BB EOYS4 Flashcards
Which fibres have a path in the lateral spinothalamic tract?
Aβ; Að & C
Að & C
Aβ & C
Aβ & Að
C
Which fibres have a path in the lateral spinothalamic tract?
Aβ; Að & C
Að & C
Aβ & C
Aβ & Að
C
Which part of the brain has reduced glucose metabolism during depression
parahippocampus
hypothalamus
hippocampus
subgenual anterior cingulate cortex
fornix
Which part of the brain has reduced glucose metabolism during depression
parahippocampus
hypothalamus
hippocampus
subgenual anterior cingulate cortex
fornix
Which fibres have a path in the Anterior Spinothalamic Tract?
Aβ; Að & C
Að & C
Aβ & C
Aβ & Að
C
Which fibres have a path in the Anterior Spinothalamic Tract?
Aβ; Að & C
Að & C
Aβ & C
Aβ & Að
C
In the transmission of the Lateral Spinothalamic Tract, the pathway synapses at the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).
From where does the third order neuron of the LST pathway go to after the mediodorsal nucleus?
Rostral insula
Mamilliary bodies
Anterior cingulate cortex (ACC)
Primary somatosensory cortex
Primary motor cortex
In the transmission of the Lateral Spinothalamic Tract, the pathway synapses at the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).
From where does the third order neuron of the LST pathway go to after the mediodorsal nucleus?
Rostral insula
Mamilliary bodies
Anterior cingulate cortex (ACC)
Primary somatosensory cortex
Primary motor cortex
In the transmission of the Lateral Spinothalamic Tract, the pathway synapses at the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).
From where does the third order neuron of the LST pathway go to after the posterior thalamus?
Rostral insula
Mamilliary bodies
Anterior cingulate cortex (ACC)
Primary somatosensory cortex
Primary motor cortex
In the transmission of the Lateral Spinothalamic Tract, the pathway synapses at the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).
From where does the third order neuron of the LST pathway go to after the posterior thalamus?
Rostral insula
Mamilliary bodies
Anterior cingulate cortex (ACC)
Primary somatosensory cortex
Primary motor cortex
In the transmission of the Anterior Spinothalamic Tract, the pathway synapses at the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).
From where does the third order neuron of the AST pathway go to finalise?
Rostral insula
Mamilliary bodies
Anterior cingulate cortex (ACC)
Primary somatosensory cortex
Primary motor cortex
In the transmission of the Anterior Spinothalamic Tract, the pathway synapses at the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).
From where does the third order neuron of the AST pathway go to finalise?
Rostral insula
Mamilliary bodies
Anterior cingulate cortex (ACC)
Primary somatosensory cortex
Primary motor cortex
Transmission (Anterior Spinothalamic Tract)
Which fibres project within the Anterior STT?
Where does the Anterior STTT project to after travelling up the spinal cord / wheres the third order neurone? [1]
Ab, Ad and C fibres
Projects to ventral posterior lateral (VPL) and ventral posterior inferior (VPI) nucleus of the thalamus. (VPL/VPI) on the contralateral anterior STT tract
Third order neurones from VPL/VPI project to the somatosensory cortex (S1 and S2) - Provide exact localisation and physical intensity of noxious stimulus.
Transmission (Lateral Spinothalamic Tract)
Which fibres project within the Lateral STT?
Describe its path
Ad and C fibres
Projects contralaterally via LSTT to mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).
From mediodorsal nucleus of the thalamus (MDvc) innervates anterior cingulate cortex (ACC)
From posterior thalamus (VPI and VMpo) which innervates the rostral insula (unpleasant emotion of pain)
Anterior STT: innervates the [] cortex via []
Lateral STT: innervates the [] & [] via the [] and []
Anterior STT
* Innervate the primary and secondary somatosensory cortex via VPL/VPI
Posterior STT:
* Innervates the anterior cingulate cortex and rostral insula via the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo)
Explain the mechansim of pain modulation at the dorsal horn via the Noradrenaline and serotonin neurons
Noradrenaline and serotonin neurons descend from locus coerulus and raphe nucleus respectively & exhibit excitatory repsonse on lamina II neurons
The lamina II neurons present here are inhibitory - so release GABA and ekephalins onto the INCOMING Aδ neurons, which reduces their activity
How can you modulate pain via Abeta afferents? (e.g. if in pain - rubbing the area might help)
Ab afferent from skin also synapse excitably onto lamina II inhibitory cell body, that are used as interneurons from descending pain pathway (from noradrenaline and serotonin)
This causes more inhbitory GABA and enkephalins to be released on INCOMING Aδ neurons, which reduces their activity
Chronic pain
What is allodynia and hyperalgesia?
Allodynia: a condition where pain is caused by a non-noxious (non-painful) stimulus (e.g. tickle with a feather).
Hyperalgesia: a condition where an abnormal increased pain sensitivity is caused by a noxious (painful) stimulus (e.g. hot water on sunburn).
What is functional pain? [2]
no underlying lesion found despite investigation
pain is disproportionate to the degree of any clinically discernable tissue injury
Peripheral sensitization
How does Capsaicin reduce pain?
The relief of pain that may follow this topical treatment is thought to be related to the temporary deactivation of heat-sensitive epidermal nociceptors expressing the Transient Receptor Potential Vanilloid 1 (TRPV1)
Capsaicin excites pain and heat rececptors; but then desensitization the receptors and reduces pain
Describe the characteristics of primary erythromelalgia [2]
What is the pathophysiology of behind primary erythromelalgia? [2]
Primary erythromelalgia is a rare autosomal dominant neuropathy characterized by the combination of recurrent burning pain, warmth and redness of the extremities.
It is a channelopathy (genetic etiology) caused by mutations ofSCN9A, the encoding gene of the voltage-gated sodium channel subtype Nav1.7 - causes the channel to open with less depolarisation
.
Which type of receptors is the midbrain periaqueductal gray full of? [1]
Which nuclei does this receptor type influence? [4]
Opoid receptors - influences the:
- parabrachial nucleus
- medullary reticular formation
- locus coerruleus
- raphe nuceli
Explain the main function of the endocannabinoid receptors
Activate Via retrograde transmission:
- Post synaptic neuron sends a message to pre-synaptic neuron to stop release of GABA and glutamate (e..g if GABA activated - will stop release of glutamate)
E.g. Activation of GABA receptor causes release of endocannabinoid, which goes retrogradly (to the pre-synaptic terminal) and decrease release GABA)
Where is the subgenual anterior cingulate cortex ? [1]
How is the subgenual anterior cingulate cortex effected during depression? [1]
What structural implications does this have? [1]
Decreased metabolism: significant reduction in glucose consumption
The mean gray matter volume of the subgenual anterior cingulate cortex is reduced
What is the DMD like in patients with depression? [2]
In which particular areas? [2]
Major depression have an increased functional connectivity within DMN
increased connectivity between DMN and fronto-parietal networks: especially left subgenual cingulate area
involved in self-reference thoughts and negative recurrent thoughts = worse :(
Describe interactions between key structures that involved in depression that cause an increase in depressive ruminations:
Which areas of the brain become hyperactive? [4]
Which areas of the brain become hypoactive
Hyperactive:
* amygdala
* hippocampus
* subgenual cingulate cortex
* medial prefrontal cortex
Hypoactive:
* Dorsolateral prefrontal cortex
* ventrolateral prefrontal cortex
Describe the mesolimbic pathway that controls reward circuits in the brain [2]
Which NT controls this pathway? [1]
dopaminergic projection from the ventral tegmental area
to the nucleus accumbens is essential in reward and drug dependence
Explain an example of how chronic drug abuse can alter gene expression and therefore change brain structure [1
Chronic drug use causes an increase in the expression of expression of ΔFosB gene
Fos family of transcription factors, accumulates within a subset of neurons of the nucleus accumbens and dorsal striatum
FosB functions as a type of sustained “molecular switch” that gradually converts acute drug responses into relatively stable adaptations that contribute to the long-term neural and behavioral plasticity that underlies addiction.
Where does damage occur in brain if create decoticate or decerebrate damage? [2]
Decorticate (Damage above red nucleus): arms adducted and flexed, legs internally rotated and plantar flexed
Decerebrate (Damage below red nucleus): arms adducted and extended, legs stiffly extended and plantar flexed: Between the vestibular nuclei and red nuclei
Describe the mechanism of assessing consciousness (Auditory stimulation) using Auditory event-related potential (AERP):
What is the overall thing trying to identify? [1]
Where in the brain do you look? [2]
What would indicate a positive outcome? [1]
Aim to identify a mismatch negativity (MMN, a negative component appearing in the primary auditory and prefrontal cortices around 100-250 ms after an auditory change in a monotonous sequence of sounds (e.g. an oddball paradigm).
Aim to identify a P300 (a positive component appearing in the primary auditory and prefrontal cortices around 300 ms after an auditory change in a monotonous sequence of sounds (e.g. an oddball paradigm).
Which imaging modalities could you use to assess consciousness? [2]
Stimulation (e.g. auditory, tactile, visual) could carried out on the patient during imaging.
PET scan
Blood oxygenation level dependent (BOLD) fMRI
