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Neuroscience > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

Compare Merkel, Meissner, Ruffini and Pacinian in terms of:

  • Rapidly/slowly adapting
  • receptive field size
  • what they detect
A

Merkel:Slowly, small RF, form and texture
Meissner: Rapid, small RF, motion and grip
Ruffini: Slowly, big RF, movement and proprioception
Pacinian; Rapid, big RF, vibration

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2
Q

Where is the ventral posterolateral thalamus’ primary projection in the cortex for touch? Where does it go then?

A

3b main output, this also converges on 1 and 2.

3a,3b,1,2 all converge on S2.

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3
Q

Where are the 3 cell bodies located in the DCML pathway?

A

Dorsal root ganglia
Dorsal column nuclei (gracile and cuneate)
Ventral posterolateral thalamus

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4
Q

What is the difference between first and second pain?

A

First pain is from Adelta fibres, it is immediate and sharp

Second pain is from C fibres, is comes after and is dull and longer lasting

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5
Q

What is inflammatory pain from? What is one receptor involved? What can it lead to?

A

Damaged/inflammed tissues releasing a soup of nociceptor sensitisers.
TRPV1
Can lead to peripheral/central sensitisation
Hyperalgesia; increased response to normally painful stimulus
Allodynia; painful response to an innocuous stimuli

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6
Q

What are the two types of maladaptive pain?

A

Neuropathic; damage to neural pathway leading to spontaneous pain and hypersensitivity (amplification of pain in primary/central)
Dysfunctional; no pathophysiology but have spontaneous pain and hypersensitivity

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7
Q

What part of the brain stem has a descending modulatory role in perception of pain?

What about cortical areas?

How can placebo/nocebo influence the descending pathway

A

Rostral ventral medulla

Cingulate cortex
Insula
Prerfrontal

Placebo; provides endogenous analgesia as have positive expectations
Nocebo; can cause hyperalgesia from negative expectation e.g. needle

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8
Q

What is the pathway in the monosynaptic stretch reflex?

A

Muscle spindles converge on the motor neuron of that muscle causing contraction. Also send an inhibitory interneuron to antagonistic muscle.

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9
Q

What is the role of golgi tendons in bicep fatigue?

A

To maintain force; e.g. if biceps fatigue the decrease in force means less activation of the inhibitory interneuron and more excitation of the muscle to increase force

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10
Q

Why is there a 1:1 ratio or nerve to muscle fibre activation?

A

The pre synapse has heaps of varicosities, and the post synapse is folded, so massive SA for AcH to cause AP

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11
Q

If muscles remain unactivated fibrillations and fasciculation can occur, why?

A

Fibrillations are contractions of one muscle cell, can be because upregulated AchR to try and be more excited and now reacted to Ach is wasn’t supposed to\
Fasciculations; group of muscle fibres contracting spontaneously probe from activation of a MN thats degenerating

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12
Q

What are signs of LMN syndrome?

A

Weakness/paralysis
Decreased tone
Decreased reflexes
Fascicculations/fibrillations/atrophy

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13
Q

What are the two corticospinal tracts and what do they control? What % of nerves is in each?

A

Lateral has 90%, controlling distal muscles

Ventromedial has 10%, controlling proximal muscles, terminates on one side of ventral horn but sends branches to other

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14
Q

What are some UMN signs? What are they proceeded by?

A 
Proceeded by spinal shock
Then get:
Spasticity; increased reflexes, clonus and increased tone
Babinski's sign
Loss of fine voluntary movements
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15
Q

What is the difference between decorticate and decerebrate rigidity?

A

Start with lesion to the corticospinal tract
In decorticate the lesion is above the red nucleus.
The rubrospinal tract usually inhibited causes flexion of the arms.
The pontine RF causes extension of the legs.
In decerebrate the lesion is below the red nucleus, so lose that drive for flexion and now reticulospinal driven extension dominates too.

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16
Q

Why is the lower face not spared in a UMN lesion to the facial nerve?

A

The lower face doesn’t have contralateral innervation like the upper face and most other cranial nerves.
The cingulate cortex gives contralateral innervation so if one UMN is damaged it will still function.
As the lower face only has innervation from MC of the contralateral side it will affected with a UMN lesion.

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17
Q

What is the role of the basal ganglia?

A
  • Initiating movement
  • Selecting complex movements, like a centre-surround model selects movements via direct pathway and not other via indirect
  • Evaluating success in achieving those goals
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18
Q

What part of the basal ganglia do you lose in:
- Parkinsons
- Huntingtons
What is the consequence?

A

Parkinsons: substantia nigra. get slow and diminished movement and tremor
Huntingtons; corpus striatum. Get chorea; jerky uncontrollable movements

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19
Q

What is the function of the cerebellum?

Are lesions ipsilateral or contralateral?

A

Coordinating timing and sequence of movement
Planning sequences
Motor learning

Ipsilateral, as crosses in midbrain before going to cerebrum, then cerebrum crosses again before spinal cord

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20
Q

What is some differences between anterior and posterior lobe cerebellar syndrome?

A

Anterior; ataxic gait and los of coordination (what happens in chronic drunks)
Posterior; dysmetria (overshoot in precision) and inability to rapidly alternate movements, speech abnormalities

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21
Q

What is in the
Tectum
Tegmentum
Basis

A

Tectum- colliculi
Tegmentum- reticular formation and cranial nerve nuclei
Basis; descending motor control

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22
Q

What is the main role of the rostral vs caudal reticular formation?

A

Rostral more involved in conscious and alert state

Caudal work with CN and SN more involved in complex motor and autonomic functions

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23
Q

What motor column is nucleus ambiguus in and what CN nuclei does it contain?

A

Brachial motor
CN9- Stylopharyngeus
CN10- Levator palati

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24
Q

What column is nucleus solitarius in?

What are its two parts and respective CN?

A

Visceral sensory
Gustatory nucleus for taste; 7,9,10
Visceral sensory division; 9,10

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25
Q

How do we test midbrain function

A

Pupillary light reflex; light in via CN2 and constriction via CN3

26
Q

How do we test pons function?

A

Corneal blink reflex; sensory input via CN5-V1 and motor output of blinking via CN7 (orbicularis oculi)

27
Q

What are the two nerve roots of the facial nerve and what do they supply?

A

Facial nerve proper–> muscles of facial expression
Nervus intermedius–> small skin behind ear, taste to anterior tongue (chords tympani) and PS to lacrimal, sublingual and submandibular glands

28
Q

How do we test medulla function?

A

Gag reflex- input via CN9, output via CN10 of pharynx

29
Q

What keeps photoreceptors depolarised in the dark?

How does the light hyper polarise them?

A

cGMP keeping a sodium channel open
Light changes the conformation of retinal activating the opsin.
This activates the G protein transducin to activate phosphodiesterase to break down cGMP into GMP so sodium influx stops.

30
Q

How does a surround photoreceptor thats receiving light depolarise the central photoreceptor?

A
  • Light in surround photoreceptors
    • Less glutamate on surround photoreceptor so it hyperpolarises
    • Less glutamate on horizontal cell so it hyperpolarises
    • Less GABA then onto the centre photoreceptor
    • Centre photoreceptor depolarises
    • Which means bipolar cell hyperpolarises
31
Q

Out of M and P ganglion cells which are bigger, what are their roles and what % of ganglion cells are each

A

M- bigger, motion, 5%

P- smaller, colour, 90%

32
Q

How many layers are in the lateral geniculate nucleus? Which have M and which have P? What about diff eyes?

A

1-2 have M, 3-6 have P
LE- 1,4,6
RE- 2,3,5

33
Q

What are intrinsically photosensitive ganglion cells?

A 
GC with a melanopsin that can be depolarised with light. 
Control the non-vision aspects such as:
- Pupil responses 
- Circadian rhythm and sleep regulation
- Light allodynia
34
Q

What is the pathway of pupil responses?

A

iPGC project to pre-tectal nucleus in the midbrain
Then to edinger-westphal nucleus (CN3 nucleus) of both eyes
Then to ciliary ganglion
Then to sphincter pupillae

35
Q

What is the pathway from ipGC that control circadian rhythm?

A

ipGC to suprachiasmic nucleus in hypothalamus

36
Q

Where does ipGC meet nerves from dura in a migraine?

A

Meets nerves from trigeminal–> brainstem in the posterior part of the thalamus

37
Q

What is the action of superior and inferior oblique? how do you test them in isolation?

A

Primary action is torsion

If adducted, inferior oblique elevates and superior oblique depresses

38
Q

What white matter tract connects the visual cranial nerve nuclei? whats the effect of an inter-nuclear ophthalmic lesion?
where are the vertical and horizontal gaze centre?

A

Medial longitudinal fasciculus
INOL- eye doesn’t follow the other eye to look one way
Midbrain reticular formation has the vertical gaze centre
Pontine reticular formation has the horizontal gaze centre

39
Q

What’s the pathway for horizontal saccade?

Where do UMN that drive gaze centres come from?

A

Frontal eye fields via superior colliculi to contralateral gaze centre PPRF
PPRF excitatory burst neurons to abducens nucleus.
It excites its own LR and goes to OCN to excite MR
PPRF inhibitory burst neurons to opposite AN
Inhibits its own LR and inhibits OCN MR

40
Q

What is the pathway for vestibular-ocular reflex?

A

Semicircular canals to VN8
Goes to opposite AN to excite
And ipsilateral AN to inhibit
Also does a cheeky path to ipsilateral OMN to excite MR faster

41
Q

What layer of the visual cortex to M neurones project to?

Then where?

A

M to 4Ca
Then to 4B (directional selectivity here)
Then to middle temporal lobe (direction-of-motion columns)

42
Q

What layer of the visual cortex to P neurones project to?

Then where?

A

P to 4CB
To V2
To V4 (shape and colour)
To inferior temporal; visual memory and perception e.g. of faces

43
Q

What is anomalous trichromacy?

A

Have all 3 cones but one doesn’t function properly

44
Q

What is protanope and protanomal?
What is duetanope and duetanomal?
What is tritanope and tritanomal?

A 
Protanope- no red cone
Protanomal- abnormal red come
Deutanope- no green cone 
Deutanomal- abnormal green cone
Tritanope- no blue cone
Trianomal- abnormal blue cone
45
Q

What is the role of ossicles?

A

Match the impedance of air to impedance of fluid in inner air so sound not reflected but transmitted

46
Q

What part of the basilar membrane responds to high vs low frequencies?

A

Apex responds to low frequencies

Base responds to high frequencies

47
Q

How do hair cells generate an AP?

A

When hair bundle deflected towards tallest sterocilia is causes K+ to come in from endolymph and depolarise.
Causes Ca to come in glutamate vesicles to be released onto nerve causing AP
K+ exits into perilymph and it depolarises

48
Q

What is the role of outer hair cells?

A

Voltage causes them to lengthen, increasing the basilar membrane movement 100 fold to allow IHC to transmit hearing.

49
Q

How is high and low frequencies localised in the superior olivary complex?

A

Duplex theory

  • Low freq location measured by time that sound arrives at each ear- so uses delay within the medial superior olivary complex
  • high freq; intraural intensity differences; get more excitation of the side which has the relative stronger stimulus in the lateral superior olivary complex. it inhibits the other side via medial nucleus of trapezoid body
50
Q

How is the auditory cortex organised?

what is the pathway leading to it?

A

Frequency columns, alternating left and right ear with excitatory input from one and inhibitory input from the other
CN8, CN8 nuceus, superior olivary complex, lateral lemniscus to superior olive, to auditory cortex in temporal lobe

51
Q

Where in the spinal cord are pre-ganglionic and post-ganglionic sympathetic neutrons located?

A

Pre: Intermediolateral cell column (T1-L3)
Post: prevertebral, paravertebral and adrenal medulla

52
Q

Where in the spinal cord are pre-ganglionic and post-ganglionic parasympathetic neutrons located?

A

Pre: intermediolateral cell column (S1-S5)
Post: bunch of micro ganglia close to organ, hypogastric plexes’

53
Q

What happens at 2 weeks, 3 weeks and 3 months post peripheral nerve injury?
What happens if unsuccessful?

A

2 weeks; peripheral nucleus, loss of nissl, wallerian degeneration and muscle atrophy
3 weeks; schwann cell cells form a cord that growing axons penetrate so supports regrowth
3 months; successful regeneration of nerve and muscle
If unsuccessful get neuroma formation

54
Q

What happens in primary and secondary CNS injury?

A

Primary; cell loss
Secondary; Degenerative insults; ischaemia, Ca2+ influx, glutamate toxicity, free radicals
Immune cells and microglia
Days later; apoptosis of axons and myelin and get gliosis

55
Q

How does gliosis in the CNS form a barrier between undamaged and damaged tissue?

A

Secretes ECM and cytoskeletal proteins which are a barrier
Upregulates axon guidance molecules on astrocytes (Cadherin, ephrins)
Myelin inhibitors on myelin debris (MAG, OMGp, Nogo binding o Nogo receptor on axon)
They both stop the growth of axons via Rho kinase pathway

56
Q

What is the genetic basis and pathology of Huntingtons disease? What are the ranges of repeats?

A

Aut dom; Mutation in HTT gene exon that get CAG (glutamine) repeat expansions; get poly Q-huntingtin which is toxic the the basal ganglia
Fully affected with > 40 repeats

57
Q

What are some symptoms of spinocerebellar ataxia?

What is the amino acid repeated?

A

Aut dom: Have degeneration of cerebellum and spinocerebellar tracts, so issues with coordination
CAG- glutamine in exon

58
Q

In freidrich ataxia what is the repeat? What are the clinical symptoms?

A

Aut rec: GAA repeat in FXN gene in introns. >66 repeats and are affected. Causing reduction in protein production of frataxin
Get ataxia as well as sometimes cardiomyopathy and diabetes

59
Q

What is an epileptic seizure? What makes it epilepsy?

A

Hyper synchronous and excessive firing of neurons in the brain, sets up a self sustaining network
Epilepsy is a group of neurological disease with a predisposition to seizures-more than 2 seizures and a propensity for more

60
Q

Out of genetic and structural epilepsy which is more likely to remit and responds better to med?

A

Genetic

61
Q

What is the most common pathology in adults with partial epilepsy (focal seizures)? What are some other possibilities?

A

Medial temporal sclerosis

Malformation of cortical development
Low grade tumours
Vascular lesions
post traumatic

62
Q

What have they found in schizophrenia in terms of neural size and connections?
What about glial cells?
How does the glial cell changes compare with autism? What genetic change is correlated with autism?

A

Both are decreased
Decrease in glia density

Increase in glia density in autism, showing as overgrowth in the DLPFC
Increased risk SNP’s and decreased protective SNP’s

Neuroscience (6 decks)

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