CNS Flashcards
(326 cards)
1
Q
Where are the sensory, motor and autonomic synapses found?
A
Sensory - dorsal horn.
Motor - ventral horn.
Autonomic - lateral horn.
2
Q
What is the most common membranous origin in a meningoma?
A
Arachnoid mater.
3
Q
What are the grey and white matter equivalents in the PNS?
A
Grey - ganglion.
White - peripheral nerve.
4
Q
What is a nucleus and what is the cortex? State the difference between a nucleus and ganglia.
A
Nucleus - a collection of functionally related cell bodies. A nucleus is found in the CNS, whereas a ganglia is found in the PNS.
Cortex - folded sheet of cell bodies found on the surface of the brain, around 1-5mm thick.
5
Q
Identify the central sulcus, pre- and post-central gyrus, lateral fissure, parieto-occipital sulcus and clacarine sulcus on the following.
A
6
Q
Identify the corpus callosum, thalamus, cingulate gyrus, hypothalamus, fornix, tectum and cerebellar tonsil on the following.
A
7
Q
How can a lack of CSF present clinically?
A
Headaches that are worse when standing up.
8
Q
How much CSF is produced per day?
A
600-700ml.
9
Q
What is the pathway of CSF?
A
Synthesised in the choroid plexus.
Drains from the lateral ventricles into the 3rd ventricle through the interventricular foramen.
Drain from the 3rd ventricle into the 4th ventricle via the aqueduct of the midbrain.
Drains from the 4th ventricle into the subarachnoid space via the median aperature, the 2 lateral aperatures and a small amount via the central canal.
It is then taken up into the venous sinuses via the arachnoid granulations.
10
Q
What is the notochord derived from?
A
Mesoderm, made from the primitive node.
11
Q
At what day does neurulation begin, and when and where does the neural tube first close?
A
It begins at day 18.
At day 21, the neural tube first closes in the cervical region.
12
Q
When do the anterior and posterior neuropores close?
A
Anterior - day 25.
Posterior - day 28.
13
Q
What is the neural tube formed from, and what do these cells form?
A
Formed from neuroepithelial cells.
These cells form glial and neuronal cells.
14
Q
What do neuroblasts, intermediate zone and marginal zone form?
A
Neuroblasts - nerve cell precursors.
Intermediate zone - future grey matter.
Marginal zone - future white matter.
15
Q
How does dorsal-ventral patterning occur?
A
Signals that are sent from the surface ectoderm, paraxial mesoderm and notochord.
16
Q
What morphogens are released and what are their functions?
A
Sonic hedgehog (Shh, from the notochord) induces floor plate production via ventralisation.
BMPs induce roof plate production via dorsalisation.
17
Q
What are the alar and basal plates’ products?
A
Alar - sensory and interneurons.
Basal - motor neurons.
18
Q
What do the lumbosacral, cranial and trunk neural crest cells become?
A
Lumbosacral - parasympathetic neurons and enteric nervous system.
Cranial - sensory cranial nerve nuclei, parasympathetic ganglia, and facial skeleton.
Trunk - sympathetic neurons.
19
Q
How do neural crest cells help form spinal nerves?
A
20
Q
What are the risk factors for neural tube defects?
A
Older and younger mothers age.
Folic acid deficiency.
Maternal diabetes/ obesity.
21
Q
What is cranial bifida?
A
Failure of the cranial neuropore to close, leading to meninges and/or parts of the brain herniating through the fontanelles.
22
Q
What are the two types of neural crest defects?
A
Defective migration or mophogenesis.
Tumours derived - teratomas.
23
Q
How many segments composes the spinal cord?
A
31.
24
Q
How do sensory deficits at the level of dorsal root/ spinal nerve, cord and above the thalamus present?
A
Dorsal root - dermatomal.
Cord - multiple dermatomes.
Above the thalamus - homuncular pattern.
25
What is the impulse direction in a funiculus and tract?
Funiculus - bidirectional.
Tract - singular direction.
26
What are the functions of the:
- Cerebellar peduncles.
- Substantia nigra.
- Red nucleus.
- Periaqueductal grey matter.
Cerebellar peduncles - descending corticospinal fibres from the ipsilateral hemisphere.
Substantia nigra - dopaminergic neurones.
Red nucleus - unconscious movement.
Periaqueductal grey matter - pain transmission and mictuition.
27
What can a basilar artery occlusion cause and why?
Locked in syndrome.
The corticospinal fibres travel ventrally.
28
What is the relevance of the visual cortex around the clacarine sulcus?
Above the sulcus provides the contralateral inferior field.
Below the sulcus provides the contralateral superior view.
29
What is the optic chiasm?
The site at which nasal retinae - lateral fields - decussate.
30
What are the metabolic and mechanical functions of the CSF?
Metabolic - contains glucose.
Mechanical - shock absorption.
31
What do the 3 swellings of the neural tube form, and how are these further subdivided?
Diencephalon also forms the optic nerves.
32
What are the sensory and motor parts of the medulla and midbrain?
Medulla:
- Sensory; lemnisci.
- Motor; pyramids.
Midbrain:
- Sensory; colliculi.
- Motor; cerebral peduncles.
33
How does the brainstem form?
It is pulled down by the cord as the vertebra grow faster than the spinal cord.
34
Which chromosome is affected in Di George syndrome?
Chromosome 22.
35
Explain the glucose-lactate shuttle.
Glycogen in the astrocyte is broken down into lactate.
Lactate is then shuttled across the astrocyte and into the neuron via MCT1 and MCT2 transporters, respectively.
The lactate is then converted into pyruvate via lactate dehydrogenase, where the pyruvate then enters glycolysis.
NOTE: it only occurs when the neurons are active or there is disrupted blood supply, inhibiting glucose transport.
36
Explain the transport of glucose into neurons.
Glucose from the brain capillaries is transported into the interstitial space across endothelial cells via the GLUT1 transporter.
The glucose is then transported into the neuron via the GLUT3 transporter.
37
Why do astrocytes remove neurotransmitters, and how?
Excess glutamate causes toxicity.
Termination of depolarisation.
Re-uptake.
38
What is the benefit of the coupling of astrocytes?
Ions can move between them, allowing for the potassium to be buffered much more greatly, in the brain extracellular fluid.
39
How are microglia activated?
State the outcome.
Recognition of foreign material via the dendrites of the microglia causes swelling and formation of phagocytic cells.
These can also act as antigen presenting cells.
40
What does the post-synaptic response depend on?
The nature of the transmitter.
The nature of the receptor.
41
What are the different types of ionotropic glutamate receptors, and what are their functions?
AMPA - facilitates the influx of sodium and potassium.
Kainate - facilitates the influx of sodium and potassium.
NMDA - facilitates the influx of sodium, potassium and calcium.
42
How do glutamate metabotropics function?
GPCR:
- changes in IP3 and Ca2+ mobilisation.
- inhibition of adenylate cyclase and decreased cAMP.
43
What does the activation of NMDA receptors cause?
Up-regulation of AMPA receptors.
Induction of long term potentiation through calcium ion entry, if strong, high frequency stimulation.
44
What is long term potentiation and what is the function of it?
Increased strength of synaptic connections between neurons.
Related to learning and long-term memory formation.
45
How is long term potentiation inhibited?
Long term depression weakens the synaptic strength over time.
46
What are the difference between the GABA receptors?
GABAa - LGIC for chloride.
GABAb - GPCR, which has a modulatory role.
47
How does ACh produce its effects in the CNS?
Acts at both nAChR and mAChRs.
Excitatory.
Often act on pre-synaptic terminals to enhance the release of other transmitters.
48
Where is ACh released from in the CNS, where does it act and what is its functions?
Released from the nucleus basalis.
It acts on cerebral cortex and hippocampus.
Has arousal, learning, memory and motor functions.
49
What is the first neuronal degeneration in Alzheimer’s and how is this treated?
Degeneration of the nucleus basalis.
Cholinesterase inhibitors increased the amount of ACh released, alleviating symptoms.
50
What are the 3 main dopamine pathways?
Nigrostriatal - substantia nigra to the striatum.
Neocortical - midbrain to the cerebral cortex.
Mesolimbic - midbrain to the limbic system (hippocampus, amygdala, etc.).
51
What are the functions of the nigrostriatal, mesocortical and mesolimbic pathways?
Nigrostriatal - motor control.
Mesocortical - mood, arousal and reward.
Mesolimbic - mood, arousal and reward.
52
What receptors do antipsychotic drugs act on?
Dopamine D2 receptors.
53
Where is noradrenaline mainly released from in the CNS, and where does it act to have what action?
Cell bodies found in the brainstem - locus coerulus.
It projects widely to act on the cortex, limbic system and cerebellum.
It has effects on mood and arousal.
54
Where is serotonin released from in the CNS and what are its functions?
Raphe nuclei.
It has an effect in sleep/ wakefulness and mood.
55
Which cell in the CNS can help to form scar tissue and repair damage?
Astrocytes.
56
How do astrocytes have a function in contributing to cognition?
They are connected to each other via gap junctions, forming a syncytium, allowing calcium waves to propagate through it.
57
When and where is glycine released, and what is its function?
It is released during REM sleep, in the spinal cord.
It inhibits lower motor neurons, causing paralysis.
58
Which dopaminergic pathway can contribute to the development of schizophrenia?
The mesolimbic pathway.
59
What is the role of histamine in the CNS?
Stimulates the cortex to maintain wakefulness.
Sleep.
60
What are the functions of the following peptides:
- Dynorphin.
- Encephalins.
- Orexin/ hypocretin.
Dynorphin - pain transmission.
Encephalins - pain transmission.
Orexin/ hypocretin - has a role in narcolepsy.
61
How do ESPS function?
The depolarisation in post-synaptic terminals causes an ESPS.
If the ESPS exceeds the threshold, action potentials are triggered with increased frequency.
62
What can cause a ‘glove and stocking’ paraesthesia?
Diabetic neuropathy, toxins, renal failure.
Demyelination of the axons.
63
Where in the spinal cord does subacute degeneration of the cord affect?
The dorsal column.
64
What is sensory ataxia? State some symptoms.
Impairment of somatosensory nerves, interrupting sensory feedback signals to the brain.
Lack of coordination and postural instability - worsens when vision is impaired.
65
What is syringomyelia?
CSF-filled cyst within the central canal of the spinal cord that grows anteriorly and laterally.
66
What is a chiari malformation?
Where the brain tissue, usually the cerebellar tonsil, pushes into the spinal canal, causing syringomyelia.
67
Which sensory tract can be affected by an expanding syringomyelia, and how is the increasing distribution seen in patients?
The spinothalamic tract - as the cyst grows laterally, it affects the cervical, thoracic, lumbar and then sacral dermatomes.
68
What are some causes of insensitivities to pain?
Peripheral vascular disease.
Diabetes neuropathy.
FAAH-OUT gene mutation.
Congenital insensitivity to pain.
69
Where in the spinal cord is Lissauer’s tract located?
Off the tip of the dorsal horn.
70
What order of neuron forms the dorsal-column and spinothalamic pathways?
Dorsal-column - first order neuron.
Spinothalamic - second order neuron.
71
What are the functions of A and C fibres?
A fibres carry impulses from mechanoreceptors in the skin.
C fibres carry pain, from nociceptors.
72
What are the type and characteristics of first order neurones?
They are pseudounipolar neurons.
They have their cell body in the DRG (or trigeminal ganglion, for the trigeminal nerve, etc.).
They receive information from one type of receptor, and collect information from a single dermatome (usually).
They project ipsilaterally into the spinal cord, to the cell body.
They synapse onto secondary neurons.
73
What is the function of pseudounipolar neurones, and how are they adapted for this?
They are sensory neurons.
Their cell body does not interrupt the continuous axon, allowing impulses to travel rapidly.
74
What are the characteristics of second order neurons?
Their cell bodies are found in the dorsal horn or medulla.
They decussate.
They project into the thalamus.
75
What are the characteristics of third order neurons?
Their cell bodies are in the thalamus.
They project to the primary sensory cortex.
76
What is the process of binding?
The ability of the CNS to bring the different senses together for perception.
77
What does the type of sensation depend on?
The receptor type.
78
What is a receptive field?
An area of skin that a primary sensory neurone supplies - it can span across more than one dermatome.
79
What is somatotropy/ topographical representation?
The organisation of the sensory system, converting dermatomal sensory information into homuncular sensory information, with great efficiency, through the exchange of information between primary, secondary and tertiary sensory neurones.
80
What does the sensation from T6 and above, and T7 and below run in, in the dorsal column pathway?
T6 and above - cuneate fasciculus.
T7 and below - gracile fasciculus.
81
Where do the second order neurones decussate in the spinothalamic tract?
The ventral white commissure.
82
How does the neural level differ between the dorsal column and spinothalamic tracts?
Dorsal column loses ipsilateral sensation at the level of the lesion and below.
Spinothalamic loses contralateral sensation at 1-2 spinal levels below the level of the lesion, and below.
83
What is the strength of the receptor activation based on?
The level of ion flux during the generator potential.
84
Through what structure do second order neurones project from the gracile/ cuneate nucleus (medulla oblongata) to the contralateral thalamus?
Medial lemniscus.
85
Where do thalamic neurones from the superior and inferior parts of the body project to?
Superior projects to the lateral somatosensory cortex.
Inferior projects to the medial somatosensory cortex.
86
How does rubbing a painful area of the body relieve the pain?
Mechanoreceptors are stimulated and the information is conveyed along ABeta fibres (sensory).
These ABeta neurones stimulate inhibitory enkephalinergic interneurones, which inhibits the transmission of pain from the second order neurone cell body.
87
How can there be cortical modulation of pain?
Cortical neurones project down to the midbrain - periaqueductal grey, stimulating the neurones there.
These neurones then stimulate the neurones in the nucleus raphe Magnus, within the medulla (part of the reticular formation).
These neurones then descend and inhibit the second order sensory pain neurones via activation of the inhibitory enkephalinergic interneurones.
88
How do inhibitory interneurones inhibit the second order sensory pain neurones?
Through the release of enkephalin.
89
How does the light pass through the retina and how does this correlate to the function of the retina?
Light has to pass through the superficial neurosensory structures before reaching the pigmented layer.
The impulses then travel from the pigmented layer, superficially, to the retinal ganglion cells.
90
What are the functions of the following:
- Pigmented layer.
- Photoreceptors.
- Horizontal cells.
- Bipolar cells.
Pigmented layer - absorbs excess light, preventing the light from scattering and glare, moderating the amount of light being processed. It also anchors the photoreceptors.
Photoreceptors - rods are for black and white vision, and cones are for coloured vision and high visual acuity.
Horizontal cells - lateral inhibition, inhibiting signals from adjacent photoreceptors.
Bipolar cells - allows for communication between photoreceptor cells and retinal ganglion cells.
91
Where is the primary visual cortex found?
Found around the calcarine fissure in the occipital lobe.
92
What is binocular vision?
Vision using two eyes with overlapping fields of vision, allowing for good perception of depth.
93
Which artery prevents central vision from being lost?
The middle cerebral artery - macular sparing.
94
What is the function of the vestibular nuclei?
To send projections through the medial longitudinal fasciculus and descending down into the spinal cord, allowing for the position of the head to be compensated for when the body is at different angles.
95
What are the posterior spinal and anterior spinal arteries supplied by, generally?
Segmental vessels from the aorta.
96
What does the adamkiewicz artery do?
Gives branches to the anterior and posterior spinal arteries around the lower spinal cord.
97
What does the anterior spinal artery arise from?
Vertebral arteries.
98
What does the anterior spinal artery reside in?
The anterior sulcus of the spinal cord.
99
What is the damage distribution in an anterior spinal artery occlusion?
Bilateral symptoms, where there is damage to the ventral horns, corticospinal tracts, spinothalamic tracts and part of the dorsal horns.
Anterior 2/3rds of the spinal cord.
100
What is the damage distribution in a posterior spinal artery occlusion?
Ipsilateral symptoms as there is one on each side:
- most of the dorsal horn.
- dorsal column pathway.
Posterior 1/3rd of the spinal cord.
101
Why does a basilar artery occlusion cause locked-in syndrome?
State why the eyes can move.
The pontine arteries branch from the basilar artery.
The pontine arteries supply the corticospinal tracts.
The eyes can still move as the midbrain is preserved, so CNs III and IV can still function.
102
Which cerebellar arteries supply the midbrain, pons and medulla?
Midbrain - superior cerebellar arteries (and posterior cerebral).
Pons - anterior inferior cerebellar artery.
Medulla - posterior inferior cerebellar artery.
103
Which other artery has a significant blood supply to the medulla?
Vertebral arteries.
104
What is the projection of the middle cerebral arteries?
They travel laterally, and give off lenticulostriate branches.
As they emerge through the lateral fissure, it gives a superior and an inferior division.
105
What are the branches of posterior cerebral artery and what do these supply?
Quadrigeminal artery supplying the midbrain.
Anterior and posterior temporal arteries, supplying the inferior temporal lobe.
Calcarine artery supplying the occipital lobe.
Thalamoperforating artery supplying the thalamus.
Thalamogeniculate artery supplying the medial and lateral geniculate nuclei, of the thalamus.
106
What artery can be occluded by a sub-falcine herniation, and why?
Raised intracranial pressure can lead to the cingulate gyrus herniating under the falx cerebri, compressing the anterior cerebral artery.
107
What does the uvea consist of?
Choroid layer and its associated vasculature.
Ciliary body and iris, anteriorly.
108
Which artery is a direct continuation of the internal carotid artery?
The middle cerebral artery.
109
What are the major areas that the posterior cerebral artery supplies?
Occipital lobe.
Inferior temporal lobe.
Thalamus.
110
What is the damage to the visual system associated with a middle cerebral artery occlusion, affecting both optic radiations?
Macular splitting - a homonymous hemianopia.
111
What do the medullary pyramids contain?
Upper motor neurones that form the corticospinal tracts.
112
Where do the leg, trunk and arm run, within the internal capsule?
Leg most posteriorly.
Arm most anteriorly.
Trunk in the middle.
All located within the posterior limb of the internal capsule.
113
What is the innervation to the trigeminal and vagus nuclei?
State why.
Bilateral innervation - contains innervation of upper motor neurones from the ipsilateral and contralateral sides.
They are important features which, if compromised, could potentially be fatal, and so have a ‘fail-safe’ mechanism, protecting from strokes.
114
What is the nucleus of the vagus nerve called?
The nucleus ambiguous.
115
What are the surrounding structures of the internal capsule?
Give further details.
Surrounding the posterior limb:
- Thalamus is medial.
- Lentiform nucleus is lateral - immediately lateral is the globus pallidum, and slightly more lateral is the putamen.
116
Where within the internal capsule is the corticobullar tract found, and what is its function?
Within the genu.
It contains upper motor neurone axons that go to supply the lower motor neurones that supply the muscles of the face.
117
What are the different aspects of the posterior limb of the internal capsule?
Medial - ascending third order sensory fibres of the somatosensory tract.
Lateral - descending upper motor neurones supplying the arm, trunk and leg.
This means that it is a bidirectional pathway.
118
What do each of the colours of the midbrain represent, and what are their functions?
Red - cerebral peduncles, which connects the cerebral hemispheres to the midbrain, containing upper motor neurones.
Blue - substantia nigra, which produces dopamine.
Green - red nucleus which has some motor control and produces a coarse tremor if damaged.
Pink - spinothalamic and medial lemniscus (containing dorsal column second order neurones).
Black - oculomotor and edingerwestphal nuclei.
Yellow - peri-aqueductal grey, involved in micturition and pain.
Light green - cerebral aqueduct, which allows CSF to drain from the 3rd to 4th ventricle.
Superior colliculi - reflex actions of the visual system.
119
What do each of the following colours represent, in regards to the corticospinal tract?
Green - UMNs which synapse onto LMNs supplying the axial musculature.
Blue - UMNs which synapse onto LMNs supplying the limb girdles.
Yellow - UMNs which synapse onto LMNs supplying the intrinsic muscles of the limbs.
Red - UMNs which synapse onto LMNs supplying the distal limb muscles.
120
Where in the corticospinal tract can the following conditions effect:
- Multiple sclerosis.
- Guillain-Barré syndrome.
MS - lower motor neurones or the cell bodies/ proximal axons of the upper motor neurones in the CNS.
GBS - lower motor neurone axons in the PNS, the peripheral nerves.
121
What does the medial longitudinal fasciculus do?
Connects different cranial nerve nuclei together (CNs III, IV, VI), to allow the for the extra-ocular muscles to move in a conjugate manner - prevents the lateral movement of the eyes forming diplopia.
122
How are spinal reflexes modulated?
State what can occur if these are damaged.
Descending influences from the brain - strokes affecting the modulatory fibres can lead to different manifestations of the reflexes, such as Babinski’s sign.
123
Why do atrophy and fasiculations occur in lower motor neurone damage?
Atrophy - lower motor neurones deliver growth factors and action potentials to the muscle, so a decrease in these leads to a decrease in muscle mass.
Fasciculations - up-regulation of nAChRs means that the muscles become over-sensitive to circulating ACh, leading to uncoordinated contraction of muscles.
124
What is the rubrospinal?
A motor pathway that originates from the red nucleus to around C1-C2.
125
What is the reticulospinal tract?
A motor pathway from the reticular formation, that helps control muscle tone. It causes paralysis during REM sleep.
126
What is the vestibulospinal tract?
Input to the spinal tract from the semicircular canals, to help keep the head stationary.
127
What is the tectospinal tract?
From the colliculi to the tectum, giving reflexive information regarding the:
- Superior = visual.
- Inferior = auditory.
128
What is the corona radiata?
White matter of the cerebral hemispheres that aggregate to form the internal capsule.
129
What is clasp knife rigidity?
Where the resistance to moving a limb is high until the Golgi tendon organs detect the high degree of stretch, and then stimulate inhibitory interneurones causing relaxation.
130
What does the anterior limb of the internal capsule do?
Connects the axons of motor cortex with the cerebellum.
131
What is the blood supply to the internal capsule?
Lenticulostriate arteries - branches of the MCA.
132
Where does the width of the cord increase from superior the inferior?
State why.
Cervical enlargement - wide as there are more LMN and 2nd order sensory cell bodies supplying the upper limb, correlating to the brachial plexus.
Lumbosacral enlargment - wide as there are more LMN and 2nd order sensory cell bodies supplying the lower limb, correlating to the lumbosacral plexus.
133
What is significant about the thoracic and sacral levels of the spinal cord?
Thoracic - the lateral horns contain sympathetic pre-ganglionic cell bodies, and extend from T1-L2.
Sacral - lateral horn (homologous, not actually) contains parasympathetic pre-ganglionic cell bodies, as well as the cell bodies of LMNs, distributing to the perineum via the pudendal nerve.
134
How does the amount of white matter differ throughout the cord?
At C1, there is the maximum there as there is the UMNs that haven’t distributed yet, and the convergence of the sensory axons from the levels below.
As we descend, there is less white matter - UMNs decrease in number.
135
How does damage to the basal ganglia cause contralateral symptoms?
The corticostriatal pathway projects from the cortex to the striatum (putamen and caudate nucleus), sending the motor plan to the basal ganglia.
Impulses are then sent from the globus pallidus to the thalamus, and from the thalamus to the motor cortex on the ipsilateral side - the pallidothalamocortical pathway - mediating and adapting the motor plan.
Dopamine is provided to the basal ganglia via the nigrostriatal pathway.
This means that the basal ganglia is unilateral, and so damage to the basal ganglia will lead to damage to the upper motor neurones before they decussate.
136
How does damage to the cerebellum cause ipsilateral symptoms?
The input from the cerebella are through the pontine nucleus, via the corticopontine pathway, and then the pontocerebellar pathway, which decussates. Together, this is the corticopontocerebellar pathway.
The cerebellum then communicates with the contralateral thalamus, via the cerebellothalamo pathway, and then the thalamus communicates with the cortex via the thalamocortico pathway. Together, this is the cerebello-thalamo-cortical pathway.
This means there is a double decussation and so there is ipsilateral symptoms.
Furthermore, the spinocerebellar tract is ipsilateral, sending sensory information from the muscle spindle to the cerebellum, and so damage to this pathway also leads to ipsilateral symptoms.
137
Where are the dopaminergic neruones that degenerate in Parkinson’s disease found?
The substantia nigra pars compacta.
138
How does the direct pathway cause excitation of the cortex?
The substantia nigra pars compacta sends excitatory dopaminergic connections to the putamen, stimulating the putamen.
The putamen then inhibits the globus pallidus internal segment.
This decreases the inhibition of the thalamus, leading to stimulation of the cerebral cortex.
139
How does the indirect pathway cause excitation of the cortex?
The substantia nigra pars compacta sends inhibitory dopaminergic connections to the putamen, inhibiting the putamen.
The inhibitory stimulations of the putamen to the globus pallidus external (GPe) are therefore inhibited, so there is less inhibition of the GPe.
This means there is more inhibitory stimulations sent from the GPe to the sub-thalamic nucleus.
The inhibition of the sub-thalamic nucleus leads to less stimulation of the globus pallidus internal.
Less stimulation of the globus pallidus interna means there is less inhibition of the thalamus, leading to increased excitation of the cortex.
140
What is the neurotransmitter that causes inhibition in the basal ganglia pathways?
GABA.
141
If there is both excitation and inhibition of the putamen, how is it that there is any movement performed?
There are differing numbers of D1 and D2 receptors that are stimulated at different times.
142
What anatomical structures are lost in the following conditions:
- Huntington’s disease.
- Hemiballismus.
- Parkinson’s disease (bradykinesia, particularly).
Huntington’s - loss of inhibitory neurones from the putamen to the globus pallidus externa.
Hemiballismus - sub-thalamic nucleus.
Parkinson’s - substantia nigra pars compacta.
143
What is past-pointing of cerebellar lesions?
Where the patient points beyond the target, due to loss of coordination.
144
What are pendular reflexes of a cerebellar lesions?
Reflexes that do not terminate.
145
What receptors are stimulated in the direct and indirect basal ganglia pathways?
Direct - excitatory D1 receptors.
Indirect - inhibitory D2 receptors.
146
What are the signs and symptoms of Parkinson’s disease?
State why they occur.
Tremor - indirect pathway dysfunction.
Rigidity - lack of co-ordination between agonists and antagonists.
Bradykinesia - loss of cortical excitation.
Hypophonia - bradykinesia of the larynx and tongue.
Decreased facial movement - bradykinesia of the face.
Micrographia - bradykinesia of the hands.
Dementia.
Depression - loss of role in cognition and mood.
147
What are the signs and symptoms of Huntington’s chorea?
State why they occur.
Chorea - increased motor cortex activation.
Dystonia (odd postures) - uncoordinated contractions of agonists and antagonists.
Loss of coordination.
Cognitive decline and behavioural disturbances - loss of inputs in higher mental function.
148
What do the superior, middle and inferior cerebellar peduncles connect to?
149
What do the cerebellar vermis and hemispheres deal with, respectively?
Vermis - trunk.
Hemispheres - ipsilateral side of the body (limbs).
150
Why does dysdiadochokinesia, ataxia, nystagmus, and slurred speech occur in cerebellar disease?
Dysdiadochokinesia - difficulty sequencing rapid movements.
Ataxia (unsteady gait) - difficulty sequencing lower limb muscular contractions, with a loss of conscious proprioception from the lower limbs.
Nystagmus - malcoordination of extraocular muscles.
Slurred speech - malcoordination of laryngeal and tongue musculature.
151
How many layers is the cerebral cortex and what is the thickness of this?
State the major output cell type in the cortex.
6 layers of dendrites and cell bodies, making it around 5mm thick.
Pyramidal cells.
152
What is the left hemisphere more dominant for?
Sequential processing:
- Language.
- Mathematics/ logic.
153
What is the right hemisphere more dominant for?
‘Whole picture’ processing:
- Body image.
- Visuospatial awareness.
- Emotion.
- Music.
154
Which white matter pathway connects the Wernicke to Broca area?
Arcuate fasciculus.
155
What influences where memories are stored?
Where the information was initially dealt at, there is a greater preference for storage there.
The different memory types - declarative in the cortex, and non-declarative in the basal ganglia and cerebellum.
156
What are the outputs of the cerebral cortex?
Projection fibres - to the brainstem.
Commissural fibres - between hemispheres.
Association fibres - regions of the cortex in the same hemisphere.
157
What connects the inputs and outputs to the cerebral cortex?
Interneurones.
158
Where is the hippocampus located, and how does it facilitate consolidation?
Temporal lobe.
Output pathways:
- Fornix to mammillary bodies.
- Mammillary bodies to thalamus.
- Thalamus to cortex.
159
What is the definition of sleep?
Readily reversible state of reduced responsiveness to, and interactions with, the environment.
160
What is the reticular formation and what can it be divided into?
Specialised interneurones that run the length of the brainstem, and are continuous with white matter tracts of the spinal cord and diencephalon.
It can be divided into the median, medial and lateral columns.
161
What are the different functions associated with each reticular column?
Median - states of arousal, sleep and mood.
Medial - somatosensory processing.
Lateral - influence on cranial nerves and autonomic function.
162
What is the general function of the reticular formation?
To integrate, relay and co-ordinate vital life functions and protective reflexes.
163
What are the different outputs to the cortical regions and their associated neurotransmitters?
Thalamus - glutamate.
Hypothalamus - histamine.
Basal forebrain nuclei - acetylcholine.
164
What is the reticular activating system?
A positive feedback loop, receiving excitation from the cortex and then exciting the cortex itself, playing a role in wakefulness, arousal and consciousness.
165
What nuclei is involved in the reticular activating system?
Median raphe nuclei.
166
What is the physiology behind sleep?
Neuronal mechanisms of deactivation of the reticular activating system, inhibition of the cortex and its activity, and reduction in sensory input, synchronising neural activity.
167
What is nocturnal bruxism?
Grinding of the teeth that occurs during REM sleep.
168
What is seen on an EEG in REM sleep and when awake, and when the eyes are closed?
Beta-waves - low voltage, thus synchronicity, but high frequency.
Alpha-waves - slightly increased synchronicity as there is less sensory input, but still high frequency.
169
What is seen in the 4 stages of non-REM sleep, on an EEG?
Stage 1 - theta waves.
Stage 2/3 - theta waves, sleep spindles and k-complexes.
Stage 4 - delta waves.
As the stages increase, the amplitude (thus, synchronicity) increases, and the frequency decreases.
170
What is the site of where conscious thoughts arise?
Cerebral cortex.
171
Why does the reticular formation send projections down the cord?
To maintain muscle tone.
172
Where do sleep spindles arise from?
The thalamus.
173
What is narcolepsy a dysregulation of?
Circadian rhythm.
174
What are some causes of a raised ICP?
Haematoma/ haemorrhages.
Tumours.
Space occupying lesions.
Cerebral oedema.
Infections.
175
What structures can be compressed by a subfalcine herniation?
Anterior cerebral artery.
Medial part of the frontal/ parietal lobes.
Corpus callosum.
176
What structures can be compressed by a trans-tentorial herniation?
Occulomotor nerve.
Posterior cerebral artery.
Superior cerebellar arteries.
177
What is a duret haemorrhage?
Haemorrhage into the brainstem, secondary to a trans-tentoral herniation.
178
What are the two types of subdural haemorrhage?
Acute - traumatic, rapid blood accumulation.
Chronic - elderly and alcoholics due to atrophy; anticoagulant therapy and liver cirrhosis is important.
179
What are the two types of subarachnoid haemorrhage?
Traumatic - basal skull fractures, contusions (bruising of the brain).
Spontaneous:
- Ruptured berry aneurysm.
- Amyloid angiopathy.
- Vertebral artery dissection.
- Arteriovenous malformations.
180
What are the vascular watershed areas of the brains blood supply that are at risk during hypotension?
State what occurs due to this.
Distal arterial territories, such as the border between the middle cerebral artery and anterior cerebral artery.
Wedge shaped liquefactive necroses occur.
181
What cerebral artery is most commonly affected by emboli?
Middle cerebral artery - increased risk of atherosclerosis here.
182
What are some common sites of thrombus formation that affect the blood supply to the brain?
Carotid bifurcation.
Origin of the middle cerebral artery.
Basilar artery.
Lenticulostriate arteries.
183
What are the causes of spontaneous intracerebral haemorrhage?
Hypertension - 60+ years, increased risk of small intraparenchymal blood vessels.
Cerebral amyloid angiopathy.
Arteriovenous and cavernous malformations.
Tumours.
184
What are the commonly affected sites in spontaneous intracerebral haemorrhage?
Basal ganglia.
Thalamus.
Pons.
Cerebellum.
185
What are some complications of hypertension in the brain?
Charcot-Bouchard microaneurysms.
Lacunar infarcts.
Slit haemorrhages - rupture of small vessels.
Vascular dementia.
Acute hypertensive encephalopathy.
Massive intracerebral haemorrhage.
186
What is the pathophysiology of cerebral amyloid angiopathy?
State the possible complications.
Amyloid deposition in the walls of small and medium sized meningeal and cortical vessels, leading to rigid and weakened walls.
Increased risk of cerebral cortex- and micro-haemorrhage.
187
What are Arteriovenous and cavernous malformations?
Arteriovenous - more common in males and between the age of 10 and 30, affecting the subarachnoid vessels, that tangle.
Cavernous - loose vascular channels, that are distended and thin. Affects the cerebellum and pons.
188
What is capillary telangiectasia and venous angioma?
Capillary telangiectasia - dilation of thin walled vessels, with microscopic foci.
Venous angioma - dilated venous channels.
189
What are some symptoms of CNS tumours?
Seizures.
Headaches.
Focal neurological deficits.
Raised ICP - nausea, vomiting, etc.
Local compression symptoms.
190
What are some different types of primary CNS tumours?
191
Where do ependymomas affect?
Ventricular system, so are often disseminated into the CSF.
192
What infection are lymphomas of the CNS associated with?
EBV, causing large B-cell lymphomas.
193
Where do medulloblastomas affect and what are they sensitive to?
Cerebellum.
Radiosensitive.
194
What are meningiomas?
Benign growths, derived from the arachnoid meningothelial cells.
195
What are the different types of meningitis?
Acute pyogenes.
Aseptic/ viral.
Chronic - mycobacterium tuberculosis/ fungi.
Carinomatosis - extensive tumour, which can affect the meninges.
196
What are some complications of meningitis?
Cerebral oedema.
Cerebral infarction.
Cerebral abscess.
Epilepsy.
Meningoencephalitis.
Septicaemia.
197
What are the causes of meningeal abscess and empyema?
Streptococci and staphylococci.
198
What are the most common causes of encephalitis in the temporal lobe, spinal cord motor neurones and brainstem - and in the foetus?
TL - herpes simplex virus.
Spinal cord MN - polio.
Brainstem - rabies.
Foetus - cytomegalovirus.
199
What are the physical damages seen due to prion disease?
Neuron cell death.
Synapse loss.
Microavacuolations.
200
What is mad cow disease?
Bovine spongiform encephalopathy.
201
What are the symptoms of creutzfeld Jakob disease?
Changes in memory.
Cerebellar ataxia.
Global dementia.
202
What are the signs and symptoms of Alzheimer’s disease?
Impaired intellectual function.
Impaired memory.
Altered mood and behaviour.
Disorientation.
203
What protein is aggregated in cells in Huntington’s disease?
Ubiquitinated huntington protein.
204
What is the function of orexin?
It regulates wakefulness via the amount of blue light present - more blue light causes it to inhibit the release of melatonin.
205
What conditions could lead to an acute on chronic dementia exacerbation in an elderly patient?
VITAMIN CDE:
- Vascular; TIA, stroke.
- Infections, such as UTIs.
- Traumatic.
- Metabolic; electrolytes.
- Iatrogenic; starting or stopping medications.
- Congenital.
- Degeneration.
- Endocrine; hyperglycaemia.
206
Where in the frontal lobe are impulses and behaviour controlled?
Pre-frontal cortex.
207
What cognitive domains are in decline in dementia?
Complex attention.
Executive function.
Learning.
Memory.
Language.
Perceptual motor function.
Social cognition.
208
What is executive function?
The ability of a person to plan and problem solve.
209
what is the function of amyloid precursor protein?
Repair neurones following damage.
210
What is amyloid precursor protein normally broken down, and incorrectly broken down in Alzheimer’s disease?
Normally broken down periodically by alpha and gamma secretase, into soluble metabolites.
Incorrectly broken down into insoluble metabolites, by beta secretase.
211
Where do the insoluble amyloid plaques aggregate, and what is the problem with this?
Fill space between neurones.
Within the blood vessel walls.
Reduce signal transmission.
Amyloid angiopathy - weakened blood vessels can bleed.
Inflammatory response causing neuronal death.
212
What is the normal function of tau proteins?
Stabilise the microtubules within the cytoskeleton, mobilising nutrients around the neuron.
213
How do neurofibrillary tangles cause damage?
Hyperphosphorylation of tau proteins, meaning they no longer support the cytoskeleton, causing neuronal death.
Tau proteins aggregate together.
214
What drug can be used to break down amyloid plaques, but what are the side effects of this?
Aducanumab - brain swelling and bleeding.
215
What is the function of acetylcholine, relating to its loss and symptoms seen in Alzheimer’s?
Loss of memory and learning.
216
What are the differences between sporadic and familial Alzheimer disease?
Sporadic is more common, with the causes being more genetic and environmental, with the prevalence increasing with age.
Familial has an early onset, and is associated with PSEN1/2 genes (mutation of gamma secretase), found on chromosome 21.
217
What are the symptoms of Alzheimer disease?
Short term memory loss often first to show - hippocampus.
Motor and language skills affected.
Long term memory loss.
Disorientation.
218
What is the most common cause of death, associated with Alzheimer’s?
Immobilisation, leading to diseases such as pneumonia.
219
What assessment is performed for assessing Alzheimer’s, and what are the functions of it?
Mini-mental state examination:
- Gives an idea of cognitive function.
- Quick test.
- Good for showing dementia progression.
220
What are some organic causes of Alzheimer’s-like symptoms?
Hypothyroidism.
Hypercalcaemia.
B12 deficiency.
Normal pressure hydrocephalus.
Delirium.
221
What protein is involved in lewy-body dementia and which anatomical structures are the misfolded proteins found?
Alpha-synuclein.
Found in the temporal and frontal lobe cortexes and substantia nigra, mostly.
Some found in the cingulate gyrus.
222
What are the cognitive and parkinsonian symptoms of lewy-body dementia?
Cognitive - hallucination, depression and REM sleep disorders: sleep walking/ talking.
Parkinsonian - bradykinesia, resting tremor, stiffness.
223
What drug is often given for lewy-body dementia?
Levodopa.
224
What is frontotemporal lobe dementia, and what is the pathophysiology behind this?
A heterogenous group of diseases, characterised by the glial type and neuronal inclusions, or underlying genetic mutation - faster progression with an earlier age onset.
Inclusion bodies - aggregated proteins.
Tau hyperphosphorylation.
225
What is seen on an MRI of frontotemporal dementia?
Unilateral or bilateral frontal/ temporal atrophy.
Ventricular enlargement.
226
What needs to occur for AIDS dementia to happen?
CD4+ count falls below a threshold.
227
What are the treatments for delirium?
228
What are some differences between delirium and dementia?
229
What are some non-cognitive symptoms of dementia?
Behavioural - agitation, aggression, wandering, sexual disinhibition.
Depression and anxiety.
Psychotic features - visual and auditory hallucinations, hostile delusions.
Insomnia and daytime drowsiness.
230
Which neurones are predominantly affected by plaques and tangles?
Cholinergic.
Noradrenergic.
Serotonergic.
Those containing somatostatin.
231
What are the symptoms of AIDS dementia?
Cognitive impairment.
Psychomotor retardation - slow thoughts and movements.
Tremor.
Ataxia.
Dysarthria.
Incontinence.
232
What is aura and what are some associated symptoms?
A transient period of neurological signs and symptoms, pathopneumonic of migraine.
Zig-zag lines, visual loss, numbness, speech disturbances.
233
What is the pathophysiology of a cluster headache?
Hypothalamic activation, with secondary trigeminal and autonomic involvement.
234
What are some sight-threatening and life-threatening causes of headache?
Sight-threatening - giant cell arteritis and acute closed-angle glaucoma.
Life threatening - meningitis, haemorrhage and tumours.
235
How long do cluster attacks last and what can be their remission time period?
Last 2-12 weeks.
Remission between 3 months and 3 years.
236
What can trigeminal neuralgia be aggravated by?
Light touch to the face.
Eating.
Cold wind.
Vibrations.
237
What are the two mechanisms that can cause ischaemia of the brain, in a subarachnoid haemorrhage?
Blood loss, decreases the perfusion pressure to the area of brain tissue.
Blood accumulation can cause vasospasm, leading to stroke.
238
What can be seen on a CT in a chronic stroke case?
Areas of decreased density, where oedema (water) and death of neurones and brain tissue has occurred.
239
What is the effect of ischaemia of the paracentral lobules?
Motor - external urethral sphincter weakness leading to incontinence.
Sensory - loss/ changes to sensation of the external genitalia.
240
What are the 3 signs that can be seen in left sided neglect?
Tactile extinction - when both sides of the body are touched simultaneously, in the affected region, the left is not felt.
Visual extinction - if something is shown to both sides of the body, the left is not seen/ acknowledged.
Anosognosia - not acknowledging their stroke, reasoning as to why they have issues with their left side of the body.
241
Where are the motor and sensory neurones within the internal capsule located?
Motor is more anterior.
Sensory is more posterior.
242
How would an occlusion at the bifurcation of the MCA present?
Global aphasia if left sided - both Broca’s and Wernicke’s areas are affected.
Contralateral homonymous hemianopia.
Weakness and sensory changes of the arm and face.
243
Why is there sensory loss in a posterior cerebral artery occlusion?
It is contralateral as there is a decrease in blood supply to the thalamus via the thalamoperforator/ thalamogeniculate branches.
244
What proportions of substances make up the pressure within the neurocranium?
Brain - 80%.
Blood - 10%.
CSF - 10%.
245
What is cerebral oedema and why may it occur?
Swelling of the brain due to an increase in fluid accumulation intracellularly or extracellularly.
Trauma.
Infection.
Ischaemia.
Infarction.
246
What are the two potential long-term shunts given for congenital hydrocephalus?
Ventriculoperitoneal.
Ventriculoatrial - right atrium.
247
What is cerebral autoregulation?
When the mean arterial pressure drops, there is vasodilation of the cerebral arterioles to maintain cerebral blood flow.
When the mean arterial pressure increases, there is vasoconstriction to maintain cerebral blood flow.
248
What are the stepwise responses to raised intracranial pressures?
Initially, there is extrusion of CSF and venous blood.
Then there is cerebral arteriole vasodilation.
Then there is increased sympathetic activity, causing an increase in mean arterial pressure.
249
What is the issue with the mechanisms to compensate an increase in intracranial pressure?
An increase in cerebral blood flow increases the volume within the cranium, further increasing the intracranial pressure.
250
What are some acute features of a raised intracranial pressure?
Headache.
Vomiting.
Visual disturbances - impaired visual acuity, papilloedema, diplopia (CN VI).
251
What are some chronic features of a raised intracranial pressure?
Difficulty concentrating.
Seizures.
Increased systemic blood pressure.
Focal neurological signs.
Reduced GCS - confusion, drowsiness and unconsciousness.
252
What are some radiological features of raised ICP?
Midline shift - subfalcine herniation.
Effacement (decrease in size) of ventricles.
Loss of grey-white matter differentiation.
253
What are the different features seen in the following herniation:
- Subfalcine.
- Transtentorial.
- Tonsillar.
Subfalcine - cingulate gyrus compresses the anterior cerebral artery.
Transtentorial - uncus compresses the oculomotor nerve and cerebral peduncles; contralateral hemiparesis.
Tonsillar - compress the brainstem, usually terminal.
254
What is Cushing’s triad?
Increased ICP:
- Initial hypertension, increasing MAP.
- The increase in MAP is sensed by the baroreceptors, causing reflex bradycardia through vagal activity.
- Compression of the brainstem damages the respiratory centres, causing irregular breathing.
255
Why are proton pump inhibitors given to patients with raised intracranial pressure?
The increased vagal activity predisposes to stomach ulcer formation.
256
What are brain protective measures performed by clinicians for raised ICP?
Elevate the head 10-15 degrees to maximise venous return.
Give oxygen to maximise oxygen delivery to the brain, preventing cerebral vasoconstriction.
Decrease cerebral metabolic rate:
- sedation.
- analgesia.
- paralysis.
- treating/ preventing seizures.
- avoiding hyperthermia.
Maintenance of normal blood pressure.
Later on, mannitol or hypertonic saline can be given.
257
What are some surgical interventions for raised intracranial pressure?
Evacuation of haemorrhage.
Extra-ventricular drainage for hydrocephalus.
Decompressive craniectomy.
258
What are the 4 dural septa?
Falx cerebri - between cerebral hemispheres.
Falx cerebelli - between cerebellar hemispheres.
Tentorium cerebelli - between the cerebellum and occipital lobe.
Diaphragma sella - covers the superior surface of the pituitary gland, allowing the infundibulum to pass through.
259
What are the enlarged areas of subarachnoid space called?
Where do they occur?
Basal cisterns - occur where the brain moves away from the skull.
260
How is CSF propelled through the ventricular system?
Continuous production of CSF.
Ciliary action of ventricular ependyma.
Vascular pulsations.
261
What are the choroid plexuses?
Capillaries and loose connective tissue that filter the plasma to form CSF.
262
What do SAHs present with?
Thunderclap headache - 1 hours to 1 week.
Meningism - neck stiffness, photophobia, headache.
Dizziness.
Orbital pain.
Diplopia.
Visual loss - anterior communicating artery aneurysm.
263
What are the 3 causes of SAH?
Rupture of saccular/ berry aneurysms.
Rupture of arterio-venous anastomoses.
Traumatic.
264
What are some complications of SAH?
Microthrombi occluding smaller distal arteries.
Vasoconstriction due to CSF irritating cerebral arteries.
Cerebral oedema - hypoxia induced.
Myocardial damage due to sympathetic activation.
Early rebleeding.
Acute hydrocephalus.
Cerebral ischaemia.
265
Where is the meningococcal rash usually found?
Trunk.
Legs.
Mucous membranes.
Conjunctivae.
Palms and soles.
266
What are the 3 most common bacterial causes of meningitis in adults?
Streptococcus pneumoniae.
Neisseria meningitidis.
Haemophilus influenzae.
267
What are two examination signs seen in meningitis?
Kernig sign - supine, flexed thigh and knee, where the knee is difficult to straighten.
Brudzinski sign - neck flexion causes involuntary flexion of the knees and hips.
268
What should be done to investigate the blood and CSF in those that have already received antibiotics?
PCR.
269
What is the thrombolysis window for strokes?
Within 4 hours.
270
What are some congenital and acquired causes of hydrocephalus?
Congenital:
- Obstructive = neural tube defects, aqueduct stenosis.
- Increased production/ decreased drainage of CSF.
Acquired:
- Meningitis.
- Trauma.
- Haemorrhage.
- Tumours.
271
What is external ventricular drainage used for?
State some drawbacks.
Medium term drainage of hydrocephalus.
Continuous pressure monitoring.
Requires inpatient monitoring.
Risk of infection.
272
Why does microvascular thrombosis occur in meningococcal septicaemia?
Sluggish circulation.
Impaired fibrinolysis.
Increased tissue factor expression in endothelial cells.
273
What is the treatment for CMV meningitis?
Ganciclovir.
274
Label the following:
275
Why do the paracentral lobules have motor and sensory functions?
They are located on the medial aspects of the hemispheres, containing components of the both the pre- and post-central gyri.
276
Why does trauma to the head cause a loss of consciousness?
It generates abnormal action potentials.
277
What is psychiatry?
The study and treatment of mental disorders.
278
What does the term psychotic mean?
The mind is no longer able to differentiate between fantasy from reality. A state of unknown mental disorder.
279
What are neurotic disorders?
Disorders where the person can no longer cope with dealing with reality due to unconscious conflicts or an intolerable condition - a condition that they are aware of.
280
What are personality disorders?
Conditions where the person has never been able to cope with the emotional and practical demands of life and faces a lifelong struggle.
281
What is the diagnosis criteria for mild/ moderate and severe depression?
Mild/ moderate - have 2/3 of the core depressive symptoms (low mood, lack of energy, lack of enjoyment and interest), and 2 other symptoms for at least 2 weeks.
Severe - have all 3 of the core depressive symptoms (low mood, lack of energy, lack of enjoyment and interest) for at least 2 weeks.
282
How long do symptoms have to last to be considered a manic episode, and how long do they usually last?
Symptoms must be present for at least 1 week.
They usually last 3-6 months.
283
What psychotic symptoms do people in mania often experience?
Delusions.
Hallucinations.
284
What is the difference between bipolar 1 and 2?
State when bipolar’s usual onset is.
Bipolar 1 is mania/ mania and depression.
Bipolar 2 is hypomania/ hypomania and depression.
Onset is usually 15-19 years old.
285
What are the functional circuits of the brain responsible for?
Cognitive processes - thoughts.
Sympathetic output.
Parasympathetic output.
Motor systems.
286
Where is serotonin produced and transported to?
Raphe nucleus, to cortical areas and the limbic system.
287
What evidence supports the role of serotonin in mood disorders?
Drugs that increase the levels of serotonin in the synaptic cleft can help to treat depression.
5-HIAA (metabolites of serotonin) is low in the CSF of patients with depression.
Tryptophan, a precursor for serotonin, depletion causes depression.
288
What are some drugs that increase the levels of serotonin in the synaptic cleft can help to treat depression?
Selective serotonin re-uptake inhibitors.
Serotonin-noradrenaline re-uptake inhibitors.
Tricyclic antidepressants.
Monoamine oxidase inhibitors.
289
Where is noradrenaline produced and where does it project to?
Locus coeruleus, to the limbic system and cortex.
290
What is the evidence to show that noradrenaline is involved in mood disorders?
Antidepressants that increase noradrenaline successfully treat depression.
Patients that have recovered from depression with low noradrenaline levels have higher rates of relapse.
Post-mortem studies of depressed patients have been shown to have lower levels of noradrenaline.
291
What are some drugs that increase the levels of noradrenaline in the synaptic cleft can help to treat depression?
Serotonin-noradrenaline re-uptake inhibitors.
Noradrenaline re-uptake inhibitors.
Tricyclic antidepressants.
292
What is the Papez circuit?
Cortical areas send inputs to the hippocampus.
The hippocampus projects to the mammillary bodies via the fornix.
The mammillary bodies project to the thalamus and hypothalamus.
The thalamus projects back to the cortex.
The hypothalamus projects to the pituitary and autonomics.
293
How may antidepressants affect the physical structure of the brain?
Changing levels of other neurochemicals.
Stimulation of neurogenesis in the hippocampus through growth factors such as brain-derived neurotrophic factor.
294
How do different levels of anxiety affect performance?
Moderate levels improve performance by improving focus and concentration.
High levels decrease performance as a person becomes internally focussed on removing symptoms.
295
What is the pathophysiology of the stress response?
Stress activated pre-ganglionic afferent neurones in the spinal cord, which project to other neurones to release adrenaline and noradrenaline.
The paraventricular nucleus in the hypothalamus is stimulated by stress to release CRH.
CRH causes the pituitary to release ACTH, which then acts on the adrenal cortex to release cortisol.
296
What is stress habituation?
Repeated mild stress exposure which leads to a reduced response in the HPA axis, and in the ANS.
297
How does chronic stress cause sensitisation?
There is dampening down of the negative feedback pathways of cortisol.
Positive drive through the amygdala increases activity in the paraventricular nucleus.
Increased activity in the ANS.
298
What does the response to stress depend on?
The perceived ability to cope with threat.
Tendency to react to stress with high arousal.
Perceived ability to copy with the arousal.
299
Who are anxiety disorders more common in?
Younger women.
300
What are avoidance phobias?
State the pathophysiology.
They are anxiety disorders that there is an involuntary need for avoidance of a situation or thing, that is perceived as irrational.
Classical conditioning, associating something with a negative outcome, can cause avoidance phobias.
301
How are avoidance phobias treated?
Guided self-help and CBT, with psychoeducation.
Systemic desensitisation - relaxation and hierarchy (increasing exposures).
Medications such as SSRIs.
302
What is agoraphobia and what ages are the most frequent onsets?
Fear of crowds, open spaces and of difficulty getting home.
It is an anticipatory anxiety, associated with avoidance and anxious thoughts.
Two peaks of onset:
- Mid twenties.
- Mid thirties.
303
What is social phobia?
Inappropriate anxiety in social situations, due to fear of scrutiny by other people. It is precipitated by an initial panic in adolescence, which leads to them fearing it again.
It can be associated with substance misuse.
304
What is panic?
Excessive arousal with fear that the symptoms are evidence of a catastrophe, where there is concern about reoccurrence.
An episodic anxiety that lasts around 20 minutes.
305
What are the treatments and treatment aims of panic?
Treatment:
- Tricyclic antidepressants = imipramine, clomipramine.
- SSRIs.
- CBT.
Aim is for improvement within 6 months.
306
What is the re-entrant loop of OCD?
Increased activity within the caudate nucleus activates the orbitofrontal cortex.
The cingulate gyrus then activates the thalamus.
The thalamus increases in activity.
307
What are some symptoms of generalised anxiety disorder?
Worries.
Feeling on edge.
Difficulty concentrating.
Motor tension - restless, fidgeting and tension headaches.
308
What are some physical symptoms of anxiety disorders?
GI, respiratory, cardiovascular, genitourinary, neuromuscular, sleep.
309
What are some factors that influence the development and maintenance of generalised anxiety disorder?
Genetics.
Upbringing - experiencing anxiety around them as a child.
Personality type.
Stressful life events.
310
What are some physical differentials for generalised anxiety disorder?
Withdrawal of substances from things like caffeine.
Thyrotoxicosis.
Phaeochromacytoma.
Paroxysmal tachycardia.
Ménière’s disease.
311
What is the stepped-care model of GAD?
Step 1 - suspected GAD = education and active monitoring.
Step 2 - diagnosed GAD = guided self-help and psychoeducation groups.
Step 3 - inadequate response to step 2 with marked functional impairment = CBT or a drug treatment.
Step 4 - risk of self-harm or self-neglect = complex drug, and/or psychological treatment regimens.
312
What are the neural elements of the stress response?
Hippocampus.
Thalamus.
Hypothalamus.
Amygdala.
Pre-frontal cortex.
313
What is the role of the hippocampus and hypothalamus in the neural element of the stress response?
Receives input from the cortex, processes the emotional content and projects to the thalamus and hypothalamus. Role in memory consolidation.
Hypothalamus - projects to the autonomic preganglionics for nervous system activation.
314
What are the inputs, outputs and role of the amygdala in the stress response?
Inputs - sensory system.
Outputs - cortex and hypothalamus.
Behavioural and autonomic emotional responses.
315
Why are benzodiazepines generally not recommended for anxiety disorder patients?
Addiction.
Sleep dependence.
Tolerance.
High street value.
Overdose.
316
What are the changes in the brain seen in OCD patients?
Reduced volume in the orbitofrontal cortex.
Reduced anterior cingulate cortex volume.
Increased activity in the cingulate cortex.
Decreased activity in the pre-frontal cortex.
317
What is the main concern for side effects of SSRIs?
There is an increased risk of suicide within the first 2 weeks of initiation.
318
State some common side effects of SSRIs.
Nausea and vomiting.
Decreased libido.
Impotence.
Diarrhoea.
Headache.
319
State some functions of the pre-frontal cortex.
Generation of and response to emotions.
Short term memory.
Attention and arousal.
Sensory processing.
320
What are hallucinations?
Perception with no stimulus, in any sensory modality.
321
What are two normal hallucinations?
Hypnogogic - when going to sleep.
Hypnopompic - waking up.
322
What is thought broadcast and thought insertion?
Thought broadcast - everyone knows what the person is thinking.
Thought insertion - thoughts are implanted by others.
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What is delusional perception?
The attribution of new meaning, usually in the sense of self-reference, to a normally perceived object.
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What are somatic hallucinations?
The perception of something being inside or affecting the body, with no stimulus.
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What are positive schizophrenic symptoms?
Symptoms that add to the patient:
- Delusions.
- Hallucinations.
- Thought disorder (incoherent thoughts).
- Lack of insight.
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What are negative schizophrenic symptoms?
Symptoms that take away from the patient:
- Underactivity.
- Low motivation.
- Social withdrawal.
- Emotional flattening (less emotionally reactive).
- Self-neglect.
