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s3 - MSK, Derm, Cardio, Neuro, Pharm > Neurology > Flashcards

Neurology Flashcards

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1
Q

Name 2 common disorders of the basal ganglia.

A

Parkinsons

Huntingtons

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2
Q

What components make up the ‘corpus striatum’?

A
  • caudate nucleus and lentiform nucleus
  • substantia nigra
  • subthalamic nucleus
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3
Q

Where does the head and body of the caudate nucleus lie?

A

Nestles into the curvature of the frontal horn of the lateral ventricles

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4
Q

Where does the tail of the caudate nucleus lie?

A

Lies in the roof of the temporal horn of the lateral ventricle. On top of the hippocampus.

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5
Q

What does the genu of the internal capsule wrap around?

How can you tell a slice shows the genu of internal capsule?

A
  • wraps around apex of lentiform nucleus (g.pallidus)

- at the level of the interventicular foramen of Monro

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6
Q

What is the anterior limb of the internal capsule between?

A

Caudate nucleus and the lentiform nucleus

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7
Q

What is the posterior limb of the internal capsule between?

What does it contain?

A

The thalamus and the lentiform nucleus

Has corticospinal tract fibres

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8
Q

What is the striatum?

What is the pallidum?

A 
Striatum = input = caudate and putamen
Pallidum = output = internal and external pallidum
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9
Q

Basic basal ganglia loops go:
frontal - striatum - pallidum - thalamus - frontal
What are the 3 loops regulated by and how?

A

Dopamine
Caudate and putamen get it via nigro-striatal tract
Ventral striatum gets it via VTA of midbrain

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10
Q

Where do the 3 BG loops originate?

What do they pass through?

A

Cognition - prefrontal cx…(passes through caudate)
Movement - motor and premotor areas (via putamen)
Emotion - limbic lobe, hippocampus, amygdala (V.striatum)

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11
Q

Which part of the substantia nigra projects to the BG?

A

The pars compacta

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12
Q

What are D1 -like receptors and what is DA’s effect on them?

A

e.g. D1 & D5,

They are excited by DA

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13
Q

What type of DA receptors do the striatal neurones express in the direct pathway?
What about in the indirect pathway?

A

Direct pathway expresses D1-like receptors

vs indirect expresses D2-like

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14
Q

What effect does the internal pallidum projection to the ventral thalamus have?
How does the direct/indirect pathway affect this?

A

Inhibitory (supress unwanted movements/thoughts)
Direct-disinhibits this (so activity occurs)
Indirect pathway-reinforces this (strengthens brake)

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15
Q

Direct pathway is from striatum->int. pallidum

Where does the indirect pathway go?

A

Striatum –> ext pallidum –> sub.thalamic nucleus –>int pallidum

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16
Q

How does the indirect pathway increase the subT nucleus excitation to int pallidum, reinforcing the inhibitory action?

A
  • striatum/putamen sends an inhibitory neurone to the ext. pallidum
  • disinhibits subT nucleus (no longer inhibited by ext.p
  • strong excitation from subT to internal pallidum
  • int pallidum inhibits thalamus more
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17
Q

Where is the ventral striatum and what is it formed by?

A

Anteriorly the caudate and lentiform nuclei are fused inferior to the ant limb of internal capsule
This is the VS and has ^^ and the N.Accumbens

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18
Q

What is the Ventral/Limbic striatum involved in?

A

Reward based learing

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19
Q

What projects to the Ventral Striatum? Function?

A

Ant. Cingulate Cx and orbiomedial pre-frontal Cx - emotions, decisions, behavior
Hippocampus - spatial/temporal contextual info about reinforced behaviours. +Amydala

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20
Q

Why may DA dysregulation syndrome/addiction to Levodopa, hypersexuality, gambling.. occur in Parkinson’s.

A

Ventral striatum activity is increased

This area is rich in receptors for addictive behaviours/substances

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21
Q

How do DAT scans show DAergic levels?

A
  • radioactive label binds to DA-Transporters

- if there’s v. low DA transmission, there will be a low signal as less DATs are active

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22
Q

What is hemiballismus?

A
  • shooting fast movements of limbs from midline

- (involuntary)

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23
Q

What is Huntington’s Disease?

A
  • AD
  • loss of GABAergic neurones in striatum
  • causes hyperkinesia and dementia
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24
Q

Braak Stages of Parkinson’s disease:
Stage 1&2-
Stage 3&4-
Stage 5&6-

A

1&2 - early degeneration, sleep and small changes
3&4 - 50-80% loss, motor symptoms
5&6 - lewy bodys, psychiatric symptoms

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25
Q

Why does Parkinson’s result in a tremor?

A
  • other NT disturbances (Ach, NA, 5-HT, GABA)

- less DA = less Ach inhibition so hyperactive Ach

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26
Q

What was the effect of MPTP (heroin metabolite) in causing Parkinson’s?

A
  • MPTP taken up by DAT and metabolised by MAO-B
  • MPP+ (metabolite) generates free radicals
  • mitochondrial and DA cell degeneration
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27
Q

Why is L-DOPA always given with peripheral DOPA-decarboxylase inhibitors e.g. Benserazide, carbidopa?

A
  • So more L-DOPA reaches brain and isnt converted into DA peripherally
  • (which cant cross BBB and has many SE.s)
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28
Q

Why may the DA antagonist Domperidone be given in Parkinson’s patients on L-DOPA?

A
  • treat nausea/vom. as CTZ has many DA receptors

- this antiemetic doesnt cross the BBB it acts just outside on D2 and D3 receptors

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29
Q

How do MAO-B blockers like Selegiline help in Parkinson’s?

A
  • less DA metabolised (+protects vs MPTP toxicity)

- only acts in brain so no peripheral SE.s

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30
Q

What type of drug is ‘Entacopone’ that may be given to treat Parkinson’s with L-DOPA?

A

COMT-inhibitor

-slows L-DOPA elimination by increasing its t 1/2

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31
Q

Bromocriptine, ropinerole, pramipexole and rotigiotine are examples of what class of drugs?

A

DA agonists

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32
Q

Why may antimuscarinics like ‘benzatropine’ be given in Parkinson’s?

A

-to decrease the tremor

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33
Q

What do the dorsal columns detect?

A

Fine touch
Proprioception
Vibration

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34
Q

What route does the corticospinal tract take?

A
  • motor area, through corona radiata, post limb of internal capsule. Decussates at pyramids
  • descends on contralateral side to muscles
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35
Q

Where is M1 located?

And pre-motor cx?

A

M1-precentral gyrus of frontal lobe, ant to central sulcus

Immediately infront = pre-motor cx

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36
Q

Where is S1 located?

A

S1-post central gyrus of parietal lobe

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37
Q

2/3rds fibres in corticospinal tract come from M1 and pre-motor cx, where does the other 1/3rd come from/function?

A
  • from parietal lobe, project to dorsal horn of cord

- to “filter out” sensations generated by movement

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38
Q

Dorsal Collumn pathway: from low-threshold mechanoreceptors…-DRG, dorsal gracile/cuneate fasiculus

A
  • reach nuclei, medulla, X, up as internal arcuate fibres
  • become medial lemniscus
  • limbs/trunk-VPL, head/neck-VPM
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39
Q

Name 4 types of movement

A
  • voluntary
  • rhythmic
  • reflexive
  • postural
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40
Q

In the Rexed laminae of the spinal cord, what would the a medial ventral part control (e.g. VIII)

A

-medial = proximal, ventral = extensors

so would supply proximal extensors

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41
Q

Touch and olfaction receptors are “all in 1” (receptor+afferent) so are resilient to injury. Name 2 receptors that are separate.

A

-auditory, -vestibuluar, -gustatory

These are delicate and irreplacable

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42
Q

Name 3 things that can damage photoreceptors.

A
  • light
  • vit A deficiency
  • mutations, metabolic disease
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43
Q

Name 3 things that can cause auditory cell receptor damage.

A
  • Noise trauma
  • mutations
  • ototoxicity (chemo, aminoglycoside antibiotics)
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44
Q

Give 2 ways sensory skin receptors increases their “dynamic range” and save the cost of unnecessary APs

A
  • lack of 2 point discrimination by summing depolarisation over 1 receptive field
  • limited temporal resolution (2 quick taps feels like 1)
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45
Q

What is the advantage of “adaptation” of receptors?

A

-damps down constant responses, allowing highlighting of salient stimuli without saturating receptor

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46
Q

What does lateral inhibition enhance?

A

Spatial discrimination

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47
Q

At what day in development do the neuroepithelial cells attach to the pial and luminal surface and proliferate? How?

A

Day 22

  • drop down to luminal surface
  • split perpendicular
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48
Q

After the NT closes, how do the neuroepithelial cells now proliferate? What is the resulting cell?

A
  • drop to luminal surface and split parallel to surface

- upper daughter cells exposed to different intracellular signal, it becomes a ‘neuroblast’

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49
Q

Name two extracellular chemicals that act as morphogens which neuroblasts have receptors for.

A
  • neuroregulins

- reelin (from Cajal-Retzus cells in marginal zone)

50
Q

What do each of the 6 cortical layers become?

  • deep 5&6
  • middle (4)
  • outer 2&3
  • Glial layer (1)
A
  • 5&6 - big pyramidal cells, axons to subcortex
  • (4) - stellate cells
  • 2&3 -small pyramidal cells, axons to cortex
  • Glial layer (1) - neuroepithelial cells drop to luminal surface and become ependymal cells
51
Q

Name a condition causing inappropriate formation of the brain/neurogenesis?

A

DCX-loss of doublecortin protein

X-linked condition

52
Q

How do simultaneous deplolarisations of an effective circuit cause long term potentiation. AMPA is stimulated by a little glutamate..

A
  • If AMPA is sufficiently stimulated, the Mg ion blocking NMDA receptors is diplaced so Glutamate binds here
  • opens Ca2+C, Ca2+ strengthens synapse
  • grows, makes more NT and more AMPA Rs
53
Q

Describe A-delta fibres. NT..respond to…feels like…

A
  • thin, myelinated, NT used is glutamate
  • respond to mechanical trauma/noxious heat
  • immediate sharp pain
54
Q

Describe C fibres. NT..respond to…feels like…

A
  • thin, unmyelinated, NT is glutamate, sub P
  • report ongoing pain/pressure/heat/inflammation
  • long, throbbing/aching pain until injury heals
55
Q

How does damage and prostoglandins activate C fibres?

A

Damage-K+/H+, hist, bradykinin…depolarise C fibres

Prostoglandins increase C fibre sensitivity

56
Q

What is sub P’s role in injury?

A

Sub P increases inflammation causing loss of function

So promotes healing

57
Q

What is the lateral pain pathway responsible for?

What areas of thalamus/cx involved

A
  • perception and sensation of pain
  • VPN - sharp localised pain
  • SS cortex - localised pain
58
Q

What is the medial pain pathway responsible for?

What areas of thalamus/cx involved

A
  • emotional response to pain (fear/aversion)
  • midline thalamic nuclei (unpleasant sensation)
  • ant. cingualte cx (mood/links to hypothal and limbic)
  • insula cx (whole body map, increases alertness)
59
Q

How can pain overrun CNS via medial pain pathways?

A
  • ruin sleep
  • disrupt concentration
  • switch attention/salient stimulus
60
Q

Descending modulatory pathways project from the RV medulla and DL pontine tegmentum to spinal cord releasing what? To do what? When?

A
  • release NA/5HT onto interneruones
  • to decrease activity in the 2dry pain afferents
  • always at a backgound level, more with opiods/anti-depressants
61
Q

What is allodynia?

A

When normal touch becomes painful

62
Q

What 3 things characterise drug addiction?

A
  • compulsion to take drug
  • loss of control limiting intake
  • emergence of a negative emotional state
63
Q

What is the timeline leading to drug addiction?

A

social drugs - escalating use - dependence - withdrawal - protracted withdrawal - recovery (+/-relapse)

64
Q

Where do the mesolimbic DAergic systems project to?

A
  • VTA and Nuc Accumbens

- mediate drug use and positive reinforcement

65
Q

What areas of the brain are involved in negative reinforcement e.g. bad emotional state –> drug taking?
NTs?

A

Amygdala, hypothalamus, hippocampus, Nuc Accumbens (orbiofrontal, prefrontal and ant.cingulate Cx)
Releasing NA, GABA and CRH.

66
Q

When your awake, impulses from thalamus and modulatory input fires, but when asleep….and REM sleep…

A

…modulatory inputs stop, thalamic cells fire spontaneously/synchronous firing.
-REM sleep cortex active, thalamus desynchronised, EO and ear muscle active, skeletal muscle paralysis

67
Q

As you drop down the 3 levels of sleep what happens in relation to thalamus?

A

Firing becomes more and more synchronous

deep sleep 4Hz/sec vs 20Hz/sec awake

68
Q

From where does ACh modulatory input originate?

A
  • Pontomesencephalic Tegmentum - (to thalamus)

- Basal Forebrain - (to hippocamp. increases cx response strength and selectivity, attentiveness)

69
Q

From where does NA modulatory input originate?

Effect?

A
  • Locus coeruleus in brainstem - (to everywhere)

- increase cx response amplitude&selectivity, vigilant

70
Q

From where does DA modulatory input originate?

Effect?

A

-Substantia Nigra (to basal ganglia)
-VTA (to frontal cx, limbic lobe, n. Accum, amygdala
Alert, adaptive motivational behaviour

71
Q

From where does Histamine modulatory input originate?

Effect?

A
  • Tuberomammilary Nucleus in hypothal

- excites wake promoting circuits -> alert to stimuli

72
Q

From where does Orexin modulatory input originate?

Effect? Pathology?

A

-Hypothal
Switch on wake-promoting centres
Narcolepsy, fragmented sleep, REM while awake

73
Q

From where does Seratonin modulatory input originate?

Effect?

A
  • Raphe Nuclei (to brainstem, cerebellum and Cx)

- active in quite wakefullness, normal stress response

74
Q

What processes are involved in waking up?

A
  • Hypothal orexigenic cells switch on histamine cells
  • they both activate 5Ht/NA/Ach brainstem ARAS centre
  • basal forebrain Ach to whole brain starts activity
75
Q

What processes are involved in falling asleep?

  • What neurones, where, controlled by?
  • what else activates these neurones?
A
  • GABAergic neurones in venerolateral preoptic nucleus (VLPN) of hypothal inhibit the orexin/Hist/ARAS
  • GABAergic cells are under the control of SCN
  • also adenosine increases with wake time which activates GABA cells so do immune byproducrs
76
Q

What might a VLPN lesion cause?

A

Intractable insomnia

77
Q

What causes REM sleep? (which NT, where)

A

Cholinergic centre in pontomesencephalic tegmentum

axons desynchronise thalamus so cortical neurones in BG wake up an higher Cx activity

78
Q

Where is Broca’s area? Responsible for?

A
  • pars triangularis and pars opercularis of inferior frontal gyrus on the left hemisphere
  • for motor/producing speech
79
Q

What is the pars orbitalis of inferior frontal gyrus responsible for?

A

-behavioural inhibition/restraint

80
Q

What does the dorsolateral part of the pre-frontal cortex do?
In what patients is it abnormally active?

A
  • executive cognition (organising planning) via basal ganglia loops involving the caudate nucleus
  • (+frontal eye fields controlling attention/gaze)
  • in OCD patients
81
Q

What does the ventromedial part of the pre-frontal cortex do?
What would a lesion here lead to?

A
  • regulation of behaviour, personality and social conduct

- lesion –> rude, inappropriate, lack of insight

82
Q

What is the sensory association Cx involved in? What important projection does it receive?

A
  • visuospatial representation of objects in space
  • ‘where’/dorasl visual stream from occipital cortex
  • where x is, speed, trajectory, object interaction
83
Q

Where is the sensory association cx?

A

Just behind S1 in the parietal lobe

84
Q

The posterior parietal region is also involved in what?

A post. parietal lesion therefore causes what?

A
  • attention/gaze

- hemineglect (sometimes anosognia-unaware their deficit exists)

85
Q

The parietal lobe does praxes. What is this? What may a parietal/frontal/white matter connection lesion cause?

A
  • semi automatic motor sequences stored in the pre-frontal cx but selected by the post. parietal lobe
  • lesion -> apraxia
86
Q

What is the dominant (L) inferior parietal lobe involved in? Lesion causes what - name of syndrome?

A
  • symbolic representation, number concepts, physics. reading and writing
  • lesion Gerstmann syndrome - L/R confusion, maths difficulty, cannot name fingers
87
Q

What is the medial parietal lobe/tne pre-cuneus involved in?

A

active in day dreaming
episodic memory recall
object visualisation

88
Q

Where does visual info relating to form/colour project to? What is it called if you can’t integrate this info?

A
  • ‘what’ pathway to lateral and inferior temporal cx to identify and categorise objects
  • failure to recognise objects = agnosia
89
Q

What does the auditory association cortex do in the language dominant cx? Wernicke’s is here, where exactly?

A
  • recognition of speech sounds

- Wernicke’s - post 1/3rd of superior temporal gyrus

90
Q

What do areas in the inferior parietal lobe, adjacent to Wernicke’s area do?

A

-understanding of written language ie. reading

91
Q

What do you get with a lesion to

  • arcuate fasiculus
  • broca’s
  • Wernicke’s
A

Arc. Fasiculus - conduction aphasia
Broca’s - non-fluent aphasia
Wernicke’s - fluent aphasia

92
Q

What is the main function of the spinocerebellum?

A

-modulates descending motor systems in brainstem via reticular formation and vestibular nuclei

93
Q

What is the main function of the vestibulocerebellum?

A

-regulates balance and eye movements via vestibular nuclei

94
Q

What is the main function of the cerebrocerebellum?

A
  • high level planning movement.

- regulates cortical motor programs (via thalamus)

95
Q

Cerebellar output is via what cells? What NT? Project where?

A

Purkinje cells. GABAergic

  • to deep cerebellar nuclei (excitatory) -> to thalamus -> Cerebral Cx
  • (also to vestibular nuclei, reticular formation)
96
Q

What are the 2 excitatory inputs to a Purkinje cell? Where do they come from?

A
  • Climbing fibres from cerebral cortex to inf olive

- Mossy fibres from brainstem nuclei –> parallel fibres from granule cells

97
Q

Name 2 local cerebellar inhibitory interneurones.

A
  • basket cells
  • stellate cells
  • golgi cells
98
Q

How is “cerebellar learning” brought about?

A
  • long term changes in responsiveness to parallel fibre inputs
  • synaptic strengthening in successful circuits
99
Q

Where does the trochlear nerve exit the brainstem?

A

-DORSALLY. lateral to the frenulum below the inferior colliculi and cruciform sulcus.

100
Q

What cranial nerve comes of the pons at the juction of pons base and middle cerebellar peducle?

A

CNV - Trigeminal Nerve

101
Q

Where do the olives in the medulla project to? For..?

A

To the contralateral cerebellar hemisphere via inf. peduncle (decussate at raphe nucleus)
For motor learning

102
Q

Which cerebellar peduncle runs up the lateral medulla like a rope and turns posteriorly sharply to enter the cerebellum?

A

Inferior cerebellum peduncle (restiform body)

103
Q

The upper 1/3 of medulla opens like a flower posteriorly, the point of transition between closed/open is called what? What is here?

A

The transition = the “obex”

This is where the CTZ is

104
Q

CN nuclei are arranged in discontinous vertical columns from medial to lateral what are the columns and their CNs?

A
  • somatic motor group (EO & tongue CNIII, IV, VI, XII)
  • visceral motor (E.West. CNIII, VII, IX, X-parasymp)
  • branchiomotor (V, VII, nuc, ambiguus IX, X, XI)
105
Q

What is the function of the Nucleus Ambiguus? (IX, X, XI) in the branchiomotor column derived from fish gill arches.

A

Muscles of speech and swallowing

muscles of soft palate, larynx and pharynx and parasymp to heart

106
Q

What muscle do the fibers of the glossopharyngeal nerve (CN IX) innervate?

A

Stylopharyngeus muscle

107
Q

What is the main sensory nerve of the head and neck for general fine touch/2 point discrimination? Where does this nerve emerge?

A

Trigeminal sensory root

-lateral to motor root (think embryo) at pons/MCP junction

108
Q

What does the motor root of the trigeminal nerve supply?

A

Muscles of mastication

109
Q

The trigeminal nucleus runs the whole length of the brainstem, what is the superior part in the midbrain responsible for? And the inferior part in medulla and C-spine?

A
  • Superior does proprioception e.g. jaw muscles

- Inferior part does pain/temp sensation via trigeminothalamic tract

110
Q

Where does the vestibulocochlear CNVIII arise from?
Fibres enter brainstem via?
And terminate at their nuclei….

A
  • cochlear+vestibular apparatus in the petrous portion of the temporal bone.
  • enter brainstem via internal auditory meatus at the CPA-cerebellopontine angle
  • nuclei in lateral recess of floor of 4th ventricle
111
Q

How many cochlear nuclei are there? How many vestibular nuclei?

A 
2 cochlear (dorsal and ventral)
4 vestibular (3 in medulla, the superior one in the midbrain)
112
Q

The V-shaped visceral afferent nucleus in the medulla is aka the solitary tract / nucleus tractus solitarius. What CN come to which part?

A
  • Top part: fibres from taste buds (CN VII, IX, X)
  • Middle: fibres from heart and lungs (CN IX, X)
  • Bottom: sensation from GIT/abdo viscera (CN X)
113
Q

V1 and V2 pass through the cavernous sinus. V3 does not. Name 3 muscles the trigeminal nerve innervates.

A
  • mylohyoid
  • ant belly of digastric
  • tensor tympani
  • tensor veli palatini
114
Q

What muscles other than facial expression muscles does CNVII innervate?

A
  • post. belly digastric
  • stylohyoid
  • stapedius
115
Q

What CN carries visceral afferents from the carotid sinus? (this nerve also does ear drum sensation)

A

-CN IX - Glossopharyngeal

116
Q

Where does the vagus nerve do pain and temperature sensation?

A
  • infratentorial dura
  • larynx
  • external ear
117
Q

CNXII innervates all the muscles of the tongue except….Which nerve innervates this?

A

Palatoglossus (innervated by vagus)

118
Q

What is the effect of the following on the HPAxis: amygdala, hippocamppus. How is this different in depressed individuals?

A

-Amygdala stimulates HPA (–> CRH –> more cortisol)
-Hippocampus negatively feeds back on HPA (less C)
In depressed you have less cortisol receptors in the hippocampus so less neg. feedback

119
Q

The motor loop of basal ganglia from motor cx to putamen goes to which part of pallidum and which part of thalamus?

A

Motor: …–> Internal segment of globus pallidus (lateral)

and to the VL nucleus of thalamus

120
Q

The cognitive loop of basal ganglia from dorsolateral pre-frontal cx to DL caudate goes to which part of pallidum and which part of thalamus?

A

Cognitive…-> Internal segment of globus pallidus (medial)

and to MD and ventral anterior nuclei

121
Q

The limbic loop of basal ganglia from Ant cingulate cx to ventral striatum goes to which part of pallidum and which part of thalamus?

A
  • Ventral pallidum

- MD nucleus of thalamus

s3 - MSK, Derm, Cardio, Neuro, Pharm (9 decks)

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