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Neuroscience Flashcards

1
Q

Define: brainstem

A

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

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2
Q

Where does the brainstem lie?

A

Posterior cranial fossa

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3
Q

What are the major divisions of the brainstem?

A

Medulla oblongata
Pons
Midbrain

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4
Q

What are the numbers of the cranial nerves?

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

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

A

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

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

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

A

Olfactory (sensory)

Structures innervated= Olfactory epithelium via olfactory bulb

Functions= Olfaction

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7
Q

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

A

Optic (sensory)

Structures innervated= Retina

Functions= Vision

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8
Q

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

A

Oculomotor (motor, parasympathetic)

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

Function= Movement of the eyeball
= Pupillary constriction and accomodation

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9
Q

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

A

Trochlear (motor)

Structures innervated= Superior oblique muscle

Function= Movement of the eyeball

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10
Q

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

A

Trigeminal (motor and sensory)

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

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

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11
Q

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

A

Abducens (motor)

Structures innervated= Lateral rectus muscle

Function= Movement of eyeball

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12
Q

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

A

Facial (sensory, motor, para)

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

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

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13
Q

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

A

Vestibulocochlear (sensory)

Structures innervated= Vestibular apparatus
= Cochlear

Function= Vestibular sensation (position of head)
= Hearing

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14
Q

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

A

Glossopharyngeal (sensory, motor, para)

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

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

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15
Q

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

A

Vagus (sensory, motor, para)

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

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

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16
Q

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

A

Accessory (motor)

Structures innervated= Stemocleidomastoid and trapezius

Function= Movement of head and shoulder

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17
Q

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

A

Hypoglossal (motor)

Structures innervated= Intrinsic/extrinsic tongue muscles

Function= Movement of tongue

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18
Q

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

A

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

Special somatic afferent
Special visceral afferent
Special visceral efferent

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19
Q

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

A

GSA= sensation from skin and mucous membranes

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

GSE= muscles for eye and tongue movements

GVE= preganglionic parasympathetic

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20
Q

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

A

Special somatic afferent= vision, hearing and equilibrium

Special visceral afferent= smell and taste

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

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21
Q

Where is the Edinger Westphal nucleus?

A

Motor GVE

Midbrain

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22
Q

Where are the oculomotor and trochlear nuclei?

A

Motor GSE

Midbrain

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23
Q

Where is the abducens nuclei?

A

Motor GSE

Pons (middle of pons)

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24
Q

Where are the trigeminal m and facial nuclei?

A

Motor SVE

Pons (trigeminal top, facial bottom)

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25
Where are the salivatory nuclei?
Motor GVE | Either side of pons-medulla junction
26
Where is the vagus m nucleus?
Motor GVE | Medulla
27
Where is the ambiguus nucleus?
Motor SVE | Medulla
28
Where is the hypoglossal nucleus?
Motor GSE | Medulla
29
Where is the accessory nucleus?
Motor SVE | Cervical spinal cord
30
Where is the trigeminal s nuclei?
Sensory GSA | Midbrain, top of pons, down pons/medulla/SC
31
Where is the vestibulocochlear nucleus?
Sensory SSA | Lower half of pons and top of medulla
32
Where is the solitarius nucleus?
Sensory GVA/SVA | Medulla
33
When substantia nigra is damaged, what happens?
Parkinson's disease
34
Where in the brainstem can the inferior colliculus, cerebral aqueduct, substantia nigra and cerebral peduncle be found?
Midbrain
35
Where in the brainstem can the 4th ventricle, middle cerebellar peduncle and transverse fibres be found?
Pons
36
Where in the brainstem can the 4th ventricle, inferior olivary nucleus and pyramids be found?
Medulla
37
Where in the brainstem can dorsal columns, central canal and pyramidal decussation be found?
Lower medulla
38
What causes lateral medullary syndrome?
Thrombosis of vertebral artery or PICA
39
What is PICA?
Posterior inferior cerebellar artery
40
What does thrombosis of vertebral artery or PICA cause?
Lateral medullary syndrome
41
What are the symptoms of lateral medullary syndrome
Vertigo Ipsilateral cerebellar ataxia Ipsilateral loss of pain/thermal sense (face) Horner’s syndrome Hoarseness, difficulty in swallowing Contralateral loss of pain/thermal sense (trunk and limbs)
42
What does the lesion in lateral medullary syndrome disrupt? (3 nuclei, 2 tracts and 1 other area)
Vestibular nucleus Spinal nucleus (trigeminal) Nucleus ambiguus Spinothalamic tract Sympathetic tract Inferior cerebellar peduncle
43
What levels are the cervical plexus?
C1-C5
44
What levels are the brachial plexus?
C5-T1
45
What levels are the lumbar plexus?
L1-L4
46
What levels are the sacral plexus?
L4-S4
47
How many pairs of spinal nerves are in each group?
``` Cervical 8 pairs Thoracic 12 pairs Lumbar 5 pairs Sacral 5 pairs Coccygeal 1 pair ```
48
Where is the lumbar enlargement?
Around T9-T10
49
Where is the conus medularis?
Between T12 and L1
50
What spinal segments are largest and smallest?
``` Around C5 (cervical enlargement) Around L3 (lumbar enlargement) ``` Smallest are sacral
51
What spinal segment is the bone notch at the base of the neck?
C7
52
What pathway goes from the primary somatosensory cortex to detect pain/crude touch?
Primary somatosensory cortex Thalamus: ventral posterior lateral nucleus (Secondary sensory neuron) Anterolateral pathway (spinothalamic tract) Spinal cord (Primary sensory neuron via DRG)
53
What is the purpose of spinothalamic tract?
To receive sensory info about pain, temperature, crude touch
54
What are the major sensory pathways?
Posterior column-medial lemniscus pathway Anterolateral (spinothalamic) pathways SEE DIAGRAMS
55
What are the major motor pathways?
The lateral corticospinal pathway The anterior corticospinal pathway SEE DIAGRAMS
56
What are the divisions of autonomic pathways?
Sympathetic Parasympathetic SEE DIAGRAMS
57
What is the cross-sectional structure of the spinal cord?
Central canal in the middle of the grey matter butterfly White matter surrounds (contains nerve fibre tracts) Sensory nerve root from top of grey matter (dorsal horn)-> sensory root ganglion-> spinal nerve Motor nerve roots leave from the front of the SC
58
What are the layers of the connective tissue that protect the SC?
Meninges Pia mater Arachnoid mater Dura mater
59
What kind of fibre tracts are found in the spinal cord?
Ascending tracts Descending tracts Bidirectional tracts SEE DIAGRAMS FOR SPECIFICS
60
What are the funiculi in white columns of the spinal cord?
Posterior funinculus Anterior funinculus Lateral funinculus
61
What parts of the spinal cord cross-section is grey matter?
``` Posterior median sulcus Grey commissure Posterior (dorsal) horn Anterior (ventral) horn Lateral horn ```
62
What receptors are part of the DRG system?
Nociceptors Mechanoreceptors Proprioceptors (also go to VH)
63
How is locomotion controlled by the SC?
Sensory afferents, corticospinal, reticulospinal and CIN Join V2a interneurons Motor neuron
64
What neurotransmitters and effector organs are involved in the somatic nervous system and autonomic nervous system?
SOMATIC ACh Skeletal muscle ANS- SYMPATHETIC ACh and NE Smooth muscle, glands, cardiac muscle ANS- PARASYMPATHETIC ACh and ACh Smooth muscle, glands, cardiac muscle
65
What effect do the somatic and autonomic NSs have on their effectors? (stim or inhib?)
SNS= stimulatory ANS= stimulatory or inhibitory depending on NT and Rs on effector organs
66
What arteries are the blood supply to the spinal cord?
``` Anterior spinal artery Vertebral artery Subclavian artery Radicular artery Great vertebral radicular artery (artery of Adamkiewicz) Lumbar radicular artery ```
67
Percentage of body weight is made up by the brain
2%
68
Percentage of cardiac output does the brain demand
10-20%
69
Percentage of body O2 consumption does the brain demand
20%
70
Percentage of liver glucose does the brain demand
66%
71
What are the 2 sources of blood to the brain?
Internal carotid arteries | Vertebral arteries
72
What do the internal carotid arteries branch to form?
2 major cerebral arteries The anterior and middle cerebral arteries.
73
What comes off the Circle of Willis?
Main venous arteries supplying brain
74
Where is a build up of atherosclerotic plaques common and why?
Bifurcation in the common carotid artery Blood gets here and suddenly becomes turbulent flow
75
Biggest in the Circle of Willis
Middle cerebral artery
76
What arteries are small and how does this affect blood supply in case of a vascular accident?
Blood supply can go to both sides if there is damage but posterior communicating arteries are often very small so compensatory flow can be difficult
77
What is involved in venous drainage (4)?
Cerebral veins Venous sinuses (folds in dura, most of drainage) Dura mater Internal jugular vein (all ends up here)
78
Define: stroke
Rapidly developing focal disturbance of brain function of presumed vascular origin and of >24hours duration
79
What percentage of strokes are infarctions and haemorrhages?
85% infarction | 15% haemorrhage
80
Define: transient ischaemic attack (TIA)
Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours
81
Define: infarction
Degenerative changes which occur in tissue following occlusion of an artery
82
Define: cerebral ischaemia
Lack of sufficient blood supply to nervous tissue resulting in permanent damage if blood flow is not restored quickly
83
Why is ischaemia different from anoxia/hypoxia?
Ischaemia relates to whole blood including oxygen, glucose, nutrients
84
What causes occlusions?
Thrombosis | Embolism
85
Define: thrombosis
Formation of a blood clot (thrombus)
86
Define: embolism
Plugging of small vessel by material carried from larger vessel E.g. thrombi from the heart or atherosclerotic debris from the internal carotid
87
How can atherosclerosis be seen on imaging?
Yellow fat where it shouldn't be
88
Outline the epidemiology of strokes
3rd commonest cause of death | 100,000 deaths in UK per annum
89
What percentage of stroke survivors are permanently disabled or show an obvious neurological deficit?
50% of survivors are permanently disabled 70% show an obvious neurological deficit
90
What are the main risk factors for strokes?
``` Age Hypertension Cardiac disease Smoking Diabetes mellitus ```
91
Where does the anterior cerebral artery supply?
Frontal area of brain | All the way back to parietal occipital fissure
92
Where does the middle cerebral artery supply?
Most lateral area of temporal lobe
93
Where does the posterior cerebral artery supply?
Around the occipital lobe area
94
What happens if there is damage to the anterior cerebral artery?
Paralysis of contralateral leg (more than arm and face) Disturbance of intellect, executive function and judgment Loss of appropriate social behaviour
95
What happens if there is damage to the middle cerebral artery?
``` “Classic stroke” Contralateral hemiplegia (more of arm than leg) Contralateral hemisensory deficits Hemianopia Aphasia (L sided lesion) ```
96
What happens if there is damage to the posterior cerebral artery?
Visual deficits - Homonymous hemianopia - Visual agnosia
97
What is a lacunar infarct?
Lacune is a small cavity Deficit is dependent on anatomical location (appear in deep structures due to small vessel occlusion) Hypertension
98
What are the subtypes of haemorrhagic strokes?
Extradural Subdural Subarachnoid Intracerebral
99
What causes an extradural haemorrhagic stroke and what are the effects?
Trauma, immediate effects Large blood clot outside dura Requires urgent attention
100
What causes a subdural haemorrhagic stroke and what are the effects?
Trauma, delayed effects
101
What causes a subarachnoid haemorrhagic stroke?
Ruptured anaerysms | Vessels rupture and fill subarachnoid space with blood
102
What causes an intracerebral haemorrhagic stroke?
Spontaneous hypertensive Health of patient important e.g. age/risk factors
103
Why should someone be admitted overnight after a stroke?
Subdural haematoma will feel ok after losing consciousness but need to be observed for 24h to check for delayed effects
104
How much blood flows into the brain?
High | 55ml/100g tissue/min
105
What happens if blood flow to the brain is reduced by more than 50%?
Insufficient oxygen delivery | Function becomes significantly impaired
106
How long does total cerebral blood flow (CBF) have to be interrupted to cause unconsciousness or irreversible damage?
4 seconds-> unconsciousness Few minutes-> irreversible
107
What is syncope?
Fainting | Common manifestation of reduced blood supply to the brain
108
What causes syncope?
``` Low blood pressure Postural changes Vaso-vagal attack Sudden pain Emotional shock ``` (All result in a temporary interruption or reduction of blood flow to the brain)
109
Approximate percentage of body glucose used by the brain
50-60%
110
Why does the brain need glucose from the body?
Brain cannot store, synthesize or utilise any other source of energy (In starvation, ketones can be metabolised)
111
What happens when blood glucose drops below 2mM?
Unconsciousness Coma Ultimately death
112
Normal fasting levels of glucose
4-6mM
113
How is the brain's constant need for oxygen and glucose regulated?
Mechanisms to maintain cerebral blood flow Mechanisms which relate activity to requirement in specific brain regions to altered localised blood flow
114
How is total cerebral blood flow regulated?
Autoregulation between MABP 60-160mmHg
115
How do arteries respond to blood pressure to allow autoregulation of CBF?
Arteries and arterioles dilate/contract to maintain blood flow Stretch-sensitive cerebral vascular smooth muscle contracts at high BP and relaxes at lower BP
116
What happens below the autoregulatory pressure range of CBF?
Insufficient supply-> compromised brain function
117
What happens above the autoregulatory pressure range of CBF?
Increased flow can lead to swelling of brain tissue (not accomodated by the closed cranium-> increased intracranial pressure-> danger
118
What is local autoregulation?
Local brain activity determines the local 02 and glucose demands Therefore local changes in blood supply are required Neural and chemical control
119
How is CBF controlled by neural factors?
Sympathetic nerve stimulation (to main cerebral arteries-> vasoconstriction) Parasympathetic (facial nerve) stimulation (-> slight vasodilation) Central cortical neurones (release vasoconstrictor NTs e.g. catecholamines) Dopaminergic neurones (-> localized vasoconstriction)
120
How do dopaminergic neurones have a local effect on CBF?
Innervate penetrating arterioles and pericytes around capillaries May divert CBF to areas of high activity DA may cause to contraction of pericytes via aminergic and serotoninergic receptors
121
What is a pericyte?
Form of brain macrophages with diverse activities e.g. immune function, transport properties, contractile
122
How are CNS tissues vascularised?
Arteries from pia penetrate into the brain parenchyma to form capillaries Capillaries drain into venules and veins which drain into pial veins
123
Is the CNS densely or sparsely vascularised?
Densely | No neurone >100um from a capillary
124
How is CBF controlled by chemical factors?
``` Vasodilators: CO2 (indirect) pH (H+, lactic acid etc) Nitric oxide K+ Adenosine Anoxia Other (kinins, prostaglandins, histamine endothelins) ```
125
How does CO2 lead to cerebral arterial vasodilation?
CO2 crosses BBB from blood into smooth muscle cells H+ crosses from neural tissue to smooth muscle cells In smooth muscle CO2 binds with H2O bicarbonate and H+ SEE DIAGRAM CO2 may also affect the production of NO (a potent relaxant of smooth muscle)
126
How is brain activity mapped?
PET and fMRI | Studying local changes to cerebral blood flow
127
Where is CSF produced?
By regions of choroid plexus in the cerebral ventricles
128
What is the choroid plexus?
Ventricles, aqueducts and canals of the brain are lined with ependymal cells Lining modified in some regions to form branched villus structures= choroid plexus
129
How is CSF formed?
By choroid plexus Capillaries leaky but adjacent ependymal cells have extensive tight junctions Secrete CSF into ventricles
130
What is the volume of CSF in circulation?
80-150ml
131
How does CSF circulate?
Lateral ventricles 3rd ventricle via interventricular foramina Down cerebral aqueduct into 4th ventricle Into subarachnoid space via medial and lateral apertures)
132
What is the function of CSF?
Protection (physical and chemical) Nutrition of neurones Transport of molecules
133
Features of capillaries
Thin-walled Abundant Provide large s.a. for exchange
134
List the different capillary types in order of leakiness
Moderately leaky= continuous Leaky= fenestrated Very leaky= sinusoid
135
How much plasma leaks out of blood vessels per day?
8L (this means entire plasma volume must pass into the interstitial space and back into the blood circulation every 9 hours)
136
What do endothelial cell-cell contacts of BBB capillaries have?
Extensive tight junctions
137
What do tight junctions at the endothelial cell-cell contacts of BBB capillaries do?
Reduce solute and fluid leak across the capillary wall Mainly applies to hydrophilic solutes e.g. glucose, AAs, toxins, and others
138
What is the difference between a brain capillary and a cardiac muscle capillary?
Cardiac muscle capillary= continuous type, with transcellular vesicular transport Brain capillary= continuous type, little transcellular vesicular transport
139
What are IEJs?
Interendothelial junctions
140
What are pericytes?
Pericytes are cells closely apposed to capillaries
141
What do pericytes do and how are their associations important to maintain BBB properties?
Maintain capillary integrity and function Peripheral vessels have sparse pericyte coverage, while BBB capillaries have dense pericyte coverage In addition, BBB capillaries are covered on “end-feet” from astrocytes
142
What prevents blood-borne infectious agents entering CNS tissue?
BBB
143
What are CVOs?
Circumventricular organs These are capillaries that lack BBB properties and are fenestrated (therefore leaky) Need access to the blood
144
Where are CVOs found?
Close to ventricles
145
What are CVOs involved in?
Generally involved in secreting into the circulation or need to sample the plasma e.g. for toxins or electrolytes to regulate water intake Need access to the blood
146
What is secreted by the posterior pituitary and median eminence?
Hormones | CVOs
147
What does the area postrema do?
Samples the plasma for toxins and will induce vomiting | CVOs
148
Why do second-generation antihistamines not cause drowsiness?
They are polar so don't cross the BBB | Old fashioned H1 blockers were hydrophobic so could cross the BBB and used as sedatives
149
How does the BBB affect the treatment of Parkinson's Disease?
Raise DA in brain DA can't pass through BBB so L-DOPA can cross the BBB and then get converted to DA in the brain Without Carbidopa very little L-DOPA gets to the brain (stops L-DOPA being converted in the body, just the brain)
150
Why is Carbidopa used with L-DOPA?
Administered with DOPA decarboxylase inhibitor (Carbidopa) Carbidopa cannot cross the BBB so doesn't affect conversion of L-DOPA in the brain but stops conversion in the body
151
How is the thalamus organised?
Divided in two by third ventricle Collection of individual nuclei with separate functions Ipsilateral connections with forebrain Nuclei are interconnected
152
What is the function of the thalamus?
Relay centre between cerebral cortex and the rest of the CNS Integrates info Involved in virtually all functional systems
153
How are the parts of thalamus described?
By their location
154
Where does the reticular nucleus extend?
Over the whole lateral surface of the left thalamus
155
What are the 4 main types of thalamic nuclei?
Specific - connected to primary cortical areas Association - connected to association cortex Intralaminar - connected to all cortical areas Reticular – not connected to cortex
156
What are the specific nuclei of the thalamus?
Connected to primary cortical areas NUCLEUS -> CORTEX Ventral lateral-> motor cortices (primary, ventral anterior premotor, supplementary) Ventral anterior-> motor cortices (primary, ventral anterior premotor,supplementary) Ventral posterolateral-> somatosensory (body) Ventral posterolateral-> somatosensory (head) Lateral geniculate-> visual Medial geniculate-> auditory
157
What are the association nuclei?
Connected to association cortex NUCLEUS-> CORTEX Anterior/lateral dorsal/dosromedial -> Mammillary bodies (ant), hypothalamus (lat dorsal), cingulate and prefrontal Lateral posterior/pulvinar -> Parieto-temporo-occipital and prefrontal
158
What thalamic nuclei are associated with RAS (reticular activating system)?
Intralaminar nuclei= diffuse cortical projections Reticular nucleus= intrathalamic projections Both receive inputs from reticular formation
159
What is RAS (relates to thalamus)?
Reticular Activating System | Has intralaminar nuclei and reticular nucleus
160
What causes thalamic syndrome and how does it present?
Posterior cerebral artery stroke Sensation - reduced, exaggerated, altered Pain Emotional disturbance
161
What is TBI?
Traumatic brain injury
162
What does TBI cause even years after brain injury?
Neuroinflammation
163
What is neuroinflammation and what can cause it?
Inflammation of the nervous tissue It may be initiated in response to a variety of cues e.g. infection, traumatic brain injury, toxic metabolites, or autoimmunity
164
What can cause neuroinflammation?
Infection, traumatic brain injury, toxic metabolites, or autoimmunity
165
How does WM damage relate to amount of inflammation?
More severe WM damage-> more inflammation | Inflammation tracks along the axons (anterograde)
166
How is the hypothalamus organised?
Divided in two by third ventricle Collection of individual nuclei with separate functions Largely ipsilateral connections with forebrain
167
List the hypothalamic nuclei seen in the midline?
``` Fornix Paraventricular nucleus Anterior nucleus Pre-optic nucleus Suprachiasmatic nucleus Supra-optic nucleus Mammilary body Posterior nucleus Dorsomedial nucleus Ventroedial nucleus Infundibular nucleus ```
168
What is the function of the hypothalamus?
Coordinates homeostatic mechanisms by the ANS, endocrine system and controlling behaviour
169
What forebrain structures are associated with the hypothalamus?
Olfactory system | Limbic system- hippocampus, amygdala, cingulate cortex, septal nuclei
170
What behaviours are controlled by the hypothalamus?
``` Eating and drinking Expression of emotion Sexual behaviour Circadian rhythms Memory ```
171
How can the hypothalamus be damaged structurally?
Craniopharyngioma (and other tumours e.g. glioma, meningioma, dermoid, chordoma, hamartoma) Sarcoidosis Langerhans cell histiocytosis
172
How might someone present with hypothalamic damage?
Anterior pituitary hormone substitution Diabetes insipidus (polyuria, polydipsia) Adipsia
173
What are 3 main somatosensory receptor classes?
Mechanoreceptor Thermoreceptor Nociceptor
174
What modalities do mechanoreceptors detect?
TOUCH Light touch Pressure Vibration PROPRIOCEPTION Joint position Muscle length Muscle tension
175
What are sensory receptors?
Transducers that convert energy (thermal/mechanical/light/chemical) from the environment into neuronal APs Typically considered as the nerve ending
176
What do sensory receptors need to trigger APs?
Adequate or threshold stimulus
177
How is a sense organ formed?
Sensory receptor(s) surrounded by non-neural cells
178
What do sense organs respond to?
Receptors in a specific sense organ respond to a specific stimulus at a much lower threshold than other receptors
179
List examples of mechanoreceptors
``` Peritrichial ending Plexuses (papillary, dermal, subcutaneous) Pacinian corpuscle End bulb Merkel ending in epidermus Meissner's corpuscle Ruffini ending ```
180
How are vibrations detected?
By rapidly adapting mechanoreceptors Each fibre type has a different threshold Receptors then generate cycles of APs Thresholds overlap, therefore for certain vibrations different fibres may fire simultaneously
181
Why might certain vibrations cause different fibres to fire simultaneously?
Thresholds overlap, therefore for certain vibrations different fibres may fire simultaneously
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What are Pacinian corpuscles and Meissner's corpuscles most sensitive to?
Body most sensitive to 250 Hz Pacinian corpuscles: 60-400 Hz (peak 250 Hz) Meissner’s corpuscles: 5-300 Hz (peak 20-50 Hz)
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What does elevated vibratory threshold indicate?
Neurodegeneration (early sign)
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What's the difference between an itch and a tickle?
``` TICKLE Relatively mild stimulation Something moving across skin May be pleasurable Areas of the body with naked unmyelinated afferent nerve fibres ``` ITCH (Pruritis) Annoying Local mechanical stimulation or chemical agents e.g. Histamine, Kinins Relieved by scratching – stimulation of large nerve fibres overwhelms spinal transmission (closes the ‘Gate’) Occurs in neuropathy, renal failure, dermatitis
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Why does scratching relieve an itch?
Stimulation of large nerve fibres overwhelms spinal transmission (closes the ‘Gate’)
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What are temperature gated channels?
Different receptor subtypes | Open and close at different ranges of temperature
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Where is temperature detection most sensitive?
Face and chest
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What do TRPV, TRPM8 and TRPV1 detect?
TRPV hot temperature and chillies TRPM8 cold & menthol TRPV1 hot but also cold (ice-burn)
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What are nociceptors?
Specialised peripheral cutaneous terminals | Respond to noxious or harmful stimuli
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How are nociceptors activated?
Typically high threshold required for activation Direct activation of ion channel proteins e.g. Transient Receptor Potential (TRP) channels, Neurotrophin and G protein-coupled receptors
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Examples of nociceptors and their stimuli
Heat-> TRPV1 receptors Cold-> TRPM8 receptors pH <7-> Acid sensing ion channels (ASIC) Intense pressure-> K+ channels
192
How does depolarisation from nociception lead to the brain detecting pain?
Depolarisation-> AP in afferent nerve-> DH of SC-> brain
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What is the most common cutaneous nociceptor? What does it respond to?
Polymodal C fibre | Responds to pressure, temperature and chemical stimuli
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What is the most common skeletal nociceptor? What does it respond to?
Chemoreceptor (e.g. for lactic acid)
195
What does loss of function mutation NaV1.7 cause?
Has protective physiological role | LoF means disabling self harm
196
What substances can modulate nociception?
``` Prostaglandin Substance P Histamine Serotonin CGRP Bradykinin Potassium Acetylcholine ``` Associated with inflammation (why inflam is painful)
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What is the stimulus threshold? How is this defined experimentally?
The weakest stimulus detectable Adequate stimulus required to elicit a specific response or reflex In experimental terms, the minimum stimulus that is detected >50% of the time Varies in relation to anatomical location and between people
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How is info regarding somatosensory stimulus intensity conveyed?
Variation of frequency of APs generated Number of separate receptors activated (recruitment) Relationship between stimulus intensity and ultimate sensory discrimination may be linear or logarithmic
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What is a receptive field?
The area from which a stimulus elicits a neuronal response | Overlaps with others
200
When there is increased stimulus intensity, what happens to the receptive field?
Recruitment of adjacent sensory receptors with increased stimulus intensity The increased number of APs may be interpreted by the brain as increased intensity
201
What is lateral inhibition?
Activation of one neural unit inhibits activation of other units Mediated by interneurones within DH of SC
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How does lateral inhibition do?
Facilitates pinpoint accuracy in localisation of the stimulus Facilitates enhanced sensory perception
203
What is two-point discrimination?
Ability to detect that two stimuli are distinct from each other
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What is the two-point threshold?
Minimum distance required between two stimuli in order to perceive that they are two separate stimuli
205
What does two-point discrimination depend on?
Peripheral mechanoreceptors Spinal posterior column Cortical function
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How does two-point discrimination vary in the body? Why?
65mm on the back 2mm on the fingers Related to: Density of innervation Area of receptive field Sensory homunculus
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What is neural adaptation?
A form of desensitisation If a stimulus of constant strength is maintained for a period of time the frequency of action potentials diminishes (e.g. wearing clothes)
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Why is neural adaptation useful?
Facilitates ability to differentiate | meaningful from irrelevant information
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How do phasic and tonic receptors differ in neural adaptation?
Phasic receptors = Rapidly adaptive | Tonic receptors = Slowly adaptive
210
What are the types of nerve fibre?
A alpha (proprioception, somatic motor), beta (touch, pressure), gamma (motor to muscle spindle), delta (pain, cold, touch) B (postganglionic autonomics) C dorsal root (pain, temperature, mechanoception), sympathetic (postganglionic sympathetic)
211
How are cortical neurones involved in pain pathways?
Involved in the perception and interpretation of pain
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How are thalamic neurones involved in pain pathways?
Ventrobasal complex and Nucleus Reticularis have important reciprocal roles in modulation of nociceptive signals
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How are superficial DH neurones involved in pain pathways?
Crucial role in processing nociceptive signals
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Ascending pathway: touch and proprioception
Dorsal Column (Lemniscal system) Decussation (crossing) in brainstem Somatotopy throughout pathway Lateral inhibition in dorsal column nuclei
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Ascending pathway: pain and temperature
Spinothalamic tract Decussation in spinal cord via interneurones Somatotopy throughout pathway Important to consider in spinal cord injury
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What is Brown-Sequard Syndrome?
Hemisection of spinal cord
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How are spinal neurones modulated? What does this mean for the cortical response to peripheral input?
Spinal neurones respond to peripheral stimuli, but are modulated by interneurones and descending inhibitory controls Therefore the cortical response may not always match the peripheral input (could be greater or lesser)
218
What is the major excitatory synaptic transmitter? What does it activate
Glutamate Activates multiple receptor classes: AMPA, NMDA, mGluR Activates NMDAr by removing Mg2+ plug
219
What does NMDAr activation cause?
NMDAr activation causes large Ca2+ influx-> multiple intracellular actions
220
What may LTP of NMDAr cause?
LTP of NMDAr may occur-> hypersensitivity to pain
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What do NMDAr antagonists do?
Can relieve pain e.g. Ketamine
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What is the gate control theory? 3 examples
Non-painful stimulation can inhibit the transmission of pain from periphery to brain E.g. Rubbing elbow after banging it Using a TENS machine Spinal Cord Stimulation
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How can non-painful stimulation inhibit the transmission of pain from periphery to brain?
Gate theory Small Aδ and C fibres transmit painful stimuli Large Aβ fibres transmit non-noxious stimuli Large Aβ fibres can prevent or reduce transmission of Aδ and C fibres within the dorsal horn of the spinal cord ‘Closing the Gate’ By activating inhibitory interneurones (GABAAR)
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What is a dorsal root ganglion?
Nerve rootlets from a central dorsal nerve root that forms the ganglion Surrounded by dural sheath and minimal CSF
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What causes neuronal dysfunction in a DRG?
Associated with channelopathy (Ca2+, Na+) or second messengers may result in depolarisation in response to minor stimuli
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How can dorsal root ganglion dysfunction be treated?
X-Ray guided techniques including - Transforaminal epidural - Nerve root block - Neuromodulation
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What is neuromodulation? How does it work?
Non-painful stimulation can inhibit the transmission of pain from periphery to brain E.g. by stimulating SC or DRG Large Aβ fibres can prevent or reduce transmission of Aδ and C fibres within the dorsal horn of the spinal cord 'Closing the gate' compensates for neuronal dysfunction Useful in neuropathic pain
228
What is descending modulation?
Descending pathways from brainstem structures can have inhibitory or excitatory influence on spinal nociceptive transmission This monitoring system is always active
229
What mediates descending modulation?
Mediated by spinal 5HT3, NA, GABAA and Glycine receptors
230
What can loss of physiological inhibition result in?
Pathological hypersensitivity
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What are the 3 key somatosensory areas?
SI = Primary somatosensory cortex (in postcentral gryus) SII = Secondary somatosensory cortex (in parietal operculum) Posterior parietal cortex
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What is included in the association cortex?
Areas outside the primary areas Essential for complex mental functions Most developed part of the brain
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What parts of the brain are studied in an fMRI looking at the pain matrix?
Cortices (SI, SII, insular, anterior cingulate, prefrontal) Brainstem Amygdala Cerebellum
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What is pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage Pain is always subjective Warns that something is wrong
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Why is pain important?
A warning that something is wrong Associated with tissue damage Has a protective function
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What pain fibres are fast and slow?
Fast (Aδ) and Slow (C fibres)
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What are the types of pain?
Nociceptive – tissue damage, typically Acute Muscle – lactic acidosis, ischaemia Superficial Somatic – well-localised Visceral – deep, poorly localised Referred – from an internal organ/structure e.g. Angina Neuropathic – dysfunction of the nervous system
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How is pain detected?
Pathology-> nerve ending-> depolarisation-> AP in afferent nerve-> DH of SC-> brain
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What is pain called when it has no known pathological cause?
Malingering
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What drugs are in the WHO analgesic ladder?
1. Paracetamol & Aspirin (& Ibuprofen) 2. Codeine (& Tramadol) 3. Morphine
241
What causes myalgia (muscle pain)?
``` Metabolic Overuse Stretching Tension Compression Ischaemia Tearing Viral infection Fibromyalgia Angina ```
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What are the features of myalgia (muscle pain)?
``` Aching Burning (lactic acidosis) Cramping Tightness Crushing Tenderness ```
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What is superficial/cutaneous somatic pain?
``` Related to the skin Pressure Too hot / cold Inflammation Injury Infection Burns ```
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What are the features of somatic pain?
``` Often well-localised Sharp Stinging Aching Burning Throbbing Tightness Sensitive ```
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What is visceral pain?
Pain arising from internal organs or viscera | Heart, oesophagus, stomach, duodenum, gallbladder, or pancreas, colon
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What is problematic about visceral pain?
Viscera have low density of sensory innervation -> vague, diffuse, poorly localised pain Not possible to reliably differentiate one organ’s pain from another Pain may be referred
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Where is visceral pain often felt?
Characteristically midline pain at level of sternum/ epigastrium
248
When does visceral hyperalgesia occur?
Neural sensitisation | IBS, dysmenorrhoea, refractory angina
249
What are the features of referred pain?
At sites of body wall whose innervation enters spinal cord at the same level as the organ Sharper, better localised then visceral pain
250
What is the wind-up phenomenon of pain?
Short lasting synaptic plasticity Repetitive stimulation of WDRs (wide dynamic range neurones) induces increased evoked response and post discharge with each stimulus May precipitate long-term potentiation (LTP) i.e. long-lasting increase in efficacy of synaptic transmission Wind-up and LTP related to neuropathic sensitisation
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What are WDRs? What do they do
Wide Dynamic Range neurones Receive input from Aβ, Aδ and C fibres Respond to full range of stimuli (touch, heat, chemical) Fire APs in graded fashion Exhibit ‘Wind-up’
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What is neuropathic pain?
Pain in an area of neurological dysfunction Sharp, burning, electric shocks, squeezing Can last after area has healed completely Difficult to manage
253
How does neuropathic pain respond to analgesic drugs?
Poor response Delayed (1 month trial) Medications generally safe
254
Define: allodynia
Pain due to a stimulus that does not normally provoke pain
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Define: hyperalgesia
Increased pain from a stimulus that normally provokes pain
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Define: sensitization
Increased responsiveness of nociceptive neurons to their normal input
257
Define: hypoalgesia
Diminished pain in response to a normally painful stimulus
258
Define: hyperpathia
Painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold
259
Define: parasthesia
Abnormal sensation, whether spontaneous or evoked
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Define: dysaethesia
Unpleasant abnormal sensation, whether spontaneous or evoked
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List examples of neuropathic pain
``` Complex Regional Pain Syndrome Phantom limb pain Chronic scar hypersensitivity/postsurgical pain Post Herpetic Neuralgia Central Post Stroke Pain Radicular low back pain (sciatica) Diabetic neuropathy Chemotherapy induced neuropathy ```
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What is Complex Regional Pain Syndrome? Symptoms? How is it treated?
Severe form of neuropathic pain due to neurogenic inflammation and overexpression of nociceptive endings Sensory: hyperaesthesia/allodynia Vasomotor: temperature asymmetry/skin colour changes/asymmetry. Sudomotor/oedema: oedema/sweating changes/asymmetry Motor/trophic: decreased range of motion/motor dysfunction (weakness, tremor, dystonia)/trophic changes (hair, nail, skin)
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How can complex regional pain syndrome be treated?
MDT rehabilitation: Physio, OT, Psychology, PMP Medications, Spinal Cord Stimulation, (nerve blocks)
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What is phantom limb pain?
Pain affecting amputeess or people with removed eyes, breasts and genitals 1/2 are painful neuropathic
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What causes phantom limb pain?
Remapping of the cortex (shown by fMRI studies)
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How is phantom limb pain treated?
Medication Mirror therapy Neuroma excision 8% capsaicin patches
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How can neuropathic pain be managed pharmacologically?
Antidepressants= Amitriptyline, Nortriptyline, Duloxetine Anticonvulsants= Gabapentin, Pregabalin Opioid trial= Tramadol, Buprenorphine, Methadone, Morphine Hybrid= Tapentadol Topical= 5% Lidocaine, Capsaicin 0.075% cream and 8% patches
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How is a response to neuropathic pain treatment defined?
30-50% less pain
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What does evidence suggest is the best treatment of chronic neuropathic pain?
1st line: TCA, SNRI, alpha-2-delta ligands (e.g. Gabapentin) 2nd line: Opioids and Tramadol 3rd line: Membrane stabilisers, NMDA antagonists, Capsaicin
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How do Qutenza 8% capsaicin patches work?
Applied to skin for a single 60min period (in hospital) Binds to TRPV1 R on nerve endings (desensitises R directly and has direct toxicity to mitochondria) HAIRCUT or PRUNING mechanism Can be repeated after 3-4 months Can get long benefit from single treatment (disease modification) 3rd line
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What patients is high strength capsaicin patch therapy useful for?
Patients with peripheral NP i.e. allodynia/hyperalgesia
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What is functional segregation of motor control?
Motor system is organised into different areas that control different aspects of movement
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What is hierarchical organisation of motor control?
High order areas of hierarchy are involved in more more complex tasks e.g. programme and decide movements, coord muscle activity Low order areas perform lower level tasks e.g. execution of movement
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Which parts of the brain/SC are higher order/lower order?
``` Highest to lowest: Association cortex Motor cortex (primary motor cortex, premotor cortex, supplementary motor area) Brain stem Spinal cord ``` NB. side loops through basal ganglia and cerebellum
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What is the basal ganglia comprised of?
``` Caudate nucleus Putamen Globus pallidus Substantia nigra Subthalamic nucleus ```
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What are the areas of the frontal lobe motor cortex? Broadmann's area numbers>
Primary motor cortex or M1= Broadmann’s area 4 Premotor cortex= Broadmann’s area Supplementary motor area= Broadmann’s area
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What is the location of M1 (Broadmann's area 4)?
PRIMARY MOTOR CORTEX Frontal lobe Precentral gyrus Anterior to central sulcus
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What is the function of M1 (Broadmann's area 4)?
PRIMARY MOTOR CORTEX Control fine, discrete, precise voluntary movements Provide the descending signals to execute movements
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Where are Betz cells in the primary motor cortex?
Grey matter | Layer V
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What are descending cortical pathways? 2 egs.
Descending motor pathways From cortex Travel down to innervate abdomen, limbs and trunk
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Outline the path of the lateral corticospinal pathway?
PMC UMN through midbrain (through cerebral peduncle) Through pons Through pyramid of medulla DECUSSATION OF PYRAMIDS Lateral corticospinal tract through SC LMN through spinal nerve To skeletal muscles in the distal parts of the limbs
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Outline the path of the anterior corticospinal pathway?
PMC UMN through midbrain (through cerebral peduncle) Through pons Through pyramid of medulla DECUSSATION OF SPINAL CORD Anterior corticospinal tract through SC LMN through spinal nerve To skeletal muscles in the trunk and proximal parts of the limbs
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Where do the anterior and lateral corticospinal paths go to?
Anterior= skeletal muscles in trunk and proximal parts of the limbs Lateral= skeletal muscles in distal parts of the limbs
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How are the tongue muscles innervated by descending muscle pathways?
CORTICOBULBAR TRACT Head region motor cortex Genu of internal capsule DECUSSATES TO GO TO Hypoglossal nucleus Hypoglossal nerve (through inferior olivary nucleus and pyramid) Intrinsic tongue muscles, geniohyoid muscle, genioglossus muscle
285
List 2 examples of pyramidal tracts?
Corticospinal tract | Cortibulbar tract
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What NTs are used between UMNs and LMNs and between LMNS and muscles?
Glutamate: from upper to lower motor neurons Acetylcholine: from lower motor neurons to muscles
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What side of the body does the left cerebral surface control?
R side
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Who discovered the motor homunculus?
Penfield
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How can the organisation of the primary motor cortex be described?
Somatotopical organization Penfield's motor homunculus Can change e.g. singer has greater area of vocalisation
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What is the location of the premotor cortex (Broadmann's area 6)?
Frontal lobe, anterior to PMC
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What is the function of the premotor cortex (Broadmann's area 6)?
Involved in planning movements | Regulates externally cued movements (e.g. reaching out for an apple that you see)
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What is the location of the supplementary motor cortex (Broadmann's area 6)?
Frontal lobe | Anterior to PMC medially
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What is the function of the supplementary motor cortex (Broadmann's area 6)?
Planning complex movements and programming sequencing of movements Regulates internally driven movements (e.g. speech) SMA becomes active when thinking about a movement before executing that movement
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What is the association cortex?
Not strictly motor area as activity doesn't correlate with motor output/act Posterior parietal cortex Prefrontal cortex
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How is the posterior parietal cortex involved in motor function?
In association cortex | Ensures movements are targeted accurately to objects in external space
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How is the prefrontal cortex involved in motor function?
In association cortex | Involved in selection of appropriate movements for a particular course of action
297
What are negative and positive signs of lesions?
``` Negative= loss of function Positive= increased abnormal motor function (due to loss of inhibitory descending inputs) ```
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What are the negative and positive signs of an upper motor neuron lesion?
NEGATIVE SIGNS Paresis: graded weakness of movements Paralysis (plegia): complete loss of muscle activity ``` POSITIVE SIGNS Spasticity: increased muscle tone Hyperreflexia: exaggerated reflexes Clonus: abnormal oscillatory muscle contraction Babinski’s sign ``` SYMPTOMS ON OTHER SIDE
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What is apraxia? What are the symptoms?
Upper motor neuron disorder of skilled movement (due to lesion of inferior parietal lobe or frontal lobe (PMC, SMA) Progressive and neurodegenerative Not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea) Patients aren't paretic but have lost info about how to perform skilled movements
300
What are the most common causes of apraxia?
Stroke and dementia
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What are the main symptoms of lower motor neuron lesions?
``` Weakness Hypotonia (reduced muscle tone) Hyporeflexia (reduced reflexes) Muscle atrophy Fasciculations Fibrillations ```
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What are fasciculations? (LMN lesions)
Damaged motor units produce spontaneous APs resulting in a visible twitch
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What are fibrillations? (LMN lesions)
Spontaneous twitching of individual muscle fibres, recorded during needle electromyography examination
304
What are the main signs in UMN disease?
``` Increased muscle tone (spasticity of limbs and tongue) Brisk limbs and jaw reflexes Babinski’s sign Loss of dexterity Dysarthria Dysphagia ```
305
What are the main signs in LMN disease?
``` Weakness Muscle wasting Tongue fasciculations and wasting Nasal speech Dysphagia ```
306
What is included in the basal ganglia striatum?
Caudate and putamen
307
What are the functions of the basal ganglia?
Elaborating associated movements e.g. swinging arms when walking Moderating and coordinating movement (suppressing unwanted moves) Performing movements in order
308
What segments are the globus pallidus divided into?
Internal and external
309
What pathways are in the circuit of the basal ganglia? Where do they project and what are there overall effects?
``` Direct pathway (no projection to STN)= overall excitatory effect on motor cortex Indirect pathway (projection to STN)= overall inhibitory effect on motor cortex ``` Balance between these-> normal functioning of the basal ganglia
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What are the main neurotransmitters in the basal ganglia circuit?
Dopamine (+) Glutamate (+) GABA (-)
311
Is basal ganglia control ipsilateral or contralateral?
It is uncrossed (unlike corticospinal tract): basal ganglia mediate function of the ispsilateral cortex
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What are the 2 classes of basal ganglia syndromes?
Hypokinetic: decreased movement (Parkinson’s Disease) Hyperkinetic: increased movement (Huntington’s Disease)
313
Is Parkinson's disease hypo or hyperkinetic?
Hypo
314
Is Huntington's disease hypo or hyperkinetic?
Hyper
315
What part of the basal ganglia is most affected in PD? What neurones does this affect?
Neuronal degeneration of substantia nigra pars compacta | Loss of >80% dopaminergic cells (nigro-striatal dopaminergic axons)
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What does degeneration of dopamine neurons in the SNc cause?
Loss of nigro-striatal dopaminergic axons in caudate and putamen Disruption of the fine balance of excitation and inhibition Reduction of the excitation of motor cortex
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What are the major signs of PD?
``` Bradykinesia Hypomimic face Akinesia Rigidity Tremor at rest Parkinson's gait (shuffling) Stooped posture ```
318
Define: bradykinesia
Slowness of (small) movements e.g. doing up buttons, handling a knife
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Define: hypomimic face
Expressionless, mask-like e.g. absence of movements that normally animate the face
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Define: akinesia
Difficulty in the initiatIon of movements becausecannot initiate movements internally
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Define: rigidity
Muscle tone increase, causing resistance to externally imposed joint movements
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Define: tremor at rest
4-7Hz starts in one hand (pill-rolling tremor) | With time spreads to other parts of the body
323
Define: Parkinsonian's gait
Walking slow, small steps, shuffling feet, reduced arm swing
324
What is Huntington's disease caused by?
Neurodegenerative genetic disorder Abnormality in chromosome 4, autosomic dominant Degeneration of GABAergic neurones in striatium (caudate first, then putamen later)
325
What does degeneration of GABAergic neurons in the striatum cause?
Disruption of the fine balance between inhibition and excitation Motor cortex gets excessive excitatory input Motor cortex continuously sends involuntary commands for movement sequences to the muscles
326
What are the main signs of Huntington's Disease?
``` Choreic movements (speech impairment, difficulty swallowing, unsteady gait) Later= cognitive decline and dementia ```
327
What is chorea? Egs?
Type of movement (in HD) Rapid jerky involuntary movements of the body (hands and face affected first, then legs and rest of body) Speech impairment Difficulty swallowing Unsteady gait
328
What are the 3 lobes of the cerebellum (horizontal division)?
Anterior Posterior Flocculonodular
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What are the 3 zones of the cerebellum divided sagittally?
Vermis Intermediate hemisphere Lateral hermisphere
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The connections of the cerebellum are with the ...... .. and the ...... cerebral hemisphere?
The connections of the cerebellum are with the same side of the body and with the opposite cerebral hemisphere
331
What are the main neurotransmitters in the cerebellum?
Glutamate (+) | GABA (-)
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What is the flocculonodular lobe connected with?
The vestibular system 'Vestibulocerebellum"
333
What is the function of the vestibulocerebellum (flocculonodular lobe)?
Regulation of gait, posture and equilibrium | Coordination of head movements with eye movements
334
What is the function of the spinocerebellum (vermis and intermediate hemisphere)?
Coordination of speech Adjustment of muscle tone Coordination of limb movements
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What parts of the cerebellum is the spinocerebellum?
Vermis | Intermediate hemisphere
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What projects to the vermis?
Spinal afferents from axial portions of the body, trigeminal, visual and auditory inputs
337
What projects to the intermediate hemisphere?
Spinal afferents from the limbs
338
What part of the cerebellum is the cerebrocerebellum?
Lateral hemisphere
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What is the function of the cerebrocerebellum (lateral hemisphere)?
Coordination of skilled movements Cognitive function, attention, processing of language Emotional control
340
What are the main functions of the cerebellum?
``` Maintenance of balance and posture Coordination of voluntary movements (timing and force-> smooth moves) Motor learning (adapting and fine-tuning, via trial and error) Cognitive functions (language) ```
341
What is vestibulocerebellar syndrome (flocculonodular syndrome)?
Damage (tumour) causes syndrome similar to vestibular disease Causes gait ataxia and tendency to fall (even when patient sitting and eyes open
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What is spinocerebellar syndrome?
Damage (degeneration and atrophy associated with chronic alcoholism) Affects mainly legs, causes abnormal gait and stance (wide-based)
343
What is cerebrocerebellar syndrome (lateral cerebellar syndrome)?
Damage affects mainly arms/skilled coordinated movements (tremor) and speech
344
What are the main symptoms of cerebellar disorders?
``` Ataxia Disturbances of posture or gait (staggering/drunken) Dysmetria Intention tremor Dysdiadochokinesia Scanning speech ```
345
What are 2 of the more common cerebellar disorders?
``` Hereditary Friedrich's Ataxia Multiple Sclerosis (acquired) ```
346
Define: ataxia
General impairments in movement coordination and accuracy
347
Define: dysmetria
Inappropriate force and distance for target-directed movement (knocking over a class not grabbing it)
348
Define: intention tumour
Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
349
Define: scanning speech
Staccato, due to impaired coordination of speech muscles
350
Define: dysdiadochokinesia
Inability to perform rapidly altering movements (rapidly pronating and supinating hands and forearms)
351
What is a synapse?
Contact or junction between presynaptic axon and postsynaptic axon Allows for contact from neurone to muscle or from neurone to neurone
352
What is the synaptic contact ratio for muscles and the CNS?
1: 1 for muscle 10000: 1 in the CNS
353
What size is a typical synaptic cleft?
10-50nm
354
How is the membrane potential of the postsynaptic neurone altered?
Altered in two direction by inputs Can be made less negative (i.e. brought closer to threshold for firing- EPSP) Can be made more negative (i.e. brought further away from threshold for firing- IPSP) Graded effects= summation - IPSPs and EPSPs summate
355
What does the degree of summation (of IPSPs and EPSPs) determine?
How readily a neuron can reach threshold to produce an AP
356
What is a NMJ?
Specialised synapse between the motor neuron and the motor end plate, the muscle fibre cell membrane
357
What happens when an AP arrives at an NMJ?
Ca2+ influx causes ACh release ACH binds to Rs on motor end plate Ion channel opens- Na+ influx-> AP in muscle fibre
358
What happens at rest to ACh release?
Individual vesicles release ACh at a very low rate | Cause miniature end-plate potentials (mEPP)
359
What is an alpha motor neuron? What do they innervate?
Lower motor neurons of the brainstem and the spinal cord | Innervate the extrafusal muscle fibres of the skeletal muscles
360
What does alpha motor neuron activation cause?
Muscle contraction
361
What does the motor neuron pool contain?
All alpha motor neurons innervating a single muscle
362
What is a motor unit?
Single motor neuron together with all the muscle fibres that it innervates Samllest functional unit with which to produce force
363
How many motor neurons do humans have?
Approx 420,000
364
How many skeletal muscle fibres do humans have?
250 million skeletal muscle fibres
365
How many muscle fibres are typically supplied by each motor neuron?
600 muscle fibres
366
What does stimulation of one motor unit cause?
Contraction of all muscle fibres in that unit
367
How many different motor unit types are there? How are they classified?
3 (I, IIa and IIIb) | Classified by the amount of tension generated. speed of contraction and fatiguability of the motor unit
368
What two mechanisms allow the brain to regulate the force a single muscle can produce?
Recruitment | Rate coding
369
How does recruitment allow the brain to regulate the force that a single muscle can produce? What does this allow?
Motor units are not randomly recruited= ordered Governed by the “Size Principle” Smaller units are recruited first (these are generally the slow twitch units) More force required-> more units recruited This allows fine control (e.g. when writing), under which low force levels are required
370
How does rate coding allow the brain to regulate the force that a single muscle can produce?
A motor unit can fire at a range of frequencies Slow units fire at a lower frequency As the firing rate increases, the force produced by the unit increases Summation occurs when units fire at frequency too fast to allow the muscle to relax between arriving action potentials.
371
What relative frequency do fast and slow units fire at?
Fast units fire at higher frequency | Slow units fire at a lower frequency
372
What are neurotrophic factors?
Type of growth factor Prevents neuronal death Promote growth of neurons after injury
373
If a fast twitch muscle and a slow muscle are cross innervated, what happens to the FDL and soleus?
``` FDL= becomes slow Soleus= becomes fast ```
374
How can muscle fibre types change properties? Which fibre types in particular?
Under different conditions-> plasticity IIB to IIA most common following training I to II in cases of severe deconditioning or spinal cord injury
375
Why does ageing lead to slower muscle contraction times?
Ageing associated with loss of type I and type II fibres (preferential loss of type II-> larger proportion of type I fibres in aged muscle-> slower contraction times)
376
What does microgravity during spaceflight do to muscle fibres?
Shift from slow to fast muscle fibre types
377
What motor and descending (efferent) pathways are pyramidal and extrapyramidal?
1. Pyramidal 1a. Lateral corticospinal tract 1b. Anterior corticospinal tract 2. Extrapyramidal 2a. Rubrospinal tract 2b. Reticulospinal tract 2c. Vestibulospinal tract 2d. Olivospinal tract
378
What does 2c (vestibulospinal motor tract) do?
Regulates posture to maintain balance, and facilitates mainly α motoneurones of the postural, anti-gravity (extensor) muscles
379
What does 2b (reticulospinal motor tract) do?
Coordinate automated movements of locomotion and posture (e.g. to painful stimuli)
380
What does 2a (rubrospinal motor tract) do?
Automatic movements of arm in response to posture/balance changes
381
What do 1b (lateral corticospinal motor tract) and the sacral region do?
Control voluntary movements
382
What is a reflex?
An automatic and often inborn response to a stimulus that involves a nerve impulse passing inward from a receptor to a nerve centre and then outward to an effector (as a muscle or gland) without reaching the level of consciousness Involuntary coordinated pattern of muscle contraction and relaxation elicited by peripheral stimuli
383
How does the reflex relate to force? Use eg of bicep being tapped
If the biceps is tapped, the reflex occurs quickly and is related in size to how hard the biceps was hit
384
Outline a reflex arc
``` Sensory receptor Sensory neuron Integrating centre Motor neuron Effector ```
385
What happens to a reflex in the dorsal roots are cut?
Decreased force | Reflex needs afferents
386
Outline the monosynaptic stretch reflex
E.g. hit knee-> kick out foot Stretching stimulates sensory R (muscle spindle) Sensory neuron excited Within integrating centre (SC)= sensory neuron activates motor neuron Motor neuron excited effector (same muscle) contracts and relieves the stretching *antagonistic muscles relax
387
What motor neuron does the Hoffman (H-) reflex involve?
Orthodromic motor
388
Outline the polysynaptic reflexes (flexion withdrawal)
E.g. stepping on tack Sensory receptor (dendrites of pain-sensitive neuron on bottom of foot) Sensory neuron excited Within integrating centre (SC)= sensory neuron activates interneurons in several SC segments Motor neuronS excited Effectors (flexor muscles) contract and withdraw leg
389
Outline the flexion withdrawal and crossed extensor reflexs
E.g. stepping on tack with RIGHT FOOT Sensory receptor (dendrites of pain-sensitive neuron on bottom of foot) Sensory neuron excited Within integrating centre (SC)= sensory neuron activates interneurons in several SC segments Motor neuronS excited Effectors: Flexor muscles contract and withdraw RIGHT leg Extensor muscles contract and extend LEFT leg
390
What is the Jendrassik manoeuvre?
Patient makes a fist of clenches teeth when having patellar tendon tapped Larger reflex response will be observed when the patient is occupied with the manoeuvre, as the manoeuvre may prevent the patient from consciously inhibiting or influencing his or her response to the hammer Relates to supraspinal control of reflex
391
What does the supraspinal control of reflexes do? How is this studied?
Higher centres of the CNS exert inhibitory and excitatory regulation upon the stretch reflex Inhibitory control dominates in normal conditions Studied with decerebration which reveals the excitatory control from supraspinal areas Rigidity and spasticity can result from brain damage giving over-active or tonic stretch reflex
392
How can higher centres influence reflexes?
Supraspinal control of reflexes ``` Activating alpha motor neurons Activating inhibitory interneurons Activating propriospinal neurons Activating gamma motor neurons Activating terminals of afferent fibres ```
393
What higher centres and pathways are involved in supraspinal control of reflexes?
Cortex= corticospinal (fine control of limb movements, body adjustments) Red nucleus= rubrospinal (automatic movements of arm in response to posture/balance changes) Vestibular nuclei= vestibulospinal (altering posture to maintain balance) Tectum= tectospinal  (head movements in response to visual information)
394
What does the gamma reflex loop do?
Involves gamma motor neurons CNS can influence the stretch reflex via the gamma motoneurons Gamma motoneurons regulate how sensitive the stretch reflex is by tightening or relaxing the fibres within the spindle
395
What is hyper-reflexia?
Loss of descending inhibition | Eg.g due to a stroke-? Clonus sign, Babinski sign
396
What is the clonus sign?
Hyper-reflexia Clonus at the ankle is tested by rapidly flexing the foot into dorsiflexion (upward), inducing a stretch to the gastrocnemius muscle Subsequent beating of the foot will result, however only a sustained clonus (5 beats or more) is considered abnormal
397
What is the Babinski sign?
Hyper-reflexia The Babinski reflex occurs after the sole of the foot has been firmly stroked The big toe then moves upward or toward the top surface of the foot-> other toes fan out This reflex is normal in children up to 2 years old
398
What is hypo-reflexia?
Below normal or absent reflexes | Mostly associated with lower motor neuron diseases
399
How is sound transmitted in the outer ear?
Air transmitted sound waves are directed toward the delicate hearing mechanisms Pinna gently funnels sound waves into ear canal
400
What is the role of the outer ear?
Focuses sound on the tympanic membrane | Boosts sound pressure
401
How is sound transmitted by the inner ear?
Air movement strikes the tympanic membrane and vibrations-> oval window (smaller surface area means increased pressure) Energy generated transferred from AIR medium to SOLID medium in middle ear Ossicular chain of the middle ear connects to the eardrum via the malleus
402
How are the ossicles connected to the eardrum?
The malleus
403
What protects the inner ear from loud noises?
Stapedius muscle contracts | Protects ossicles and inner ear
404
Describe the joint between the incus and stapes
Flexible | Ossicles use leverage to increase the force on the oval window
405
What are the 3 ossicles?
Stapes Incus Malleus
406
What is the function of the inner ear?
Transduce vibrations into nervous impulses Also, produces frequency (or pitch) and intensity (or loudness) analysis of sound
407
How is pressure of vibrations increased in the middle ear?
Change in surface area (tympanic membrane to oval window)-> increased pressure
408
What are the 3 compartments of the inner ear and what do they contain?
``` Scala vestibuli (perilymph) Scala media (endolymph) Scala tympani (perilymph) ```
409
Which inner ear compartment is closest to the basilar membrane?
Scala tympani
410
The round window and oval window are found by which compartments of the inner ear?
``` Oval= scala vestibuli Round= scala tympani ```
411
What is the function of the perilymph?
Cushioning agent for the delicate structures of the centre chamber Connected to CSF
412
How is sound transduced in the inner ear?
Ossicular chain transfers energy from a solid medium to a fluid medium (of inner ear via stapes) Stapes connects to oval window which moves when sound is transferred Movement of oval window-> motion in cochlear fluid and along basilar membrane Basilar membrane excites frequency specific areas of organ of Corti-> stimulates nerve endings
413
How is the basilar membrane arranged?
Like a xylophone | BM is sensitive to different frequencies at different points along its length
414
How many inner and outer hair cells are there in a normal adult?
20,000 OHCs | 3,500 IHCs
415
What do hair cells in the inner ear do?
Adjust sensitivity of nerve signal from sound stimulus
416
What happens to hair cells due to higher amplitude (louder) sounds?
Greater deflection of sterocilia and K channel opening | Movement-> depolarisation
417
What causes the hair cell to depolarise?
Upward movement of the basilar membrane displaces stereocilia away from modiolus-> K+ channels open-> K+ enters from endolymph-> hair cell depolarises
418
What causes the hair cell to hyperpolarise?
Downward movement of the basilar membrane displaces stereocilia towards modiolus -> K+ channels close-> hair cell hyperpolarises
419
What cranial nerve is involved in the central auditory pathway?
Vestibular nerve (VIII)
420
Outline the central auditory pathways. (Note ipsilateral/bilateral parts)
Spiral ganglions from each cochlea project via auditory vestibular nerve (VIII) to the ipsilateral cochlear nuclei (monoaural neurons) After this point all connections are bilateral
421
Why is deafness in one ear due to central causes rare?
Must only be affecting the cochlear nucleus or VIII nerve | Because after cochlear nuclei, all connections are bilateral
422
How is hearing organised in the brain?
Tonotopically organised Based on sound frequency In primary auditory cortex (which is surrounded by secondary auditory cortex)
423
What are the main characteristics of sound?
Compressed and rarefied air Frequency/pitch (Hz) Amplitude/loudness (dB)
424
What frequency is heard by humans?
20-20,000Hz
425
How is the decibel scale organised?
Log scale because of the range of sensitivity (very large)
426
How is hearing loss affected with age?
Hearing loss increases with age (from about 20y) | Particularly higher frequencies associated with human speech (2-5Hz)
427
What is the main clinical condition associated with the outer ear?
The cartilage of the ear can become inflamed | Causes swelling, redness and pain of the outer ear= perichondritis
428
How can the ear be evaluated?
``` Otoscopy (to study tympanic membrane) Tuning fork (to differentiate between conductive and sensorineural hearing loss) ```
429
What features of the tympanic membrane are being looked for?
Light reflection Differentiation of its part Mobility
430
How is the tympanic membrane divided for description in clinic?
Posterior superior Anterior superior Posterior inferior Anterior inferior
431
Where are the pars flaccida, handle of malleus, umbo and a cone of light found?
Tympanic membrane
432
What tuning forks are typically used and how does their size affect their frequency?
256Hz, 512 Hz and 1024 Hz are used | Larger forks vibrate at slower frequency
433
How are tuning fork tests carried out?
Activated by striking examiner's elbow or heal | Placed 2cm away from EAC for air conduction and on mastoid for bone conduction
434
How is air conduction studied with a tuning fork?
Vibrating tuning fork is placed vertically in the meatus about 2 cm away from the EAC opening
435
How is bone conduction studied with a tuning fork?
Foot plate of vibrating tuning fork is placed on the mastoid bone Cochlea is stimulated directly by the vibrations conducted through the skull
436
What are the two main types of tuning fork tests? What's their difference?
Rinne and Weber tests Rinne= evaluates hearing loss by comparing air conduction to bone conduction Weber= evaluates conductive and sensorineural hearing losses
437
How is the Weber test carried out?
Ask where they can hear the tuning fork when its placed in middle above head (normal= middle, if stronger in one hear that means there is a problem)
438
How is hearing assessed?
Audiometry= speech audiometry or pure tone audiometry Tympanometry Otoacoustic emission To check if hearing is normal, degree of hearing loss and type of hearing loss
439
What is an audiometer?
Device used to produce sound of varying intensity and frequency in an audiometry test
440
Audiometer results: what do the following mean? - Air conduction hearing level lower than bone conduction - Air conduction hearing level the same as bone conduction - Air conduction hearing level higher than bone conduction
Air conduction hearing level lower than bone conduction= conductive hearing loss Air conduction hearing level the same as bone conduction= sensorineural hearing loss Air conduction hearing level higher than bone conduction= mixed hearing loss
441
What does tynpanometry show?
The condition of the middle ear and mobility of the eardrum (tympanic membrane) and the conduction bones by creating variations of air pressure in the ear canal SEE GRAPH- What is meant
442
What does spontaneous otoacoustic emission show?
Measures OAEs | Often part of a newborn hearing screening program
443
What are OAEs?
Otoacoustic emissions Produced by cochlea along with sound Cochlear OHCs as they expand and contract
444
What are the main types of hearing loss?
Conductive hearing loss (outer or middle) Sensorineural hearing loss (inner) Mixed hearing loss
445
What dB represents different kinds of hearing loss?
``` Normal hearing= 0-20 Mild hearing loss= 20-40 Moderate hearing loss= 40-70 Severe hearing loss= 70-90 Profound hearing loss= 90+ ```
446
What are the main outer ear causes of conductive hearing loss?
``` Congenital malformations Impacted wax Foreign bodies External otitis Exostosis ```
447
What congenital malformations can cause outer ear conductive hearing loss?
Congenital atresia= collapse or closure of air canal | Typically associated with congenital malformations of the middle ear
448
How does impacted wax lead to mild hearing loss?
Blockage | Can be removed
449
How can foreign bodies causing conductive hearing loss be removed?
Alcohol/oily solution or lidocaine (in case of insects) | More common in children (may need removal under GA)
450
What is external otitis?
Swelling and redness EAC Otorrhoea Pain on mobilization of the ear and tragus Systematic symptoms in severe cases May be fungal infection
451
What is exostosis?
Benign bone growth, usually in people with a history of exposure to repeated cold water Usually multiple, bilateral (possible extension to the middle ear) Hearing loss, external repeat ear infections, accumulation of ear wax
452
What are the main middle ear causes of conductive hearing loss?
Acute otitis media Otitis media with effusion Chronic otitis media Otosclerosis
453
What is acute otitis media?
Inflammation of the middle ear | Common health problem in children
454
What is otitis media with effusion?
Otitis media characterized by the accumulation of fluid Common with history of flu Hearing loss, ear fullness, autophonia
455
What causes chronic otitis media?
Cholesteatomatous - Congenitally acquired (primary, secondary) OR No cholesteatomatous - Without perforation (OME, retraction TM) - With perforation (inactive, active)
456
What is a cholesteatoma?
Destructive and expanding growth consisting of keratinizing squamous epithelium in the middle ear and/or mastoid process Serious but treatable ear condition
457
What are the 2 main types of TM retraction?
Pars tensa | Pars flaccida
458
What are the 2 main types of TM active?
Inactive | Active
459
What is otosclerosis? How is it treated?
Begins as soft, spongy growth of new bone (normally near oval window but can be anywhere in middle ear) 90% people have no symptoms 10% have growth causing mobility of stapes to be reduced-> conductive hearing loss Stapedectomy (removal and replacement with an artificial stapes)
460
What are the sensorineural causes of hearing loss?
``` Presbyacusis Sudden hearing loss Ototoxic drugs Infections Noise-induced hearing loss ```
461
What is presbyacusis?
Presbycusis is the loss of hearing that gradually occurs in most individuals as they grow older Gradual and symmetric Affects frequencies of speech Begins in adolescence Often associated with tinnitis
462
Why is presbyacusis increasing?
Ageing european population Decreased fertility, increased average life expectancy Men 2x more affected (earlier and more significant)
463
What is sudden sensorineural hearing loss?
SSHL (sudden deafness) Unexplained, rapid loss of hearing usually in one ear >30dB hearing reduction over at least 3 continuous frequencies, occurring over <72h
464
What are ototoxic drugs?
Certain drugs that can cause sensorineural hearing loss Mild and temporary to severe and permanent ``` E.g. Antibiotics: aminoglycosides, tetracyclines Chemotherapeutic agents: cisplatin, 5-flurocilo Acetylsalicylic acid Diuretics Beta Blockers Tricyclic antidepressants Antimalarials: quinine, chloroquine ```
465
What infections can cause sensorineural hearing loss and/or disruptions of vestibular function?
Bacterial or viral infections that invade the inner ear Other infectious diseases: Mumps, measles, meningitis, encephalitis, chicken pox, influenza, and syphilis can also invade the inner ear
466
What is noise-induced hearing loss? (2 types)
ACOUSTIC TRAUMA Injury due to brief exposure to very intense sounds such as gun shots, artillery fire, explosions, etc. Hearing loss may be severe and permanent, but substantial recovery is common LONG-TERM NOISE EXPOSURE Damage results from long-term exposure to high levels of noise Common in some occupational settings – heavy manufacturing and agriculture being the most common
467
What is the dizziness triad?
Anxiety Cardio-vascular disease/autonomic dysfunction Spatial disorientation syndrome (especially vestibular disease)
468
What can lead to spatial disorientation syndrome?
Migraine and epilepsy Hyperventilation (due to anxiety) CV disease/autonomic dysfunction
469
How are spatial disorientation syndrome and CV disease/autonomic dysfunction related?
Motion sickness control of orthostatic tension CV disease/autonomic dysfunction can lead to spatial disorientation syndrome
470
What parts of the ear are most related to the vestibular system?
Semi-circular canals | Otolith organs
471
What are semi circular canals stimulated by and what does this signal?
Stimulated by angular acceleration | Give approx signal of angular velocity
472
What are otolith organs stimulated by and what does this signal?
Stimulated by linear acceleration and gravito-intertial force Give signal of head acceleration and tily
473
What are the signals from the semi-circular canals and otolith organs used for?
Control balance reactions Provide spatial reference for other sensory motor co-ordinations Provide compensatory reflexes (VOR) Tune CV function for re-orientations Serve perception of motion in space
474
What is the different between self motion and world motion?
Self motion is when you feel as though you’re moving World motion is when you see moving (e.g. on train)
475
What are the main dysfunctions of the vestibular system? What functions do they affect?
ATAXIA Problems of controlling balance reactions and spatial referencing OSCILLOPSIA Total loss of compensatory ocular reflexes (VOR) NYSTAGMUS Unilateral loss of compensatory ocular reflexes (VOR) HYPOTENSION Problems of tuning CV function for re-orientations DIZZINESS Problems of perception of motion in space MOTION SICKNESS Unusual stimulation of balance organs
476
What kinds of vestibular disorders are there?
Structural Functional Both
477
What are structural and functional vestibular disorders?
Structural = destructive or irritative disease Functional = misinterpretation of sensory input = maladaption = loss of rules of correspondence between senses over awareness/magnification of sensory input Both = structural disorder provoking chronic dysfunction ALL TREATED THE SAME WAY
478
What is the vestibular system?
The sensory system that provides the leading contribution about movement and sense of balance Together with the cochlea it constitutes the labyrinth of the inner ear in most mammals, situated in the vestibulum in the inner ear Created to deduce orientation and motion in space (self and external entities)
479
What are the labyrinths in the vestibular system?
Bony labyrinth= bound by petrous bone filled with perilymph | Membraneous labyrinth= 2 membranous sacs filled with endolymph: utricle and saccule (the otolith organs)
480
What does the saccule give rise to?
Cochlear duct
481
What does the utricle give rise to?
Semi-circular canals
482
How long can vertigo last?
Seconds, minutes (most common), hours, days Can also be fluctuating/continuous or silent
483
What are the common causes of vertigo that lasts seconds?
Benign positional vertigo BPPV Debris in canals -> intense vertigo and nausea Paroxysmia (ephaptic) responds to Tegretol
484
What are the common causes of vertigo that lasts minutes?
Vertebrobasilar insufficiency? Migraine can lead to brief mild vertigo (possibly strong vertigo)
485
What are the common causes of vertigo that lasts hours?
Meniere's syndrome-> intense vertigo and nausea, hearing disturbance, pressure in repeated attacks
486
What are the common causes of vertigo that lasts days?
Vestibular neuritis-> intense vertigo and nausea, hearing disturbance in an isolated attack Herpes (Scarpa's ganglion)? Infarction of labyrinth?
487
What are the common causes of vertigo that has a fluctuating duration or is continuous?
Uncompensated vestibular lesion-> mild vertigo and nausea Functional midl vertigo and disproportionate disability
488
What are the common causes of vertigo is silent?
Acoustic neuroma-> mild imbalance, tinnitis, hearing loss
489
What is the vestibular ocular reflex? What does it do?
A reflex where activation of the vestibular system causes eye movement Stabilises images on the retina during head movement by producing an eye movement in the opposite direction to head -> preserves image on centre of visual field Controlled by canal
490
When the head is stationary, what happens to the canals?
Equal resting tonus on canals
491
What happens if a person sees a stimulation on the left?
``` Stimulation on L Canal drives eyes L Head turning leading canal is stimulated Head turning trailing canal is turned off Stimulated canal drives eyes R ```
492
What is the head rotation test? What are the positive and negative results?
Rapid head rotation separately to R and L whilst patient views examiner's eye POSITIVE During rotation towards the intact labyrinth the patient maintains fixation NEGATIVE During rotation towards the lesioned labyrinth the patient looses fixation Eyes go with the head and after the movement the patient makes REFIXATION SACCADES back to the fixation point
493
What does the abnormal head-thrust test test?
Detects unilateral hypofunction of the peripheral vestibular system caused mainly by acute vestibulopathy Normally= functional vestibular system will ID any movement of head position and rapidly correct eye movement Looking for presence/ absence of any corrective movement
494
What is the vestibulo-ocular pathways?
Superior and medial vestibular neurons project to motor nuclei supplying extraocular muscles Axons ascend in the MLF and excite the ipsilateral oculomotor (III) nucleus and the contralateral abducens (VI) nucleus
495
What happens to the canals and nerve firing when the head accelerates to the R?
When the head accelerates to the R, the right canals are stimulated by increased firing on right vestibular nerve (firing decreases on left nerve) (Opposite with L side)
496
If the head is stationary, what happens to the L and R vestibular nerves?
Support a tonic resting discharge | Firing on l and r is equal and opposite they cancel each other out
497
What happens if there is a vestibular lesion on one side (LEFT)?
Vestibular lesion on left side Resting discharge on right side signals to the brain as if the head is moving towards the right Patient feels like they are spinning to the right and has a nystagmus Then right canal signals drive the eyes in a slow phase movement to the left (lesioned side) Periodically, the brainstem generates fast phases (saccades) which drive the eyes back to the centre This creates a VESTIBULAR NYSTAGMUS (Right beating vestibular nystagmus in this case)
498
What are the parameters when measuring the rotational response?
Peak velocity VN/VS the ‘high frequency gain of the response End point in time Long ‘time constant’ of decay of nystagmus (roughly 1/4 end point time) Compare parameters for 2 R and 2 L accelerations
499
What is the caloric reflex test? How does it work?
Tests vestibulo-ocular reflex by irrigating cold then warm water into the external auditory canal (alternately) Stimulates individual horizontal canals of the labyrinth 44 degrees C= canal excitation- eyes driven contralateral 30 degrees C= canal inhibition- tonus of opposite canal drives eyes ipsilateral COWS= cold opposite, warm same Assessment of the caloric response: nystagmus duration, peak velocity, subjective sensation 4 measurements: R + L, hot + cold
500
What are the assessments that can be made by the caloric reflex test?
Normal= 40s irrigation normal response lasts for 1.5-2.5 minutes Small amplitude short duration response to both hot and cold on one side-> canal paresis Bilateral small short responses-> bilateral hypofunction Asymmetry of hot/cold responses (a directional preponderance) is of little significant
501
What are the symptoms, signs, course and treatments of typical vestibular neuritis?
Symptoms= vertigo, ocillopsia, imbalance, nausea, vomiting, abrupt onset Sign= nystagmus, pallor obvious ataxia Course= intense 1-2 days, recovery over week or so Treatment= steroids and anti-viral (cyclovirs) and anti-emetic
502
What are the signs of acute vestibular lesion?
Ipsilateral tilt Attempted compensation Ipsilateral head tilt and skew upwards
503
What are the vestibulospinal pathways?
Lateral vestibulospinal tract | Medial vestibulospinal tract
504
Outline the lateral vestibulospinal tract
Descends ipsilaterally in ventral funiculus of spinal cord Axons terminate in lateral part of ventral horn and influence motor neurons to limb (especially extensor antigravity) muscles
505
Outline the medial vestibulospinal tract
Descends bilaterally in medial longitudinal fasciculus (MLF) to cervical and upper thoracic spinal cord Axons terminate in medial part of ventral horn and influence motor neurons to neck and back muscles
506
How can vestibular disorder be treated?b
Reassurance that patient is understood Pharmaco-treatment: steroids, anti-viral (-cyclovirs), anti-emetic. (tegretol for vestibular ‘paroxysmia’) Treat associated anxiety, depression Cognitive behaviour therapy with desensitisation and physiotherapy Behavioural anxiolytic tactics Minimise risk factors
507
In benign positional vertigo (BPPV) how are people tested?
Placed on specific chair apparatus Asked what they feel Can study: - Compensatory eye movement for tilt - Compensatory eye movement for motion
508
What are the symptoms of motion sickness?
PRIMARY Signs of pallor and sweating Nausea and vomiting ASSOCIATED Headache including triggering migraine attacks Dizziness possibly with nystagmus Instability and in-coordination Postural discomfort and restlessness (provoking further motion sickness) Drowsiness (sopite syndrome) Feeling of eye strain
509
How can motion sickness be treated?
Non-pharmacologically: - Cognitive behavioural therapy with desensitisation (repeated small doses, no prolongs immersion) - Behavioural anti-emetic and anxiolytic exercises (controlled breathing posture relaxation)
510
What is the bony orbit?
Socket where the eye sits Made up of different bones and holes SEE DIAGRAM
511
What is the opening of the eyelid called?
Palpebral fissure
512
What are the lateral and medial canthi?
Canthus (pl. canthi) is either corner of the eye where the upper and lower eyelids meet At medial and lateral ends/angles of the palpebral fissure
513
Where is the lacrimal gland?
Located within the orbit | Latero-superior to the globe
514
What is the difference between basal tears and reflex tears?
Basal tears= produced at constant level (in absence of irritation or stimulation) Reflex tear= increased tear production in response to ocular irritation
515
What is the tear reflex pathway?
Afferent pathway, CNS, efferent pathway, lacrimal gland
516
How does a tear go from the lacrimal gland to exit the tear sac?
Tear produced by the Lacrimal Gland Tear drains through the two puncta, opening on medial lid margin Tear flows through the superior and the inferior canaliculi Tear gathers in the Tear Sac Tear exits the Tear Sac through the tear duct into the nose cavity
517
What is the purpose of the tear film?
Coves a healthy cornea with a thin layer of fluid Lubricates eye
518
What are the layers of the tear film? What does each layer do?
Superficial oily layer= lipid layer protects tear film from rapid evaporation (produced by a row of Meibomian Glands along the lid margins) Aqueous tear film (tear gland)= forms bulk of tear film, delivers O2 and nutrients to surrounding tissue and protects from bacteria Mucinous layer= on the Corneal Surface to maintain surface lubrication
519
How do mucin molecules in the tear film act?
Bind water molecules | to the hydrophobic corneal epithelial cell surface
520
What is the conjunctiva?
Thin, transparent tissue that covers the outer surface of the eye Nourished by ting blood vessels that are nearly invisible to the naked eye
521
Where is the conjunctiva found?
Begins at outer edge of cornea, covers visible part of the eye and lines the inside of the eyelids
522
How big is the eye?
Anterior-posterior= 24mm in adults
523
What are the 3 layers of the coat of the eye? What are the main features and functions of them?
Sclera= hard and opaque with high water content (white of the eye), for protecting eye and maintaining shape of eye Choroid= pigmented and vascular, for providing circulation to the eye and shielding out unwanted scattered light Retina= neurosensory tissue, for converting light into neurological impulses (to go to brain via optic nerve)
524
What is the cornea?
Front-most part of anterior segment Continuous with the scleral layer Transparent 5 layers
525
What does the cornea do?
Refraction – 2/3 of light focusing power Physical barrier Infection barrier
526
Why is the cornea involved in refraction?
Refraction – 2/3 of power Convex curvature Higher refractive index than air -> light focusing power
527
Why does prolonged contact lens wearing compromise corneal tissue health?
Reduces oxygen supply to the cornea Very prolonged-> increased risk of serious corneal eye infection
528
What are the 5 layers of the cornea?
``` 1- Epithelium 2- Bowman’s Membrane 3- Stroma (thickest layer) 4- Descemet’s Membrane 5- Endothelium ```
529
What does the stroma of the cornea do?
Regularity contributes towards transparency Corneal nerve endings provides sensation and nutrients for healthy tissue No blood vessels in normal cornea
530
What does the endothelium of the cornea do?
Pumps fluid out of corneal and prevents corneal oedema Only 1 layer of endothelial cell No regeneration power Endothelial cell density decreases with age Endothelial cell dysfunction may result in corneal oedema and corneal cloudiness
531
Where does the cornea get its nutrients and oxygen supply?
Tear film and aqueous fluid
532
What is the UVEA? Where is it?
The vascular coat of the eyeball Between the sclera and the retina 3 parts- iris, ciliary body, choroid
533
What is the uvea composed of?
3 parts- iris, ciliary body, choroid These are intimately connected (allows disease to spread)
534
What are the anterior and posterior segments of the eye?
Anterior segment refers to the anatomical structures of the eye, in front of the lens Posterior segment refers to the anatomical structures of the eye, behind the lens
535
What are the two anatomical chambers within the eye?
``` Anterior chamber (smaller) Posterior chamber ```
536
Where is the anterior chamber and what does it do?
Between cornea and lens Filled with clear aqueous fluid Supplies nutrients to surrounding tissue
537
Where is the posterior chamber and what does it do?
Between Lens and the Retina Filled with a jelly substance= vitreous humour Provides mechanical support
538
What is the vitreous humour composed of?
98-99% water trapped in jelly matrix (collagen and glycosaminoglycan gel)
539
Where is the choroid of the eye and what does it do?
Lies between the retina and sclera | Composed of layers of blood vessels that nourish the back of the eye
540
What is the iris?
Coloured part of the eye Controls light levels inside the eye similar to the aperture on a camera Round opening in the centre of the iris called the pupil Iris is embedded with tiny muscles that dilate (widen) and constrict (narrow) the pupil size
541
What is the structure of the lens?
Outer acellular capsule Regular inner elongated cell fibres (NB. important for transparency) May loose transparency with age-> Cataracts
542
What is the function of the lens?
``` Transparency (regular structure) Refractive power (1/3 power) Accommodation (elasticity) ```
543
What is the lens zonules?
Fibrous ring which has the lens suspended in it Consists of passive connective tissue Tension along the stretched lesn zonules-> holds surface of the lens flat and tort
544
What is the retina? What is the function of it?
Very thin layer of tissue that lines the inner part of the eye Responsible for capturing the light rays that enter the eye Light impulses then sent to brain for processing via optic nerve
545
What is the structure of the retina? What do the layers do?
Outer thin layer of retinal pigment epithelium (nutrient support to retina, removes metabolic debris from photoreceptors) Right behind is the choroid (Blood supply to the outer 1/3 retina (photoreceptors), pigment reduces light scattering) Then an inner thicker layer (neuroretina made of photoreceptors and neurons, has outer, middle and inner layer)
546
What are the layers of the neuroretina?
Outer layer- photoreceptors (1st order neuron)= detection of Light Middle layer- bipolar cells (2nd order neurons)= local signal processing to improve contrast sensitivity, regulate sensitivity Inner layer- retinal ganglion cells (3rd order neurons)= signal transmission from the eye to brain
547
What does the optic nerve do?
Optic nerve transmits electrical impulses from the retina to the brain Connects to the back of the eye near the macula
548
What is the optic disc?
The visible portion of the optic nerve
549
What is the macula?
Macula lutea (yellow patch)= pigmented region at the centre of the retina of about 6 mm in diameter Small and highly sensitive Fovea in the centre
550
What is the fovea?
Fovea= at the centre of the macula Characterized by an anatomical dip (foveal pit) due to the absence of the overlying ganglion cell layer Has the highest concentration of photo-receptors required for fine vision High concentration of cones, but low concentration of rods
551
How can the macula and fovea be clinically assessed?
With an OCT scan (Optical Coherence Tomography)
552
What is the ciliary body?
Ring-shaped tissue surrounding the lens (between anterior and posterior segment) Behind the iris
553
What is the iris?
Fat and ring-shaped tissue that regulates the amount of light entering into the eye Immediately in front of the ciliary body and lens
554
What are the 2 layers are the iris?
Thin posterior pigmented epithelial layer Thick anterior layer, composed of stromal tissue and smooth muscles
555
How do you treat raised intraocular pressure using the uvea-sclera pathway?
Prostaglandin analgoues (reduce pressure 20%, works on uvea-sclera pathway)
556
Retina gives rise anteriorly to....
Ciliary body epithelium | Posterior (epithelial) layer of iris
557
Choroid gives rise anteriorly to...
Ciliary body stroma | Anterior (stromal) layer of iris
558
How is the ciliary body involved in nutrient supply?
Secretes aqueous fluid in the eye (into anterior chamber) | Aqueous fluid supplies nutrients
559
Where does intraocular aqueous fluid flow?
Anteriorly into the anterior chamber
560
What does the trabecular meshwork of the eye do?
Drains fluid out the eye
561
What is normal intraocular pressure?
12-21mmHg
562
Outline what the aqueous flow includes
80-90% TM Canal of Schlemm | Rest= uveal-scleral outflow
563
What is glaucoma?
Eye condition characterized by sustained high intraocular pressure Retinal ganglion cell death and enlarged optic disc cupping Leads to gradual and cumulative damage to the optic nerve tissue in the posterior segment of the eye If untreated-> loss of peripheral vision progressively, eventual blindness
564
What are the main types of glaucoma? How do they present?
Primary open angle glaucoma= commonest, normally asymptomatic until advanced stages of the disease Closed angle glaucoma= can be acute or chronic, can be sudden painful red eye and drop in vision
565
What causes primary open angle glaucoma?
Trabecular meshwork dysfunction (functional blockage)
566
What causes closed angle glaucoma?
Forward displacement of iris, narrowing the trabecular meshwork drainage angle Occurs commonly in patients with hypermetropia, or long-sightedness
567
``` Which organ produces aqueous fluid in the eye? Iris Ciliary body Trabecular meshwork Choroid ```
Ciliary body
568
``` Which type of cells in the eye are primarily affect in glaucoma? Photoreceptors Retinal pigment epithelial cells Bipolar cells Retinal ganglion cells ```
Retinal ganglion cells
569
Where is the blind spot?
Where the optic nerve meets the retina | There are no light sensitive cells
570
``` What is the corresponding anatomic landmark for the physiological blind spot? Macula Fovea Optic disc Ora serrata ```
Optic disc
571
What can be seen by central and peripheral vision?
CENTRAL (foveal, focus) Detail day vision, colour vision Reading, facial recognition Central fine vision PERIPHERAL (motion) Shape, movement, night vision Navigation vision
572
How are central and peripheral vision assessed?
Central= visual acuity assessment (loss of foveal vision-> poor visual acuity) Peripheral= visual field assessment (extensive loss of visual field-> severe loss of peripheral vision)
573
What happens if a patient loses central vision?
Problems with reading, | and recognizing faces
574
What are the main classes of photoreceptors?
Rods and cones
575
Wha is the difference between rod and cone photoreceptors?
ROD Longer outer segment with photo-sensitive pigment 100 times more sensitive to light than cones Slow response to light Responsible for night vision (Scotopic Vision) 120 million rods CONE Less sensitive to light, but faster response Responsible for day light fine vision and colour vision (Photopic Vision) 6 million cones
576
How are photopigments synthesized in photoreceptors?
Photopigments are synthesized in the inner segment and transported to the outer segment disks Distal disks are shed from the tips and absorbed by retinal pigment epithelium cells by phagocytosis
577
What photopigment is found in rods? How does it lead to an AP?
Rhodopsin (reacts maximally to one single light frequency, namely at 498 nano-meters in humans) ``` Opsin= transmembrane Protein Cofactor= 11 cis-Retinal (Vitamin A derived) ``` Cofactor reacts to photon - > Conformal changes to Rhodopsin - > G-protein pathway - > Closure of ion channels and hyperpolarization - > Action potential
578
What photopigment is found in cone photopigments?
3 subtypes of photopsin | React to 3 light frequencies
579
Describe the photoreceptor distribution
Cone photoreceptors are distributed only within the macula Rod photo-receptors are widely distributed all over the retina, with the highest density just outside the macula The density of rod photo-ceptors gently tails off towards the periphery Completely absent within the macula SEE DIAGRAM
580
What is scotopic vision?
Night vision
581
What is photopic vision?
Day vision
582
``` Where is the highest concentration of rod photoreceptors in the retina? Optic disc Fovea 10-20 degrees away from fovea 20-40 degrees away from fovea ```
20-40 degrees away from fovea
583
How is colour vision determines by frequency spectrum?
Rod photopigment – 498nm (blue-green) Cone photopigments (in human) S-Cone 420-440nm (blue) M-Cone 534-545nm (green) L-Cone 564-580nm (red) M (green) and L (red) peaks are much closer to each other
584
What is the most common form of colour deficiency?
Commonest form of colour vision deficiency – M Cone peak shifted to L Cone peak resulting in red-green confusion (Deuteranomaly)
585
What cones does yellow light stimulate?
Yellow light has a wavelength between the peak sensitivity wavelengths of M-Cones and L-Cones Yellow light stimulates both M-cones and L-cones equally Biologically, we experience yellow light as a combination of green and red light
586
What percentage of congenital colour deficiencies affect males and females?
8% male | 0.5% females
587
What is the ishihara test?
Colour perception test Ishihara isochromatic plates can test for red-green deficiencies only Patients with colour vision deficiencies will not recognize any pattern or recognize the wrong pattern
588
What is dark adaptation and how does it occur?
Increase in light sensitivity in dark Biphasic Process - Cone adaptation 7 minutes - Rod adaptation 30 minutes (need regeneration of rhodopsin)
589
What is light adaptation and how does it occur?
Adaptation from dark to light Occurs over 5 minutes Bleaching of photo-pigments Neuro-adaptation Inhibition of Rod/Cone function
590
Which is the commonest form of colour vision deficiency in humans?
Red-green confusion
591
What are the landmarks in a digital image of the retina with a fundus camera?
Optic disc Ganglion cells exit via optic nerve, physiological blind spot Macula (and macula lutea yellow patch) Superio-temporal retinal artery and vein (vein darker and thicker) Superio-nasal retina artery and vein
592
What do retinal arteries do?
Retinal arteries provide circulation to the inner 2/3 of the retina
593
What happens in an ageing vitreous?
Liquifies and collapses with age resulting in posterior vitreous detachment Vitreous separates from retina Patient experiences vitreous detachment as seeing “floaters” May be occasionally associated with retina tear Patients are advised to see an ophthalmologist for retina examination to exclude retinal tear
594
What is refraction?
Light passing through one medium to another, strikes a boundary at some angle of incidence (measured from normal line) -> changes speed due to change in material density Leads to sensation of 'bending' of light- light doesn't travel in straight line through multiple mediums More dense= slower movement of light Use indices of refraction
595
What is the index of refraction?
The index of refraction is defined as the speed of light in vacuum divided by the speed of light in the medium Denominator will always be smaller so index will be equal to or greater than 1 Index regards to the new medium
596
What happens to light when it reaches a new medium?
Some light reflects off the boundary (angle of incidence) Some light refracts to the boundary (angle of refraction) Angle of i being bigger or smaller (NOT THE SAME) as angle of r depends on angle of light
597
What are the 2 basic types of lenses?
Convex (takes light rays and converges them on to a point) | Concave (takes light rays and diverges them outwards)
598
How is the eye like a camera?
LIGHT REFRACTION It focuses the incoming light ray from a distance onto the retina to form a clear image REGULATION OF LIGHT ENTRY INTO THE EYE Pupil, pigmented uvea MAINTENANCE OF THE SHAPE OF EYE Scleral coat Maintenance of intraocular pressure- ciliary body, trabecular meshwork VISUAL INFO PROCESSING Retina, optic nerve The retina converts image into nerve impulses, to be transmitted to the brain via the optic nerve
599
What is emmetropia?
When the cornea and the lens have just the right refractive power, to focus a clear image from distance onto the retina Parrallel rays converge exactly on the fovea (retinal surface)-> clear image formed-> SEE CLEARLY AT A DISTANCE NB. Cornea contributes 2/3 of refractive power Lens contributes 1/3 of refractive power
600
What is ametropia? List examples
Refractive error Mismatch between axial length and refractive power Parallel light rays don't fall on the retina (no accomodation) e.g. myopia, hyperopia, astigmatism, presbyopia
601
What is myopia?
Short-sightedness
602
What causes myopia?
In myopia (short sightedness), light ray from distance objects focuses IN FRONT OF the retinal surface Globe too long or high corneal curvature Image from near object converges on the retinal surface Patient see near objects clearly without glasses but need concave lenses to see clearly at distance
603
What is hypermetropia?
Long-sightedness
604
What causes hypermetropia/hyperopia?
In hypermetropia (long sightedness), parallel rays (distant image) focus BEHIND the retinal surface Caused by short globe or flat corneal surface Probably inherited Blurred vision without optical correction (glasses) Can be corrected with convex lens to provide additional converging power Blurred vision exacerbated by near vision
605
What are the symptoms of hyperopia?
Visual acuity at near tends to blur relatively early Blurred vision is more noticeable if person is tired or weak lighting Asthenopic symptoms= eyepain, headache in frontal region, burning sensation in eyes, blepharoconjunctivitis Amblyopia= lazy eye from uncorrected hyperopia
606
What is astigmatism? What happens without correction?
In astigmatism, the cornea is oval rather than spherical-shaped (hereditary) Parallel rays come to focus in 2 focal lines rather than a single focal point The refractive power varies along different meridians, or planes so see distant objects as blurred ellipses Without correction, patients see round objects as blurred ellipses, instead of blurred discs.
607
What are the symptoms of astigmatism?
Asthenopic symptoms Blurred vision Distortion of vision Head tilting and turning
608
How is astigmatism treated?
Patient requires special astigmatic glasses correction, with variable correction for every meridian Regular= cylinder lenses with or without spherical lenses Irregular astigmatism= rigid CL, surgery
609
What is the near response triad?
Adaptation for near vision TRIAD: 1) Pupillary miosis (sphincter pupillae) to increase depth of field 2) Convergence (medial recti from both eyes) to align both eyes towards a near object 3) Accommodation (circular ciliary muscle) to increase the refractive power of lens for near vision
610
What is presbyopia?
Naturally occurring loss of accommodation (focus for near objects) Onset from age 40 years Distant vision intact
611
How can presbyopia be treated?
Corrected by reading glasses (convex lenses) to increase refractive power of the eye Some people may need bifocal/trifocal glasses or progressive power glasses (all with convex lenses in near vision)
612
What is the mechanism of accommodation?
Contraction of the circular ciliary muscle inside the ciliary body This relaxes the zonules that are normally stretched between the ciliary body attachment and the lens capsule attachment NB. Zonules= passive elastic bands with no active contractile muscle Without zonular tension, the lens returns to its natural convex shape due to its innate elasticity -> increased refractive power of the lens Mediated by the efferent CNIII
613
What are the disadvantages and complications of contact lenses?
DISADVANTAGES= careful daily cleaning and disinfection, expense COMPLICATION= infectious keratitis, giant papillary conjunctivitis, corneal vascularization, severe chronic conjunctivitis
614
What are intraocular lenses?
Replacement of cataract crystalline lens Give best optical correction for aphakia Avoid significant magnification and distortion caused by spectacle lenses
615
What surgical options are available for myopia?
``` Keratorefractive srugery Intraocular surgery (clear lens extraction) ```
616
Which statement is false for myopia? 1. May be associated with large globe 2. Light ray converges behind the retina 3. May be associated with increased corneal curvature 4. Unable to see objected clearly at distance without glasses or other optical correction
Light ray converges behind the retina
617
In accommodation, which of the following events doesn't take place? 1. Relaxation of circular ciliary muscle 2. Relaxation of zonules 3. Thickening of lens 4. Increase of lens refractive power
Relaxation of circular ciliary muscle
618
Outline the visual pathway anatomy
Eye Optic nerve- ganglion nerve fibres Optic chiasm- half of the nerve fibres cross here Optic tract- ganglion nerve fibres exit as optic tract Lateral geniculate nucleus- ganglion nerve fibres synapse at LGN Optic radiation- 4th order neuron Primary visual cortex or striate cortex- within the occipital lobe Extrastriate cortex
619
What does the visual pathway do?
Transmits signal from eye to the visual cortex
620
What are the first, second and third order neurons in the visual pathway?
``` 1st= rod and cone retinal photoreceptors 2nd= retinal bipolar cells 3rd= retinal ganglion cells ```
621
What cranial nerve is involved in the visual pathway?
Optic nerve (CN II)
622
How many fibres cross the midline at the optic chiasma?
53% | Partial decussation
623
How is visual signal modulated?
2nd and 3rd order neurons within the retina modulate visual signal, before transmitting the signal to the brain Involves receptive fields
624
What is the receptive field of a neuron in vision?
Retinal space within which incoming light can alter the firing pattern of a neuron
625
What is the difference between the receptive field of photoreceptors and ganglion cells?
The receptive field of ganglion cells covers a much larger area than that of a single photo-receptor Photo-receptor receptive fields synapse upon the ganglion cells indirectly via bipolar cells SEE DIAGRAM
626
What is difference in convergence on the receptive field of rods and cones? What does this mean?
In general, fewer number of cone photo-receptors synapse upon the same ganglion cell than rod photo-receptors Cone system has lower convergence This means that ganglion cells in the cone system have a smaller receptive field than ganglion cells in the rod system
627
How does convergence of rod systems differ by location?
Rod system near macula has lower convergence than the rod system at the peripheral retina
628
Do ganglion cells in the cone or rod system have a larger receptive field?
Rods
629
What does a small receptive field (eye) mean?
Low convergence Fine visual acuity Low light sensitivity
630
What does a large receptive field (eye) mean?
High convergence Coarse visual acuity Higher light sensitivity
631
What can retinal ganglion cells be divided into?
On-centre | Off-centre
632
What stimulates/inhibits on-centre ganglion?
Stimulated by light at the centre of the receptive field | Inhibited by light on the edge of the receptive field
633
What stimulates/inhibits off-centre ganglion?
Inhibited by light at the centre of the receptive field | Stimulated by light on the edge of the receptive field
634
Why are on-centre and off-centre ganglion cells important?
Contrast sensitivity | Enhanced edge sensitivity
635
Outline the route of crossed fibres and uncrossed fibres through the optic chiasma
Crossed fibres- originating from nasal retina, responsible for temporal visual field Uncrossed fibres- originating from temporal retina, responsible for nasal visual field
636
What happens if there is a lesion anterior to the optic chiasma?
Affect visual field in one eye only
637
What happens if there is a lesion posterior to the optic chiasma?
Affect visual field in both eyes Right sided lesion-> left homonymous hemianopias in both eyes Left sided lesion-> right homonymous hemianopias in both eyes
638
What happens if there is a lesion at the optic chiasma?
Damages crossed ganglion fibres from nasal retina in both eyes Leads to temporal field deficit in both eyes- bitemporal hemianopia
639
What are the most common types of damage to a patient's visual field? (6)
``` Monocular blindness Bitemporal hemianopia Right/left nasal hemianopia Homonymous hemianopia Quadrant anopia Macular sparing ```
640
What is bitemporal hemianopia usually caused by?
Enlargement of pituitary gland tumour (presses on optic chiasma from below)
641
What is homonymous hemianopia usually caused by?
Stroke or cerebrovascular accident in the brain
642
Where is the primary visual cortex (striate cortex)?
Situated along calcarine sulcus | DIstinct stripe in the optic radiation myelinated fibres projecting into the visual cortex
643
What is the primary visual cortex representation?
Disproportionately large area representing the macular central vision within the PVC Above calcarine fissure= inferior visual field Below calcarine fissure= superior visual field Left PVC= right hemifield from both eyes Right PVC= left hemifield from both eyes
644
What does the primary visual cortex specialise in?
Processing visual information of static and moving objects
645
What are the columns in the primary visual cortex sensitive to?
Columns with unique sensitivity to visual stimulus of a particular orientation Right eye and left dominant columns intersperse each other
646
What is macular sparing? Why does it happen?
Homonymous hemianopia of contralateral side to lesion (e.g. from stroke) Macula area spared Area within PVC representing the macula is well protected because dual blood supply (R and L posterior cerebral arteries)
647
What is the extrastriate cortex?
Area around the PVC within the occipital lobe Converts basic visual information such as position and orientation, into complex human precepts like motion and object representation
648
What are the extrastriate dorsal and ventral pathways? What does damage cause?
Dorsal= how pathway= PVC to posterior parietal lobe (deals with motion detection) - Damage-> motion blindness Ventral= what pathway= PVC to temporal visual cortex (deals with object representation and face recognition) - Damage-> cerebral achromatopsia
649
What is the pupillary function?
Regulates amount of light entering into the eye
650
What happens to the pupil in light?
Pupil constriction Decreases spherical aberrations and glare Increases depth of field Reduces bleaching of photo-pigments Pupillary constriction mediated by parasymapthetic nerve (within CN III)
651
What happens to the pupil in dark?
Pupil dilatation Increases light sensitivity in the dark by allowing more light into the eye Pupillary dilatation mediated by sympathetic nerve
652
Outline the AFFERENT pupillary reflex pathway
Rod and cone photoreceptors synapse on bipolar cells which synapse on retinal ganglion cells Pupil-specific ganglion cells exits at posterior third of optic tract before entering the lateral geniculate nucleus (synapse at pretectal nucleus in brain stem) Afferent pathway from each eye synapses on Edinger-Westphal nuclei on both sides in the brainstem
653
Outline the EFFERENT pupillary reflex pathway
Edinger-Westphal nucleus - > oculomotor nerve efferent - > synapses at ciliary ganglion - > short posterior ciliary nerve - > pupillary sphincter
654
What is the direct pupillary reflex?
Constriction of pupil of the light in stimulated eye
655
What is the consensual pupillary reflex?
Constriction of pupil of other eye (not the stimulated one)
656
What is the neurological basis of the direct and consensual reflex?
Afferent pathway on either side alone will stimulate efferent (outgoing) pathway on both sides
657
What is the right afferent defect (pupil)?
E.g. damage to optic nerve No pupil constriction in both eyes when right eye is stimulated with light Normal pupil constriction in both eyes when left eye is stimulated with light
658
What is the right efferent defect (pupil constriction)?
E.g. Damage to right 3rd nerve No right pupil constriction whether right or left eye is stimulated with light Left pupil constricts whether right or left eye is stimulated with light
659
What is the unilateral afferent defect (pupil)?
Different response pending on which eye is stimulated
660
What is the unilateral efferent defect (pupil)?
Same unequal response between left and right eye irrespective which eye is stimulated
661
What does the swinging torch test study?
Relative afferent pupillary defect Partial pupillary response still present when the damaged eye is stimulated Elicited by the swinging torch test- alternating stimulation of right and left eye with light Both pupils constrict when light swings to left undamaged side Both pupils paradoxically dilate when light swings to the right damaged side
662
Why is eye movement necessary?
Voluntary or involuntary of movement of eyes | Necessary for acquiring and tracking visual stimuli
663
How is eye movement facilitated?
6 extraocular muscles (innervated by 3, 4, 6 CNs)
664
What is eye duction?
Eye movement in one eye
665
What is eye version?
Simultaneous movement of both eyes in same direction
666
What is eye vergence?
Simultaneous movement of both eyes in opposite direction
667
What is eye convergence?
Simultaneous adduction (inward) movement in both eyes when viewing a near object
668
How can looking up be described?
Elevation Supraduction- one eye Supraversion- both eyes
669
How can looking down be described?
Depression Infraduction- one eye Infraversion- both eyes
670
How can looking right be described?
Dextroversion Right abduction Left adduction
671
How can looking left be described?
Levoversion Right adduction Left abduction
672
What is torsion of the eye?
Rotation of eye around the anterior-posterior axis of the eye
673
What is a saccade? (e.g.s)
Short fast burst of eye movement (up to 900deg/sec) Voluntary or involuntary Reflexive saccade to external stimuli Scanning saccade Predictive saccade to track objects Memory-guided saccade
674
What is slow pursuit (eye movement)? (e.g.s)
Smooth pursuit- sustained slow movement Involuntary Slow movement – up to 60°/s Driven by motion of a moving target across the retina
675
What is nystagmus?
Oscillatory eye movement
676
What is optokinetic nystagmus?
Smooth pursuit and fast phase reset saccade
677
Why is the optokinetic nystagmus reflex useful?
To test visual acuity in pre-verbal children by observing the presence of nystagmus movement in response to moving grating patterns of various spatial frequencies Presence of optokinetic nystagmus in response to moving grating signifies that the subject has sufficient visual acuity to perceive the grating pattern
678
What are the 6 extraocular muscles responsible for eye movements? Where do they originate from?
Superior rectus, medial rectus, inferior rectus, lateral rectus- originating from orbit apex and attached to the anterior globe and pull backwards * rectus= straight muscles Inferior oblique, superior oblique- attached to the posterior globe and pull forwards
679
What do the lateral and medial recti do?
Lateral (external) rectus= abduction (attached to temporal side of eye, moves eye towards outside of head) Medial (internal) rectus= adduction (attached on nasal side of eye, moves eye towards nose)
680
What do the superior and inferior recti do?
Superior rectus= maximal elevation when eye is in abducted position Inferior rectus= maximal depression eye is in abducted position
681
What do the superior and inferior oblique muscles do?
Superior oblique= maximal depression when eye is in adducted position (attached high on temporal side of eye, passes under superior rectus, travels through trochlea)-> DOWN AND IN Inferior oblique= maximal elevation when eye is in adducted position (attached low on nasal side of eye, passes over inferior rectus)-> UP AND OUT
682
What extraocular muscles are controlled by CN 3, 4 and 6?
``` THREE (occulomotor) Superior rectus Inferior rectus Medial rectus Inferior oblique ``` FOUR (trochlear) Superior oblique SIX (abducens) Lateral rectus
683
What CN is lesioned if one eye goes out and down?
Third
684
What CN is lesioned if one eye goes in?
Sixth
685
How does the muscle of the vertical rectus act?
When the eye is adducted, the anterior-posterior axis of the eye is no longer aligned with the vertical rectus muscle action Torsion motion is produced instead of vertical movement -- When the eye is abducted, the anterior-posterior axis of the eye is aligned with the vertical rectus muscles Superior rectus- elevation Inferior rectus- depression
686
How do oblique muscles act?
Attach behind globe equator Pull forwards and nasally When the eye is abducted, the anterior-posterior axis of the eye is no longer aligned with the action of the oblique muscles as in the diagram Torsion motion is produced instead of vertical movement ---- When the eye is adducted, the anterior-posterior axis of the eye is aligned with the vertical rectus muscles Superior rectus- depression Inferior rectus- elevation
687
How do different parts of the third cranial nerve innervate the extraocular muscles?
SUPERIOR BRANCH Superior rectus= elevates eye Lid levator= raises eyelid ``` INFERIOR Inferior rectus= depresses eye Medial rectus= adducts eye Inferior oblique= elevates eye Parasympathetic nerve= constricts pupil ```
688
How is the fourth cranial nerve involved in innervation of the extraocular muscles?
Superior oblique= depresses eye
689
How is the fourth cranial nerve involved in innervation of the extraocular muscles?
Lateral rectus= abducts eye
690
What happens in complete third nerve palsy?
Affected eye down and out Droopy eyelid Unopposed superior oblique innervated by fourth nerve (down) Unopposed lateral rectus action innervated by sixth nerve (out)
691
What happens in sixth nerve palsy?
Affected eye unable to abduct and deviates inwards Double vision worsen on gazing to the side of the affected eye
692
How can you test the function of the 6 extra-ocular muscles?
Need to isolate the action of each of them by maximising the action of the muscle to be tested and minimizing the action of other muscles Lateral rectus muscle action is best tested in the abducted position Medial rectus muscle action is best tested in the adducted position Superior rectus muscle action is best tested in the elevated and abducted position Inferior rectus muscle action is best tested in the depressed and abducted position Inferior oblique is best tested in the elevated and adducted position Superior oblique is best tested in the depressed and adducted position
693
What does Hering's Law of Equal innervation state?
There is equal innate innervation to both muscles from both eyes, involved in conjugate or paired eye movements E.g. in dextroversion, or right gaze, there is simultaneous right eye abduction and left eye adduction
694
What is the Medial Longitudinal Fasciculus (MLF) in the midbrain for?
Responsible for coordinating eye movements in both eyes during R and L gaze
695
What is internuclear ophthalmoplegia?
Damage to medial longitudinal fasciculus (MLF) e.g. due to MS Right eye abduction not accompanied by left eye adduction Accompanied by nystagmus on right gaze Violates Herring's Law of Equal Innervation
696
What is Sherrington's Law of Reciprocal Innervation
Agonist muscles contract while antagonist muscles relax E.g. in dextroversion (R gaze), right eye lateral rectus and left eye medial rectus contract, while right eye medial rectus and left lateral rectus relax Violated in Duane's Syndrome
697
What is vertigo?
Illusion of movement | Usually rotational or 'true vertigo'
698
What are the most common types of spinning felt by vertigo patients?
Spinning world | Head spinning
699
What are symptoms of disorders of balance?
Vertigo Dizziness/giddiness Unsteadiness
700
How many people experience dizziness at some time?
1/4 people experience dizziness | 80% severe enough to see doctor
701
What are the main types of vestibular disorders? (E.g.s)
Peripheral e.g. labyrinth and VIII nerve Vestibular neuritis, BPPV, Meniere's disease Central e.g. CNS (brainstem/cerebellum) Stroke, MS, tumours
702
``` For peripheral vestibular disorders: Onset of vertigo Severity of vertigo Paroxysmal/continuous Relation with head/body position/movement Nausea/vomiting Type of nystagmus Intensity of nystagmus affected by fixation Nystagmus fatigability Hearing loss CNS symptoms/signs Catch up saccade ```
Onset of vertigo= sudden/gradual Severity of vertigo= intense Paroxysmal/continuous= paroxysmal Relation with head/body position/movement= yes Nausea/vomiting= frequent, prominent Type of nystagmus= horixontal or torsional (NEVER VERTICAL) Intensity of nystagmus affected by fixation= intensity decreased Nystagmus fatigability- decreases or disappears with repeated testing Hearing loss= may be present CNS symptoms/signs= absent Catch up saccade= one side will have
703
``` For central vestibular disorders: Onset of vertigo Severity of vertigo Paroxysmal/continuous Relation with head/body position/movement Nausea/vomiting Type of nystagmus Intensity of nystagmus affected by fixation Nystagmus fatigability Hearing loss CNS symptoms/signs Catch up saccade ```
Onset of vertigo= sudden/gradual Severity of vertigo= less intense Paroxysmal/continuous= constant Relation with head/body position/movement= no Nausea/vomiting= infrequent, less severe Type of nystagmus= horizontal, torsional, VERTICAL Intensity of nystagmus affected by fixation= unaffected Nystagmus fatigability= remains prominent on repeated testing Hearing loss= frequent CNS symptoms/signs= very frequent Catch up saccade= no
704
How can vestibular disorders be classified by duration/recurrence? (E.g.s)
Acute Intermittent (starts and stops e.g. within day) Recurrent (comes back maybe 6 months later) Progressive ACUTE INTERMITTENT (starts and stops e.g. within day): RECURRENT (comes back maybe 6 months later:
705
List 2 examples of vestibular disorders that are acute
``` Vestibular Neuritis (‘labyrinthitis’) Labyrinthine concussion ```
706
List 1 example of a vestibular disorder that is intermittent
Benign Paroxysmal Positional Vertigo (bppv)
707
List 2 examples of vestibular disorders that are recurrent
Meniere’s Disease - rare | Migraine - common
708
List 1 example of vestibular disorders that is progressive
Acoustic neuroma (8th nerve)
709
What does an acute unilateral vestibular lesion cause?
Syndrome | Many ethiologies
710
What part of the vestibulo-ocular reflex is involved in angular acceleration?
3 semi-circular canals
711
What part of the vestibulo-ocular reflex is involved in linear acceleration?
2 otolith organs
712
What vestibular projection lesions cause nystagmus?
Vestibuo-ocular
713
What vestibular projection lesions cause unsteadiness?
Vestibulo-spinal
714
What vestibular projection lesions cause nausea?
Vestibulo-autonomic
715
What vestibular projection lesions cause vertigo?
Vestibulo-cortical
716
What physiology of the vestibulo-ocular reflex is affected in vestibular disorders?
``` Vestibular tone Lesion induced asymmetry Visual suppression of nystagmus VOR suppression Vestibular compensation ```
717
Outline the symptoms of vestibular neuritis (vest neuronitis/viral labyrinthitis)
Sudden, unilateral vestibular loss Vertigo, nausea, unsteadiness, nystagmus Hearing spared No CNS symptoms or findings Viral ‘flavour’ (after URTI- mini-epidemics) Days to weeks
718
Outline the symptoms of BPPV?
Benign paroxysmal position vertigo Onset sudden (notice when they wake up and sit up) Actual attack = 10secs (autonomic features-> feel like 2-3 mins) ``` Dizziness Vertigo Loss of balance or unsteadinesss Nausea Vomiting ```
719
What test is used clinically for BPPV? How does it show BPPV?
Dix-Hallpike manoeuvre Patient rapidly moved from sitting to supine (head 45 degrees turned to right) After 20-30s-> patient returned to sitting position CHECK FOR NYSTAGMUS Pathognomonic= classic rotatory nystagmus with latency and limited duration Negative test only means active canalithiasis not present at that moment
720
What is Meniere's disease caused by and what are the symptoms?
Build up of endolymphatic pressure (‘hydrops’) causes rupture of membrane This-> perilymph and endolymph mix-> violent sensation of pressure-> vertigo attack ``` Hearing impaired (Meniere’s triad: vertigo, tinnitus and deafness) Low frequency hearing loss ```
721
How is Meniere's disease treated?
Eventually disease burns itself out (takes 15-20 years) but can’t wait so: ``` Reduce salt intake Medication- antihistamine (betahistine) Inject gentamicin (destroys balance part of the inner ear) ```
722
What are symptoms of recurrent vesibular disorder migraine?
History of migraine Migraine symptoms during vertigo attack Hearing usually spared Response to treatment
723
What causes chronic vestibular disorder? Why is it chronic?
Dizzy patient- can have many aetiologies Anxiety= confounding factor Reasons for chronicity: Lack of full vestibular compensation Inadequate testing Idiosyncratic reactions
724
What can cause central vestibular disorders?
Acute brainstem or cerebellar lesion e.g. MS or vascular Chronic/progressive= cerebellar degeneration
725
What are possible causes of dizziness that are not vestibular?
``` Heart disorders Presyncopal episodes Orthostatic hypotension Anaemia Hypoglicemia Psychological Gait disorders ``` Cause unsteadiness rather than true vertigo
726
How many different odours are there?
2000-4000
727
What kind of cells are found in the olfactory epithelium?
Bipolar olfactory neurons Sustentacular cells Basal cells
728
What happens to cells in the olfactory epithelium over time?
Progressive loss with age
729
What is found in the cribriform plate?
Olfactory receptor cells | Extend upwards to glomeruli in olfactory bulb
730
What happens to olfactory receptor cells that enter the olfactory bulb?
Form glomerulus | Second-order olfactory neuron extends away from cribriform plate to form olfactory tract
731
Outline the olfactory system from olfactory bulb to the cortex
``` Olfactory bulb (mitral cells) Olfactory tract (splits into mediate and lateral striate) -> Olfactory stria Piriform and orbitofrontal cortex ```
732
How are autonomic responses to smell promoted?
Connects from the cortex to the brainstem
733
What is anosmia?
Inability to smell | Commonly due to face trauma
734
What are prodromal auras? What are they caused by?
Many epilepsy patients have focal area in temporal lobe | Before seizure piriform area-> sensation of a smell
735
What can loss of smell be indicative of?
Normal ageing or sign of degenerative disease
736
What/where is the limbic system?
Structurally and functionally interrelated areas considered as a single functional complex Rim or limbus of cortex adjacent to corpus callosum to diencephalon
737
What are the functions of the limbic system?
Maintenance of homeostasis (via activation of visceral effector mechanisms, modulation of pituitary hormone release and initiation of feeding and drinking) Agonist (defence and attack) behaviour Sexual and reproductive behaviour Memory
738
Where is the hippocampus?
Sits in floor of ventricle | Posterior to amygdala
739
What kind of axons are in the amygdala?
GM- unmyelinated (sits in WM)
740
What does the Papez circuit show?
Neural circuit for the control of emotional expression= basis of emotional experiences
741
What are the components of the Papez circuit?
*He-Man ate a cat* ``` Hippocampus (limbi system) VIA FORNIX Mamillary body (hypothalamus) VIA MTT Anterior thalamic nucleus (thalamus) Cingulate cortex (limbic system) VIA CINGULUM BUNDLE Back to hippocampus ``` NB. Also neocortex contributed to cingulate cortex
742
What part of the Papez circuit....? Emotional colouring Emotional experience Emotional expression
Emotional colouring= neocortex Emotional experience= cingulate cortex Emotional expression= hypothalamus
743
What are the main connects of the hippocampus?
``` Afferent= perforant pathway to entorhinal cortex Efferent= fimbria/fornix ```
744
What is the entorhinal cortex
Main interface b/w hippocampus and neocortex | Lays down new memories
745
What are the functions of the hippocampus?
Memory and learning
746
What conditions are caused if the hippocampus is damaged?
Alzheimer's disease | Epilepsy
747
What is tau immunostaining?
A histologic technique in which multiple sections of brain tissue from a postmortem examination of a patient with dementia of unknown aetiology are stained with anti-tau protein antibodies to see the type of dementia
748
What plaques are involved in AD?
Amyloid beta plaque aggregation in parenchyma | Affects hippocampus early and hard
749
Outline the anatomical progression of AD and the symptoms they cause
EARLY Hippocampus and entorhinal cortex Short-term memory problems MODERATE Parietal lobe Dressing apraxia LATE Frontal lobe Loss of executive skills
750
What are the main connections of the amygdala?
``` Afferent= Olfactory cortex, septum, temporal neocortex, hippocampus, brainstem Efferent= Stria terminalis ```
751
What are the functions of the amygdala?
Fear and anxiety | Fight or flight
752
What is Klüver-Bucy syndrome?
Syndrome resulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus) ``` Symptoms= Hypersexuality Hyperorality Visual agnosia Docility ```
753
What structures of the brain are associated with aggression?
Hypothalamus Brainstem (periaqueductal grey) Amygdala Raphe nuclei (5-HT)
754
What are the main connections of the septum?
``` Afferent= amygdala, olfactory tract, hippocampus, brainstem Efferent= stria medularis thalami, hippocampus, hypothalamus ``` NB. some output via fornix
755
What is the pathway involved in drug dependence?
Mesolimbic pathway (dopamine) Midbrain (A10)-> MFB-> cortex/nucleus accumbens/amygdala
756
What do opioids, nicotine, amphetamines, ethanol and cocaine do to the limbic system?
Increase DA release in nucleus accumbens Stimulate midbrain neurons, promote DA release or inhibit DA reuptake
757
What is consciousness?
Consciousness is the brain state that enable us to experience the world around us and within one-self Distinct from automatic behaviours that occur in a rather unconscious manner Consciousness is not the same as being alert or attentive
758
How are levels and contents of consciousness different?
Levels reflect the level of alerting Contents= QUALIA experience/subjectivity and impression of visual world Alertness vs subjective experience and metacognition
759
What is metacognition?
Awareness and understanding of one's own thought process 'Cognition about cognition'
760
Is an alert/attentive state sufficient for consiousness?
No
761
What is the reticular activity system in the midbrain responsible for?
Reticular formation (RF) regulates many vital functions In consciousness- neurotransmitters alert the cortex Degree of activity in reticular system is associated with alertness/levels of consciousness
762
Where/how does the reticular formation project?
Thalamus and cortex Allows sensory signals to reach cortical sites of conscious awareness e.g. frontoparietal cortex Projects from locus coeruleus with noradrenergic neurones (to cortex) From ventral tegmental area (to cortex) with dopaminergic neurones Also have cholinergic neurons (to thalamus) Involves mesolimbic, nigrostriatal, mesocortical and tuberoinfundibular tracts
763
What do cholinergic neurons in the reticular formation do?
Boost the level of activity in cerebral cortex via the thalamus
764
What can electroencephalography (EEG) be used to measure when studying consciousness?
Monitor level of arousal
765
What Hz are delta, theta, alpha and beta waves?
``` Delta= up to 4Hz Theta= 4-8 Hz Alpha= 8-13 Hz Beta= 13-30Hz ```
766
What do higher frequency neural oscillations (gamma range approx 40Hz indicate)?
40 Hz associated with the creation of conscious contents in the focus of the mind’s eye, via thalamocortical feedback loops
767
What wave predominates in sleep?
Delta
768
What wave predominates in drowiness?
Theta
769
What wave predominates when relaxed/eyes closed?
Alpha
770
What wave predominates during waking consciousness?
Beta
771
What happens if there is damage to the RF/thalamus or a massive bilateral cortical insult (-> coma)?
State of unconsciousness Persistent vegetative state (due to disconnection of cortex from brainstem or widespread cortical damage) Brain death (due to brainstem death)
772
What can cause a coma?
``` Persistent vegetative state Brain death (due to brainstem death) Metabolic (e.g. hypoxia, hypoglycaemia, intoxication) ```
773
What are the categories in the Glasgow coma scale? What scores can be given?
``` Eyes open (1-4) Verbal responses (1-5) Motor responses (1-6) ```
774
What do scores in the GCS tell you?
Score of 3= lowest possible, severe brain injury and brain death Higher the score, the better
775
What are the GCS requirements for eyes open?
``` 1-4 none in response to pain in response to speech spontaneous ```
776
What are the GCS requirements for verbal responses?
``` 1-5 none incomprehensible sounds inappropriate words disoriented speech oriented speech ```
777
What are the GCS requirements for motor responses?
``` 1-6 none extensor response to pain flexor response to pain withdrawal to pain localisation of pain obeys commands ```
778
What kinds of brain injuries can lead to altered states of consciousness?
Contusion Concussion Diffuse axonal injury
779
What is a brain contusion?
A region of injured tissue or skin in which blood capillaries have been ruptured; a bruise Cerebral contusion can be associated with multiple microhaemorrhages, small blood vessel leaks into brain tissue
780
What is a diffuse axonal injury?
Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area.
781
What is a concussion?
Concussion is the sudden but short-lived loss of mental function that occurs after a blow or other injury to the head It is the most common but least serious type of brain injury
782
Is attention necessary for conscious awareness?
Yes but not sufficient | Being alert and aware not sufficient for conscious processes
783
What is a persistent vegetative state?
Irreversible coma due to disconnection of cortex from brainstem or widespread cortical damage Brainstem still functioning so reflexes, postural movements and sleep-wake cycle may be present In coma, can be aroused THIS IS DIFFERENT but both groups are unconsciouss
784
What is brain death?
Irreversible coma due to brainstem death Body kept alive artificially Decision to cease treatment depends on demo of absence of brainstem reflexes and response to hypercapnia Spinal reflexes and some postural movements may be present
785
What brain lesion causes achromatopsia?
Eliminate awareness of colour | Lesion in extrastriate cortex
786
What brain lesion leads to lack of awareness for stimuli in contralateral visual field?
Parietal lesion
787
What causes left visual neglect?
Breakdown of conscious awareness after right parietal damage (40-60% patients= due to right hemisphere stroke) Patients remain unconscious of info from left visual field despite PVC in occipital lobe being intact (ignore L side) Info doesn't reach awareness (RF is disrupted)
788
How can visual neglect bet investigated?
``` Star cancelation test (patients cancel fewer stars) Visual exploration (patient will not cross midline to look left) ```
789
Does visual neglect syndrome result from damage to occipital region?
No- primary visual cortex is intact | RF is disrupted
790
Why can fMRI be used to study consciousness?
Pictures of brain as patients complete tasks (holding certain info in their mind which activates certain areas) Active areas picked up by scanner Networks which are important for different tasks can be seen
791
What is blindisght?
Brain-damaged (occipital visual cortez) patients who are perceptyally blind of their visual field but can demonstrate some responses to visual stimuli I.e. they display aspects of consciousness e.g. manually interacting with unseen objects and avoiding unseen obstacles
792
How can you detect awareness in the vegetative state? Coma, 'vigil'
Still studying neural correlate of consciousness (recently use MRIs to detect level of consciousness in vegetative state) ``` No single brain region for consciousness Feed-forward processing (subliminal or non-conscious) Top-down recurrent processing (conscious access) ```
793
What is feed-forward processing?
Subliminal or non-conscious
794
What is top-down recurrent processing?
Conscious access
795
Brain activation for unconconsious info in patietns with visual neglect (Rees et al, 1993) showed...
Patients performed a face/house detection task inside the MRI scanner and indicated when they could see objects Study showed activation in the brain (striate and extrastriate) for info which could be received but not processed therefore patient can't 'see' the objects
796
What are the behavioural criteria of sleep?
Stereotypic or species-specific posture Minimal movement Reduced responsiveness to external stimuli Reversible with stimulation – unlike coma, anaesthesia or death
797
How is the physiological criteria of sleep recorded?
Brain activity with EEG (electroencephalogramm) Eye movements with EOG (electrooculogramm) Muscle movements (tone)with EMG (electromyogramm)
798
What are the stages of sleep?
Awake Stage 1 & 2= NREM Stage 3 & 4= NREM Stage 5= REM
799
What do the EEG, EOG and EMG show in an awake patient?
``` EEG= Fast activity (beta) EOG= Some eye movements EMG= Strong muscle tone ```
800
What do the EEG, EOG and EMG show in a patient in stage 1 & 2 of sleep?
``` EEG= Slowing of brain activity (theta) EOG= None EMG= Reduced muscle tone ```
801
What do the EEG, EOG and EMG show in a patient in stage 3 & 4 of sleep?
``` EEG= Even slower brain activity (delta) EOG= None EMG= Further reduced muscle tone ```
802
What do the EEG, EOG and EMG show in a patient in stage 5 of sleep (REM)?
``` EEG= Speeding up of brain activity (similar to beta in awake person) EOG= Rapid and wide EMG= Minimal tone (almost none) ```
803
What is NREM sleep?
Non-REM | Slow wave sleep
804
How long does each sleep stage last in an average cycle?
1 hour and half overall (70 mins excluding REM) ``` 12 min= awake 13 min= stage 1 13 min= stage 2 12 min= stage 3 10 min= stage 4 10-20 min= REM sleep ``` Very quickly into REM sleep
805
What controls the sleep/wave cycle?
Lateral hypothalamus (LH) promotes wakefulness (stimulates RAS) Ventrolateral preoptic (VLP) nucleus promotes sleep (inhibits RAS) Suprachiasmatic nucleus synchronises sleep with falling night level (affects VLP, LH and pineal) Pineal-> melatonin
806
What system in the brain maintains arousal?
Reticular activating system Controls consciousness Modulate activity of cerebral cortex directly or through thalamus
807
What controls the circadian synchronisation of sleep/wake cycle?
Suprachiasmatic nucleus Synchronises sleep with falling night level As light level falls, input from retina activates suprachiasmatic nucleus and has relationships with nuclei controlling sleep/wake cycle Affects VLP, LH and pineal Pineal-> melatonin secretion (main function- on pituitary)
808
How do we know sleep is necessary?
Most/all animals sleep Sleep deprivation is detrimental Sleep is regulated accurately
809
What are the effects of sleep deprivation? What happens in rats and humans?
Sleepiness, irritability Performance decrements/ increased risk of errors and accidents Concentration/learning difficulties Glucose intolerance Reduced leptin/increased appetite Hallucinations (after long sleep deprivation) Death- rats (14-40 days), humans (fatal familial insomnia)
810
What does sleep loss do to ability brain activation when performing mathematical tasks?
Reduced ability | Lower brain activation
811
After sleep loss what happens to regulate sleep?
Reduced latency to sleep onset Increase of slow wave sleep (NREM) Increase of REM sleep (after selective REM sleep deprivation)
812
What are the functions of sleep? Why can these be argued against?
Restoration and recovery- but active individuals do not sleep more Energy conservation- 10% drop in BMR (but lying still is just as effective) Predator avoidance Specific brain functions
813
When do dreams occur?
Can occur in REM and NREM sleep Most frequent in REM sleep More easily recalled in REM sleep Contents of dreams are more emotional than ‘real life’
814
Where is brain activity high during dreams?
Brain activity in limbic system higher than in frontal lobe during dreams
815
What are the functions of dreams?
Safety valve for antisocial emotions Disposal of unwanted memories Memory consolidation NREM sleep: declarative memory REM sleep: procedural memory
816
What memory consolidation happens in NREM and REM?
NREM sleep: declarative memory | REM sleep: procedural memory
817
List sleep disorders
Insomnia | Narcolepsy
818
What is insomnia?
High prevalence Most cases transient Causes of chronic cases: - Physiological e.g. sleep apnea, chronic pain - Brain dysfunction e.g. depression, fatal familial insomnia, night working Treatment: most hypnotics enhance GABAergic circuits
819
What is narcolepsy?
Falling asleep repeatedly during the day and disturbed sleep during the night Cataplexy = suddenly all muscles in body lose their tone -> fall Dysfunction of control of REM sleep Orexin deficiency –genetic or autoimmune?
820
What effect does shift work have on sleep?
Night working causes physiological processes to become desynchronised This can lead to sleep disorders, fatigue and an increased risk for some conditions such as obesity, diabetes and cancer
821
What is found in the cerebral cortex?
``` Grey matter structure White matter association fibres Grey matter function Testing grey matter function Hemispheric specialisation ```
822
What is in the GM of the brain?
Neuronal cell bodies, dendrites, synaptic connections, glial cells 50 billion neurons and x10 glial cells Only 30% surface easily visible as 70% hidden within sulci
823
What is in the WM of the brain?
Myelinated neuronal axons forming white matter tracks
824
How many cortical layers are there?
``` 6 Roman numerals (with letters for laminar subdivisons) ```
825
True or false: each of the cortical laminae in the neocortex (which covers the bulk of the cerebral hemispheres and is defined by six layers) has characteristic functional and anatomical features
True
826
Where are smaller pyramidal neurons found in the cortical layers? What kind of connections predominate?
Layers II and III | Primarily corticocortical connections
827
What kind of connections predominate in Layer I
Neuropil
828
Which cortical layer has the most stellate neurons?
Layer IV is typically rich in stellate neurons with locally ramifying axons
829
Where do the neurons in layer IV of the cortex receive input from?
In the primary sensory cortices, these neurons receive input from the thalamus, the major sensory relay from the periphery
830
What layer are pyramidal neurons whose axons typically leave the cortex found?
Layer V, and to a lesser degree layer VI, contain pyramidal neurons whose axons typically leave the cortex
831
How many distinct cortical regions or cytoarchitectonic did Brodmann describe?
About 50 Histological map of brain
832
Which cortical layers receive input and which give output?
Layer 4 receives input Layers 1- 3 send output to cortex Layers 5 and 6 send output to non-cortex
833
Which layer of the cortex is closer to the dorsal surface?
Layer I | Layer VI closest to ventral layer
834
What cortical layer has the primary visual cortex?
Layer IV
835
What is the relationship between cortical columns?
Columns stacked next to each other are connected (but looser than within each column) Some are functionally connected
836
Outline the role of the occipital lobe (and how lesions may affect this)
Visual association cortex analyses different attributes of visual image in different places Form and colour analyzed along ventral pathway; spatial relationships & movement along dorsal pathway Lesions affect specific aspects of visual perception
837
Outline the role of the parietal lobe (and how lesions may affect this)
Posterior parietal association cortex creates spatial map of body in surroundings, from multi-modality information Injury may cause disorientation, inability to read map or understand spatial relationships, apraxia, hemispatial neglect (primarily associated with right hemisphere)
838
Outline the role of the temporal lobe (and how lesions may affect this)
Language, object recognition, memory, emotion Injury leads to agnosia, receptive aphasia
839
Outline the role of the frontal lobe (and how lesions may affect this)
Judgement, foresight, personality, appreciation of self in relation to world Injury leads to deficits in planning and inappropriate behaviour
840
What are association fibres?
Connect areas within the same hemisphere
841
What are commissural fibres?
Connect left hemisphere to righ hemisphere
842
What are projection fibres?
Connect cortex with lower brain structures e.g. thalamus, brainstem and SC
843
What is another name for short association fibres?
U fibres | Connecting neighbouring gyra usually
844
What are 4 examples of long association fibres and what do they connect?
Superior Longitudinal Fasciculus (connects frontal and occipital lobes) Arcuate Fasciculus (connects frontal and temporal lobes) Inferior Longitudinal Fasciculus (connects temporal and occipital lobes) Uncinate Fasciculus (connects anterior frontal and temporal lobes)
845
What does the superior longitudinal fasciculus connect?
Frontal and occipital lobes
846
What does the arcuate fasciculus connect?
Frontal and temporal lobes
847
What does the inferior longitudinal fasciculus connect?
Temporal and occipital lobes
848
What does the uncinate fasciculus connect?
Anterior frontal and temporal lobes
849
What kind of fibres is the corpus callosum?
Commissural
850
What kind of fibres is the anterior commissure?
Commissural
851
What are the functions of the frontal lobe GM?
PRODUCTION OF VOLUNTARY SKELETAL MUSCLE MOVEMENTS Primary motor cortex, BA 4 (precentral gyrus) Premotor cortex, BA6 (Motor association area) COORDINATES INFO FROM OTHER ASSOCIATION AREAS Prefrontal association area
852
What are the functions of the parietal lobe GM?
RECOGNITION AND INTERPRETATION OF SENSORY INFO FROM SKIN, MUSCLES, TASTE BUDS Sensory association area Primary somatosensory cortex (postcentral gyrus)
853
What are the functions of the occipital lobe GM?
VISION Visual association area Primary visual cortex
854
What are the functions of the temporal lobe GM?
HEARING Auditory association area Primary auditory cortex
855
What does a lesion in the primary motor cortex cause?
Paralysis (full or partial loss of fine voluntary movements in the contralateral side Paresis (muscular weakness)
856
What does a lesion in the motor association area cause?
Apraxia (difficulty with motor planning to perform voluntary movements and tasks)
857
What happened to Phineas Gage?
Damage to prefrontal association area
858
What happens when the prefrontal association area is damaged? (e.g. Phineas Gage)
``` Changes to: Personality Self-control Attention Planning Emotions Motivation Decision making Reasoning Judgment ```
859
What is Broca's motor aphasia?
Prefrontal lesion | Impaired speech production but preserved comprehension
860
What happens if there is a lesion in the primary somatosensory cortex?
Sensory deficits (in PERCEPTION of basic sensory information)
861
What happens if there is a lesion in sensory association areas?
Sensory deficits (in INTERPRETATION of sensory information)
862
What is spatial neglect? What can it affect?
Unawareness of the contralateral side ``` Affects: Tactile recognition Flavour recognition Spatial orientation Ability to read maps Reading (alexia) Writing (agraphia) Calculations (acalculia) ```
863
What happens if there is a lesion in the primary visual cortex?
Blindness in the corresponding part of the visual field (deficit in perception of basic visual information)
864
What happens if there is a lesion in the visual association area?
Visual deficits (in interpretation of visual information)
865
What is prosopagnosia?
Inability to recognise familiar faces or learn new faces (aka face blindness) Usually due to lesion of the visual posterior association area
866
What happens if there is a lesion of the primary auditory cortex?
Deafness (deficit in perception of basic auditory information); unilateral lesions cause partial deafness in both ears
867
What happens if there is a lesion of the auditory association areas?
Visual deficits (in interpretation of auditory information)
868
What is Wernicke's receptive aphasia?
Impaired comprehension but preserved speech production
869
What happened to HM?
Amnesic patient Most of hippocampus and adjacent tissues in medial temporal lobe were removed Lead to anterograde amnesia
870
What is anterograde amnesia?
Inability to form new memories
871
What is the difference between primary and association cortices?
PRIMARY Function predictable Organised topographically Left-right symmetry ASSOCIATION Function less predictable Not organised topographically Left-right symmetry weak or absent
872
What does TMS measure?
Transcranial magnetic stimulation Measures effects of interference with normal info processing due to electro-magnetic stimulation of neurons
873
What are the advantages of TMS over lesion/patient studies?
The effects of stimulation are generally more spatially precise than naturally occurring lesions, which are often large and vary greatly across patients (i.e., better spatial resolution); Healthy participants can be used as their own controls (within-subject design), thereby avoiding the issue of potential differences in pre-morbid abilities between patients and controls; There is insufficient time for functional reorganization to take place during TMS, meaning that recovery processes are unlikely to confound the results; Allows to investigate temporal dynamics of on-line neuronal processing
874
What does PET study in the brain?
Measures changes in amount of blood flow directly to a brain region Uses radioactive tracer attached to a molecule to locate brain areas where that particular molecule is being absorbed in the brain
875
What does fMRI study in the brain?
Measures changes in amount of blood oxygen in a brain region
876
What does electroencephalography measure?
Electric signal generated by the brain Electrophysiological monitoring method to record electrical activity of teh brain
877
What does magnetoencephalography measure?
Measures magnetic field generated by the electric currents in the brain Functional neuroimaging technique for mapping brain activity
878
What does hemispheric specialisation mean?
LEFT Verbal and analytic functions Language dominant RIGHT Non-verbal and creative functions Spatial processing
879
What is tractography?
Diffusion tensor imaging Measure the effect of lesions in white matter or how these lesions might disconnect different brain areas Movement of water molecules in the brain can be used to infer the underlying structure of white matter

LCRS2- Neuroscience (1 decks)

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