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Neuroanatomy > Thalamus/Basal Ganglia/Reticular Formation (2) > Flashcards

Thalamus/Basal Ganglia/Reticular Formation (2) Flashcards

1
Q

What are the subdivisions of the basal ganglia?

A

striatum- consists of the caudate, putamen and the nucleus accumbens; globus pallidus and substatia nigra

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2
Q

Where can the caudate nucleus be found?

A

C-shaped structure that is immediately adjacent to the lateral ventricle

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3
Q

Where is the putamen located?

A

lateral and ventral to the caudate and is separated from it by the internal
capsule.

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4
Q

Where is the nucleus accumbens located?

A

rostral-ventral to the putamen

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5
Q

Where is the globus pallidus located?

A

immediately medial to the putamen

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6
Q

What is jointly referred to as the lenticular nucleus?

A

putamen and globus pallidus

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7
Q

What are the components of the substantia nigra?

A

pars reticulata- ventral portion of this nucleus and pars compacta- dorsal portion of the nucleus (immediately dorsal to the cerebral peduncle)

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8
Q

What portion of the substantia nigra contains dopaminergic neurons?

A

pars compacta

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9
Q

Glutaminergic neurons from many regions of the cerebral cortex project to where?

A

striatum via the corticostriatal pathway

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10
Q

GABAergic medium spiny neurons of the striatum project to where?

A

globus pallidus

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11
Q

What causes huntingtons chorea?

A

degeneration of GABAergic medium spiny neurons of the striatum, caused by a mutation in the Huntingtin gene which results in CAG repeats, codes for glutamine, polyglutamine tracts within the protein are formed

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12
Q

GABAergic neurons in the internal segment of the globus pallidus project to where?

A

ventral anterior (VA) nucleus of the thalamus via the lenticular fasciculus and ansa lenticularis

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13
Q

Neurons in the VA of the thalamus project to where?

A

supplemental motor cortex

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14
Q

Dopaminergic neurons of the substantia nigra, pars compacta project to where? Degeneration causes what?

A

caudate and putamen via the nigrostriatal pathway; Parkinson’s

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15
Q

Dopaminergic neurons of the ventral tegemental area project to where? What is this path thought to be involved in?

A

nucleus accumbens; drug addiction

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16
Q

Glutaminergic neurons in the subthalamus project to where? Damage results in?

A

internal segment of the globus pallidus; hemiballismus

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17
Q

What would be the effect on a patients movement be after a lesion of the striatum?

A

uncontrolled dance like movements-> Huntington’s chorea

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18
Q

What would be the effect on a patients movement be after a lesion of the substantia nigra?

A

resting tremor, parkinsons, trouble initiating movement

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19
Q

What would be the effect on a patients movement be after a lesion of the subthalamic nucleus?

A

hemiballismus- one limb, sharp, uncontrolled movement, cant stop

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20
Q

What separates the thalamus from the hypothalamus?

A

hypothalamic sulcus

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21
Q

What are the different nuclei of the thalamus?

A

Anterior division (AN), Medial division (mediodorsal N), Lateral division: Dorsal N (lateral dorsal, lateral posterior, pulvinar), Ventral N (ventral anterior, ventral lateral, ventral posterior lateral, ventral posterior medial, medial geniculate, lateral geniculate); Intralaminar N (centromedian and reticular)

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22
Q

What is the input to the pulvinar and LP? ouput from the pulvinar and LP?

A

retina to pretectal n. to superior colliculus; to posterior parietal cortex

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23
Q

What is the input to the LGN? ouput from LGN?

A

retina; optic radiations to striate cortex (primary visual cortex)

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24
Q

What is the input to the MGN? ouput from the MGN?

A

inferior colliculus via braichi of inferior colliculus; auditory radiation to Herchel’s gyrus (primary auditory cortex)

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25
Q

What is the input to the VPL? ouput from the VPL?

A

gracilis and cuneatus nuclei (ST) via ML; somatosensory radiations to post central gyrus

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26
Q

What is the input to the VPM? ouput from the VPM?

A

solitary n, spinal n. of V, primary sensory n of V; post central gyrus

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27
Q

What is the input to the VL? ouput from the VL?

A

dentate nucleus of cerebellum via dentatorubrothalamic; motor and premotor cortex

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28
Q

What is the input to the VA? ouput from the VA?

A

basal ganglia and globus palidus via thalamic fasciculus; supplementary cortex

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29
Q

What is the input to the MD? ouput from the MD?

A

septal n to amygdala; prefrontal cortex

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30
Q

What is the input to the anterior nucleus? ouput from the anterior nucleus?

A

mammillary bodies via mammilothalamic tract; cingulate gyrus

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31
Q

Where is the lateral geniculate nucleus located?

A

along the banks of the calcarine fissure

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32
Q

Sensory information is conveyed by which thalamic nuclei?

A

lateral posterior, pulvinar, VPL, VPM, medial geniculate, and lateral geniculate

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33
Q

Motor information is conveyed by which thalamic nuclei?

A

ventral anterior, ventral lateral, centromedian

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34
Q

Limbic information is conveyed by which thalamic nuclei?

A

anterior, medialdorsal, pulvinar

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35
Q

Consciousness information is conveyed by which thalamic nuclei?

A

reticular and centromedian

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36
Q

What symptoms might a thalamic lesion elicit?

A

ataxia, loss of fine touch, pain- ex of neuropathic central pain not caused by damage to body tissues but possibly by a stroke

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37
Q

What is the input to the basal ganglia?

A

straitum- caudate nucleus and putamen and nucleus accumbens

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38
Q

What is the output of the basal ganglia?

A

pallidum- lateral and medial segment; pars reticulata of substantia nigra

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39
Q

What are the highways to the basal ganglia?

A

lenticular fasciculus, thalamic fasciculus, and ansa lenticularis

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40
Q

Where does the pars compacta of the substantia nigra project to?

A

striatum

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41
Q

What are the intrinsic nuclei of the basal ganglia?

A

globus pallidus-external segment, ventral pallidum-intrinsic part, subthalamic nucleus, substatia nigra pars compacta, and ventral tegmental area

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42
Q

What are the components of the direct system with the basal ganglia?

A

cerebral cortex (frontal lobe) to input nuclei to output nuclei to thalamus back to cerebral cortex (frontal lobe)

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43
Q

What are the components of the direct system with the basal ganglia?

A

Cerebral cortex (frontal lobe) to input nuclei to globus pallidus external segment/ventral pallidum to subthalamic nucleus (can go backward) to output nuclei to thalamus to cerebral cortex

44
Q

The output nuclei of the basal ganglia projects to where besides the thalamus?

A

brain stem motor areas thru SCP to the parapontine area

45
Q

What dopaminergic cell groups input to the frontal lobe prior to input nuclei and the input nuclei of the basal ganglia?

A

SN compacta and Ventrotegmental area

46
Q

What is the function of the direct path of the basal ganglia?

A

inhibit the brake to activate desired pathway

47
Q

What is the function of the indirect pathway of the basal ganglia?

A

inhibitory to the inhibitor-> more excitation to internal segment of globus pallidus to inhibit unwanted programs

48
Q

What is the function of the subthalamic nucleus?

A

inhibit unwanted programs

49
Q

What is the function of the D1 of the putamen/caudate?

A

excitatory reinforcing desire to move

50
Q

What is the function of the D2 of the putamen/caudate?

A

reinforcing the desire for inhibition, have more unwanted movements

51
Q

What are the 4 principle input-output loops of the basal ganglia?

A

skeletomotor loop, occulomotor loop, associative loop, and the limbic loop

52
Q

What are the componnents of the skeletomotor input-output loop of basal ganglia?

A

somatic sensory/primary motor/premotor/supplementary motor area to putamen to GPi and SNr to VA and VL and back around

53
Q

What type of information is input to the caudate nucleus (head)?

A

cognition or executive function

54
Q

What type of information is input to the putamen?

A

skeletal motor

55
Q

What is the input and output to the limbic loop of the basal ganglia?

A

nucleus accumbens; ventral pallidum

56
Q

What goes wrong in the basal ganglia loops in a hypokinetic movement disorder like Parkinson’s?

A

no SNc to D2 or D1, decreased output of D1 (GABASPDYN) to GPm/SNr, increase output from D2 (GABAENK) to GPi, GPi has a decrease in output to STN and GPm/SNr, STN has increased output to GPm/SNr which has increased output to GPi, VL/VA, tectum and rectic nuclei, all of which have decreased output

57
Q

What is Akinesis?

A

delay in initiation or starting movement

58
Q

What is Bradykinesis?

A

prolonged execution of movements

59
Q

What is Hypokinesis?

A

paucity of normal spontaneous movements

60
Q

What are the features of parkinsonism?

A

akinesis, bradykinesis, hypokinesis, rigidity, resting tremor (4-5hz, pill rolling), cogwheel rigidity (resting tremor +rigidity), and parkinsonian gait

61
Q

What are the causes of Hypokinetic or Parkinsonian Syndrome

A

Idiopathic Parkinson disease, Encephalitis lethargica, Head trauma- dementia pugilistica, MPTP- designer drug, Carbon monoxide and manganese poisoning, Drug induced- neuroleptics (dopamine blocking drugs), Wilson disease- hepatolenticular degeneration, Rigidity plus other deficits in multiple neurodegenerative diseases

62
Q

What is chorea?

A

spontaneous, rapid, jerky, arrhythmic involuntary movements which are purposeless or “fragments of motor programs”

63
Q

What is Athetosis?

A

inability to sustain the body part in one position. Movements are writhing or snake-like. Often seen with chorea, hence the term choreoathetosis

64
Q

What is Ballismus?

A

flailing, flinging movement of the whole extremity seen in lesions of the contralateral subthalamic nucleus

65
Q

What is Dystonia?

A

persistence or fixing of the posture at the extreme of an athetoid movement of either the extremities or the trunk.

66
Q

What are the changes in basal ganglia loops in hyperkinetic disorders like huntigton’s?

A

D2 interrupted output to GPl which has an increase to GPm/SNr and STN which has a decrease to GPm/SNr which has a decrease to GPl, VL/VA, Tectum and Retic nuclei, all have increased output and motor cortex has an increased output

67
Q

Hyperkinetic disorders are characterized by involuntary movements such as?

A

twitching head, grimacing movements of face, lips and tongue, gesticulating movements in distal parts of upper limbs and jerking in distal lower limbs

68
Q

What are some causes of hyperkinetic disorders?

A

Huntington- loss of medium spiny stellate neurons (GABA neurons of indirect pathway), Sydenham chorea (rheumatic chorea), Drug induced, Lupus erythematous, Thyrotoxicosis
Part of other neurodegenerative diseases

69
Q

Hypokinetic disorders occur when?

A

there is too little direct pathway effect and too much indirect pathway effect.

70
Q

Hyperkinetic disorders occur when?

A

there is too little indirect pathway effect?

71
Q

The reticular formation contains several populations of what?

A

of neurons with long dendrites surrounded by interlacing bundles of fibers.

72
Q

The raphe nuclei include many what?

A

serotonergic neurons; Rostrally projecting-active in sleep, Caudally projecting- receive afferents from periaqueductal gray matter, modulate pain sensation

73
Q

The central group of nuclei includes the cells of origin of what? Rostral projections are concerned with what?

A

motor reticulospinal fibers; eye movements

74
Q

The paramedian pontine reticular formation is involved in what?

A

control of eye movements

75
Q

What kind of neurons are in the locus coerulus? What processes are they involved in?

A

Catecholaminergic neurons; probably to increase the speed of reflexes and the general level of alertness

76
Q

The laterally located parvocellular, parabrachial, and superficial medullary reticular areas are concerned with what?

A

regulation of the respiratory and circulatory systems

77
Q

Reticular formation is activation is responsible for what?

A

REM stage of sleep

78
Q

The lateral column of the reticular formation contains what? whose function is what?

A

small-sized cholinergic cells, parvocellular regions, receive afferent fibers from both neighboring regions of the brainstem

79
Q

The medial column of the reticular formation contains what? These areas serve as what?

A

different groups of large-sized cells, called magnocellular regions; effector regions

80
Q

The median column of the reticular formation contains groups which lie along or adjacent to what? This comprises what?

A

midline of the upper medulla, pons, and midbrain; raphe nuclei, Serotonergic.

81
Q

Locus ceruleus is located in what? IT contains ½ of the brain’s what?

A

pontomesencephalic junction; noradrenergic neurons

82
Q

Interneurons of the reticular formation receive what? These fibers innervate what?

A

some of the corticobulbar fibers from the motor cortex; innervate the three cranial nerves involved in eye movement

83
Q

The descending reticular nuclei in the brain are involved in what?

A

reflexive behavior such as coughing, chewing, swallowing and vomiting

84
Q

Theascending reticular formationis also called what? It is responsible for what? This portion projects to where?

A

reticular activating system; the sleep-wake cycle, mediating various levels of alertness; the mid-line group of the thalamus (wakefulness) then to cortex

85
Q

Thedescending reticular formationis involved in what? Receives input from where?

A

posture, equilibrium, ANS activity, plays a role in motor movement; hypothalamus

86
Q

Where in the reticular system can a lesion result in a coma?

A

ascending system bilaterally

87
Q

Medullary raphe neurons receive afferents from where? project to where?

A

Spinal cord, Gracile and cuneate nuclei, Trigeminal nuclei, Periaqueductal gray matter (PAG); Dorsal horns, trigeminal nuclei, and preganglionic autonomic neurons of BS/SC

88
Q

Pontine nuclei receive afferents from where? Projects to where?

A

Prefrontal cortex, Limbic system (hypothalamus, hippocampal formation); Forebrain, Cerebellum, Noradrenergic neurons of the brainstem

89
Q

What are the different raphe nuclei?

A

medullary and pontine, nucleus raphe magnus

90
Q

It is believed that the sensory and emotional information transmitted to the thalamus mediates affective components of pain. What is the pathway and the end result?

A

projection from cells in PAG to serotonergic nucleus raphe magnus (NRM), NRM projects to dorsal horn entire length of spinal cord and inhibits ST tract neuron; pain reduction

91
Q

What are the central group nuclei of the reticular formation?

A

Gigantocellularis nucleus, oral pontine reticular nuclei, Paramedian pontine reticular formation (PPRF);

92
Q

Gigantocellularis nuclei receives input from where? projects to where? Mediates what effect?

A

cortical input (premotor and motor) and project to the spinal cord as the lateral reticulospinal tracts in ventrolateral funiculus. Inhibitory influence on motor neurons. Inhibits extensor motor tone.

93
Q

oral pontine reticular nuclei receives input from where? projects to where? mediates what effect?

A

cortical input (premotor and motor) and project to the spinal cord as the medial reticulospinal tracts in ventral funiculus. Excitatory influence facilitates extensor tone.

94
Q

PPRF is involved in what?Receives afferents from where?

A

lateral conjugate movements of eyes. Saccades; contralateral cerebral cortex, the superior colliculus, and vestibular nuclei

95
Q

PPRF projects to where and with what information?

A

abducens nucleus; frontal eye fields (corticoreticular) and superior colliculus (tectoreticular fibers); VI to lateral rectus and contralateral III nucleus via MLF

96
Q

Locus coeruleus contains what kind of neurons? Receievs input from where? Project to where?

A

Catecholemine (NE and Epi NT); central group nuclei and nucleus prepositus; MANY areas in CNS, notably cortex, limbic system structures (excitatory modulation)

97
Q

What is paradoxical sleep? What modulates it>

A

REM, muscles of the trunk and limbs are relaxed and it takes a significant sensory stimulus for arousal but the brain very active; reticular system

98
Q

Electrical stimulus to reticular activating system results in?

A

sleeping to awake

99
Q

Electrical stimulus to thalamus results in?

A

awake to asleep

100
Q

What occurs in stage 1 sleep?

A

“drowsiness” , EEG lower frequency and increased amplitude; increase in anterior thalamic GABA and a decrease in noradrenergic and cholinergic activity

101
Q

What occurs during stage 2 sleep?

A

further decrease in frequency and increase in amplitude of EEG; sleep spindles-arise as a result of interactions between thalamic and cortical neurons.

102
Q

What occurs during stage 3 sleep?

A

moderate to deepsleep, the number of spindles decreases, whereas the amplitude of low-frequency waves increases still more.

103
Q

What occurs in stage 4 sleep?

A

deepest, EEG activity consists of low frequency (1–4 Hz), high-amplitude fluctuations-> delta waves; 1hr to here, only first two cycles.

104
Q

What occurs in REM sleep?

A

stagesofsleepreverse, similar waves to stage I, lasts 10 min and cycle back to non-REM

105
Q

What are the physiological characteristics of deep sleep? Modulated by what brain areas?

A

parasympathetic dominance: Decreased heart rate/respiration, Increased gastric mobility, blood pressure decrease, dysregulation of temperature; cortex and thalamus

106
Q

REM sleep is characterized by what physiological changes? Reticular formation in REM causes what changes?

A

Increased eye movements (PPRF), Penile erection (female equiv.), locus ceruleus- NE signaling activates limbic system, Raphe nucleus- serotonin signaling in forebrain

107
Q

The increase inlimbic systemactivity, coupled with a marked decrease in the influence of the frontal cortex during REM sleep, presumably explains what?

A

characteristics of dreams (e.g., their emotionality and the often inappropriate social content); frontal area is area of social inhibition; possibly involved in learning

Neuroanatomy (17 decks)

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