machanically amplifies sound with progressively lower frequencies along its length.
198
What is Tonotopy
Place on basillar membrane = frequency
199
Describe the structure of the basillar membrane
One row of inner hair cells and 3 rows of outer hair cells.
200
Functions of inner and outer hair cells
Inner sense sound
Outer amplify sound
Mechanically tuned by location and electrically tuned by expression of particular ion channels .
Both contain stereocillia to sense sound
201
What is the tectorial membrane?
attached to the hair bundles. Not sure of function. When basilar moves?
202
Exlain How bending of stereocillia triggers a nerve AP
Bending opens K channels = depolarisation as endolymph at high conc. Larger if more displacement.
Ca influx
Triggers transmitter release onto spiral ganglion neurones (SGN) - afferent axons of CNVIII
203
What is the olivocochlear system?
Regulates OHC amplification via efferent feedback
204
How are loud sounds interpreted and location
More APs from SGN, recruitment of neighbouring fibres. Goes to choclear nucleus in the auditory brainstem. Goes to Medial nucleus of trapezoid body on both sides. Delay allows left/ right and difference in volume/ amplitute.
205
What constitutes the auditory brainstem?
Lateral and medial superior olives and the medial nucleus of the trapezoid body.
206
The auditory pathway
```
Cochlear
SGN
Dorsal and ventral cochlear nuclei
Suppeior olive
Inferior colliculus
Medial geniculate nucleus
The auditory cortex
```
207
Causes of hearing impairment
```
Age, presbyacusis
Infection
Congenital
Loud noises
Gentamicin
TraumA
```
208
Explain the assessment of hearing
Otoscope
Audiograph - sensitivty against frequency (higher lost with age)
Otoacoustic emissions (sound generated by OHC - test in babies)
Auditory brainstem response - electrodes on the brain
209
Treatments fr hearing loss
Hearing aid
Cochlear implant
Cochlear nucleus
implant.
210
Congenital causes of hearing loss
DFN - X linked
DFN - AD
AFNB AR
Hair hells, tectorial ....
211
Where do most strokes occur?
Middle cerebral artery
212
Describe the vertebral arteries
Tortuous
Posterior ineferior cerebellar artery is the largest branch.
Also the spinal arteries
213
Describe the Basilar artery
Supplies most of brainstem. Located over pons.
| Superior and anterior inferior cerebellar arteries. supplies most of PCA
214
Describe PCA distribution
Occipital, midbrain, thalamus, half on temporal
215
Define stroke
Abrupt loss of brain function lasting more than 24 hours or causing death due to inadequate blood supply or spontaneous haemorrhage
216
Causes of cerebral infarct
Atheroma, embolism, idiopathic, arterititis, blood disorder
217
Describe intracerebelar haemorrhage causes
Primary or Secondary
Haemorrhagic transformation of infarct
Hypertensive, microaneurysms, lipophyalinosis (wall problem), AV or aneurysm, amyloid, haemostatic, cocain, amphetamines, tumour, venous thrombosis
218
Define TIA
Sudden focal disturbance of brain functioning (global or local) which resolves within 24 hours
219
Temporal lobe stroke signs
CNVIII, taste and smell
Wernicke's area
Memory
Optic radiation - superior quadrantanopia
220
Pariatal lesion
Primary sensory cortex
Neglect
Speech
Optic radiation either inferior or hemianopia
221
Describe TACS - total anterior circulation stroke
```
Proximal occlision
Contralateral hemiparesis/ hemianaesthesia
Higher dysfunction
Hemianopia
High mortality
```
222
Describe PACs
Occlusion of MCA or restricted infarct
2 signs from TACS or restricted motor deficit (one thing e.g. face) or isolated cortical signs
High early recurrence
223
Describe LACS (lacunar stroke)
Single perforating artery in the basal ganglia or pons.
Pure motor, sensory, sensory motor, ataxic or hemiparesis.
Silent and underdiagnosed
224
Describe POCS
Brainstem, cerebellar or occipital involvement.
| Complex presentation
225
Atypical symptoms of stroke
Delerium, confusion, collapse, incontinence
226
Write note for telangiectasia
k
227
Investigations for stroke
```
BM
HAematology
Biochem
CT/ MRI
Carotid US
ECG
Echocardiogram
```
228
Treatment for stroke
IV thrombolysis - alteplase
Early asprin
Acute stroke unit
229
Damage to spinal cord blood supply
```
Aortic damage
Vasculitis - giant cell arteritis
Sickle cell
Hypotension
Cardiac emboli
Disc Herniation
```
230
Symptoms of spinal artery occlusion
Spinal shock. (seen in urinary spincter too)
Normal ant so dorsal is fine (proproception and touch)
Normally motor
231
What is a flaccid bladder? (same as areflex)
Lesion at S2-4 lower motor neurone
232
Describe reflex bladder
UMN lesion.
Works fine but detrusor is more sensitive.
No control.
Increased muscle tone.
233
Describe motor and sensory areflexic bladder
Aware on unaware of filling - no release in response. Lesion of the sacral spinal cord or sensory nerve or detrusor
234
Describe the management of head trauma
ABCD (disability)
History
Examination
235
RAS control
dd
236
What is a coup and contrecoup injury
```
Coup = front
Contrecoup = rebound`
```
237
What are contusions?
Damaged blood vessels around the brain (like bruising)
238
Describe primary and secondary insult in brain
```
Primary = haematoma, contusion, haemorrhage, diffuse axonal injury
Secondary = preventable, hypoxiam hypoperfusion, oedema, ICP.
```
239
BBB disruption?
More permeable so vasogenic oedema.
240
What is cytotoxic oedema?
Inflam mediatorys and oxiditive stress. NA retention
241
ICP compensation?
```
CPP = MAP-ICP.
Venous blood and CSF can move out of brain to lower ICP.
MAP increases (mean arterial pressure) via Cushings.
```
242
Uses of propofol
Decreases Cerebral metabolic rate of O2 (CMRO2) like hibernation.
Dose dependent
243
USe of Thiopentone (barbiturate)
Decrease CMRO2
Hypotension
EEG monitoring - birst suppression.
Vary heavy = seizures- very bad as high O2 requirement
244
Describe use of opiods
Pain relief
Reduces stress response
Reduce cough so can intubate
Can exacerbate hypotension
245
Benefits to ketamine? and disadvantages?
No effect on BP
Predictable
No loss of airway relfexes, semi conscious, hallucinations/ terrors.
246
Use of neuromuscular blocking agent
Need for intubation
247
Use of mannitol
Potent osmotic diuretic to remove cererbral oedema but can worsen if passes the BBB
248
Explain vasopressors
Adjust BP
Invasive BP monitoring
given IV (impair venous drainage?)
249
MEasures in medically induced coma?
EEG
Bispectral index - depth of anaethesia 1 number from many imputs
ITU nurse and wakefullness
250
Evidence and reasoning behind medically induced comas?
Relieve swelling and brain decrease brain damage.
| Mixed evidence.`
251
Describe the reticular formation
Central core of brain stem, includes raphe and nucleus coeruleus.
Sleep regulation
Motor control
Cardio/ Resp control
Autonomic functions
Motivation and rewards.
Ascending reticular activating system = consciousness
252
Imputs on the reticular formation
Senses, hypothalamus, drugs and alcohol. Activate/ inhibit arousal/sleep.
253
Outputs of RF
Motor system (make more sensitive), autonomic, thalamus, cortex. Many different neurotransmittors. Ach sensitises thalamus to sensory stimuli but quiet during sleep.
254
RF in sleep
Ach silent.
| Cortex can inhibit RF if wanting sleep- waves on EEG. e.g. whilst driving
255
Describe EEG and waves
Algebraic sum of electrical activity.
Less info when eyes are shut so higher amplitude and lower frequency. Hihger frequency when open and wavees cancel each other out.
256
Describe specific wave forms
Delta large - deep sleep and brain conditions
Theta intermediate Parietal and temporal children concentrating or meditating adults
Beta like theta but irregular = awake parietal and frontal
Alpha small = awake occipital
257
Describe locked in syndrome
Loss of RAS descending pathways e.g. lesion below the mid pons - patient is alert and aware but quadriplegic and mute.
258
What is persistent vegative state?
loss of cortex PVS different from coma as they show some signs of consciousness. Brain death is the irreversible loss of all features of the brain
259
What is a coma?
State of unconsciousness from which a patient cannot be roused using pain, sound, light. No voluntary movement.
260
Describe the purpose of sleep
Allows CNS to reset and memories to process
261
What controls the sleep wake cycle?
RF and hypothalamus (by inihibiting the RF)
262
Describe a sleep cycle
Quickly into stage 4 (1 hour), straight back to REM, then cycle between stage 3 and REM with progressively more REM
263
Describe REM sleep
```
Active brain, inactive body
EEG as if awake
Waves from pons to thalamus to occipital = dreaming
Difficult to disturb
Irregular HR and RR
Increased BMR
Descending inhibition of motorneurones
Penile erection
Reduced by alcohol
Na and 5HT inhibited - explains memory without emotion
```
264
Describe non REM sleep
```
Slow wave sleep
Active body, inactive brain
e.g. sleepwalking
3/4 stages
Waves decreasein amplitude to stage 3 then become delta waves- slows.
Restorative
Neuroendocrine
Decreased cerebral bloodflow, O2 consumption, temp, BP, RR, lower BMR
```
265
Describe waking
Na and 5HT start to be released. Ach from brainstem sensitises thalamus and allows wakefulness - thalamo-cortical neurones and communication
266
What is parasomnia
Sleep paralysis
267
What is hypersomnia
Day time sleepiness e.g. OSA
268
What is Narcolepsy
Disorder of arousal - constant hypersomnia
269
Conditions that affect RAS?
Parkinsons and Schizophrenia, PTSD, Depression(NA, 5HT), Alzheimers (Ach)
270
Loss of consciousness, where is damage?
Not cortex but RF
271
Initial management of loss of consciousness?
ABCD
Airway - jaw thrust- not neck extension. Nasopharyngeal better tolerated with suction in mouth. High conc O2
Breathing - mist mask, chest, breast sounds, indicator mask, assist e.g. bag valve mask (BVM) and intubation
Circulation - pulse, breathing effort, cough, movement, ETCO2 (end tidal vol) if ventilated, cap refill, IV access BM stix.
Disability - GCS
Monitor
272
Treatment loss of consciousness
High flow O2 if hypoxic
Hypoglycaemia - glucose IV
If fitting then Lorazepam IV
273
Explain the Glasgow coma scale (not score)
Eye 1-4:
None, pain, speech, spontaneous
Verbal 1-5
None, incomprehensible, inappropriate words, confused, orientated
Motor 1-6
None, extension pain, flexion, flexion pain, localise pain, obey command
Use to find pattern of change - if decreasing then bad..
274
Extradural presentation
Trauma, torn MMA, slow onset, decline in GCS
275
Subdural presentation
Trauma- brain move in skull/ (boxing).
| Slower onset - days to weeks but can be acute, alcohol, age, atrophy of brain (dementia
276
Subarachnoid presentation
Thunderclap - berry aneurysm
277
Decorticate response in terms of RF
Intact. Thalamus and cortex connection lost. Unconscious but respond to pain.
278
Decerebrate response
Rigidity, lower brain/brainstem injury
Inhibition of RF on motor tracts removed
Relexive extension to pain
