Lecture 4: White matter, basal ganglia and diencephalon Flashcards

1
Q

Cerebral white matter is a major contributor to

A

cerebral volume

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2
Q

cerebral white matter is responsible for …

A

communication (i) between cerebral areas & (ii) between the cerebral cortex & lower CNS centres

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3
Q

What does cerebral white matter largely consist of?

A

Consists largely of myelinated axons bundled into large

tracts

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4
Q

Projection tracts

A

• extend vertically from brain to spinal cord forming internal capsule

it is a white matter tract

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5
Q

Commissural tracts

A
  • cross from one hemisphere to the other
  • corpus callosum is wide band of myelinated axon tracts (about 300 million axons)

it is a white matter tract

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6
Q

Parts of the corpus callosum seen in a midsagittal section

A

splenium (most posterior) - temporal and occipital lobes
body - other parts of frontal lobe and parietal lobe
Genu - anterior parts of frontal lobe, part that has the bend in it
rostrum

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7
Q

Split brain

A

Split-brain patients (due to transection, or being born with no corpus callosum = acallosal)
– no obvious changes in intellect and behaviour – problems with certain tasks such as naming objects
e.g. object in right hand with eyes closed, can be named (because foes to left and broca’s area is on the left); object in left hand can not be named (because goes to right and needs to go across corpus callosum in order to verbalise the name).

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8
Q

Corpus callosum transection

A

Corpus callosum transection

  • a form of treatment in patients with severe and disabling epilepsy
  • preventing the spread of epileptic discharge from one hemisphere to the other
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9
Q

Anterior commissure

A

Includes axons that connect the middle & inferior temporal gyri of the two sides

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10
Q

Association fibres

A

cerebral white matter

• connect lobes & gyri within the hemisphere

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11
Q

Basal ganglia is made up of

A

3 structures - caudate nucleus, putamen, globus pallidus

functionally associated with sub thalamic nuclei and substantial nigra

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12
Q

corpus striatum =

A

caudate nucleus

putamen

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13
Q

lentiform nucleus =

A

putamen

globus pallidus

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14
Q

striatum

A

putamen and caudate nucleus (sometimes called caudate putamen)

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15
Q

Pallidum

A

globus pallidus -external (GPe) & internal (GPi) divisions

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16
Q

all of the components of the basal ganglia =

A

corpus striatum + subthalamic nuclei + substantia nigra

17
Q

The caudate nucleus looks like

A

a comma that’s turned 90 degrees to the left, there is a head and body and tail

head is most anterior

18
Q

amygdaloid nucleus is part of

A

the limbic system

19
Q

internal capsule

A

projection fibres to and from the spinal cord, run deep to lentiform nucleus

20
Q

Posterior limb of internal capsule

A

between lentiform nucleus and thalamus

21
Q

Anterior limb of internal capsule

A

between lentiform and caudate nuclei

22
Q

Major connections of the basal ganglia

A

Receive inputs from substantia nigra &
motor cortex and send signals back to these regions

Access to motor neurons in the cerebral cortex is through the thalamus. NO direct access.

Hence have cortical-basal ganglia-thalamic-cortical loop

23
Q

Function of the basal ganglia

A

Motor Control

  • inhibit unnecessary movements
  • acts as a brake so that only have ordered exquisite movement when needed - preventing movement when you do not actually want to move
  • brake can be released by input (has to go through the loop) from the cerebral cortex and the substantia nigra to start movement

Regulating attention and cognition.

24
Q

The basal ganglia and its influence on the spinal cord

A

The basal ganglia influence the function of spinal cord motor neurons indirectly (compared to cerebral cortex, direct synaptic input)

the inhibitory neurons of the basal ganglia affect the spinal cord indirectly through the thalamus and the cortex compared to the cerebral cortex which has a direct effect on the spinal cord motor neurons by the crticospinal pathway

25
Q

At rest - neurons in the basal ganglia

A

There are inhibitory neurons in the basal ganglia and then from the thalamus there are excitatory neurons, at rest when you do not want to move the neurons that are in the basal ganglia (that are part of the globus pallidus) they are tonically active and they are inhibitory so they are constantly firing and inhibiting the thalamic neurons and because these are inhibitiory on the thalamic neurons you are not getting the generation of movement from the firing of thalamic neurons

26
Q

When the cortex wants movement - neurons in the basal ganglia

A

inhibition of inhibitory neurons causes movement

Inhibitory neuron which is tonically active which means that the thalamic neurons are not firing, to take away the inhibition you have to put in neurons that inhibit them (neurons that inhibit the inhibitory neurons). Cortical/cortex neurons that are excitatory decide they want to do this movement and these excitatory neurons depolarise and cause the inhibitory neuron to release its inhibitory neurotransmitter and this inhibits the other inhibitory neuron therefore taking away the inhibition on the thalamus and then these thalamic neurons are able to fire and they do which can generate a movement. Once the thalamic neurons are active/depolarised then they actually activate the corticospinal tract neurons which then go down to the spinal cord which means that you can actually do the movement.

27
Q

Parkinson’s disease cause

A

substantia nigra dopamine neuron degeneration

28
Q

Motor deficits with Parkinson’s disease

A
  • rigidity
    – tremor (at rest)
    – difficulty initiating movement
    – postural instability (leaning forward)
    – shuffling gait
    – stiff facial expression (mask-like face)
29
Q

Treatment of Parkinson’s disease

A

(i) replacement of dopamine e.g. leva dopa - most standard treatment
(ii) stem cell therapy
(iii) deep brain stimulation

30
Q

Diencephalon structure

A

Contains three- paired structures thalamus,
hypothalamus, epithalamus - pairedd meaning that there is one on each side

associated with the third ventricle

31
Q

hypothalamic sulcus separates

A

the thalamus and the hypothalamus

32
Q

thalamus

A
• egg-shaped structure
• makes up 80% of the
diencephalon
• forms the superolateral
walls of the third ventricle
• contains about a dozen nuclei
 • can be divided into several groups
• interthalamic adhesion (intermediate mass - connects the 2 thalamus to the other side): - a midline connection which joins
each thalamus to the other
• Plays a key role in relaying sensation, motor activities, cortical arousal, learning and memory
33
Q

thalamus role

A

• Plays a key role in relaying sensation, motor activities, cortical arousal, learning and memory

sensory relay station
also has a motor component

34
Q

The thalamus is the

A

gateway to the cerebral cortex

35
Q

Hypothalamus

A
• located below the thalamus
(hypothalamic sulcus)
• forms the inferolateral wall of the third ventricle
• extends from the optic chiasma
• superior to the brainstem
36
Q

pituitary gland

A

hypothalamus is closely associated, gives neurone control of pituitary and what hormones it release

37
Q

Main Homeostatic Roles of Hypothalamus

A

• Autonomic control centre (eg. respiration)
• Centre for emotional response (limbic system)
• Body temperature regulation
(thermosensitive neurons)
• Regulation of food intake (appetite and satiety centres)
• Regulation of water balance and thirst (thirst centre)
• Regulation of sleep-wake cycles
(with pineal gland)
• Control of endocrine system functioning (eg. ovaries, testes to produce egg, sperm)

38
Q

Hypothalamic lesion

A

Shows that hypothalamus has a role in food intake

Leptin deficient - decreases/inhibits food intake, acts on hypothalamus

39
Q

Damage to the hypothalamus

A

• various neuroendocrine disturbances
• autonomic dysfunction (respiratory,
cardiovascular and gastrointenstinal systems)
• disturbances in temperature regulation, water balance, sexual behavior and food intake
• changes the level of consciousness, sleep- wake cycle and emotional behavior

Most common cause - tumors

Early symptom - visual field defects
(encroaching on the optic chiasm or optic tract)