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neuro final exam > Neuro WEEK 12 PT 1 (1-7) > Flashcards

Neuro WEEK 12 PT 1 (1-7) Flashcards

1
Q

Striatum

A

Caudate nucleus & the Putamen

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2
Q

Substantia Nigra is comprised of

A

cell rich Pars compacta & fiber rich Pars reticulate

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3
Q

Basal Nuclei Includes

A

Caudate nucleus, Putamen, Globus Pallidus, Substantia Nigra & Subthalamus

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4
Q

Basal Nuclei also includes the: PeNS 

A

Pedunculopontine nucleus Nucleus Accumbens Subthalamic nucleus

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5
Q

Where is the Pedunculopontine nucleus located? 

A

in brainstem just caudal to substantia nigra.

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6
Q

The Pedunculopontine N is part of the

A

Ascending reticular activating system (ARAS) and descending connections thru reticulospinal tracts to LMNs

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7
Q

Nucleus Accumbens is also known as

A

ventral striatum

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8
Q

Which system is the Nucleus Accumbens densely connected with?

A

limbic system.

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9
Q

Nucleus Accumbens is a part of which pathway? MMR

A

mesolimbic motivation & reward pathway

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10
Q

What runs through specific parts of the basal nuclei?

A

Distinct, parallel operating circuits or loops

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11
Q

Naturally occurring disorders of the basal ganglia such as Parkinson’s disease (PD) or Huntington’s disease (HD) may affect

A

multiple loops

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12
Q

Symptoms presented with basal ganglia disorders such as Parkinson’s disease (PD) or Huntington’s disease (HD) - MEC

A
  • Motor
  • Emotional
  • Cognitive,
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13
Q

What is the key to basal nuclei function in motor activities?

A

Disinhibition.

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14
Q

Thalamocortical (VA/VL to motor cortex) projections are

A

Excitatory (glutaminergic)

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15
Q

In order for the thalamus to excite the cortex, basal nuclei must

A

Physically remove the inhibition of the motor nuclei of the thalamus (VA/VL).

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16
Q

Excitatory (glutaminergic) motor nuclei are tonically inhibited (GABAnergic) by

A

Globus pallidus & substantia nigra pars reticulate

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17
Q

Removal of inhibition of disinhibition is done by

A

The striatum via the GPi in the direct pathway

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18
Q

Indirect pathway begins with excitatory glutaminergic pathway from

A

Cortex to striatum.

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19
Q

In the indirect pathway striatal GABAnergic inhibitory neurons produces inhibition of inhibitory GABA output from

A

GPe to subthalamus.

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20
Q

In the indirect pathway, the disinhibited subthalamus excites

A

GPi (again with glutamate).

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21
Q

What happens when the GPi is excited in the indirect pathway?  .

A

The VA/VL thalamus is inhibited & cortex can no longer be excited - motor cortex will not produce movement

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22
Q

what type of movement does the indirect pathway inhibit?

A

voluntary movement

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23
Q

Balance of the direct & indirect pathways produces

A

movement or not.

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24
Q

Pars Reticulata is very similar in structure and function to

A

Globus pallidus internus.

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25
Q

Pars Reticularis has input from which fibers?

A

Striatum – striatonigral fibers

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26
Q

Which part of the thalamus does Pars Reticularis inhibit?

A

VA/VL thalamus with GABAnergic inhibitory neurons

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27
Q

Neurotransmitter released by Pars Compacta Neurons

A

Dopamine (DA)

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28
Q

Dopamine has two actions on the striatum. 

A
  1. Produces inhibition via D2 receptors on striatal neurons of the indirect pathway - ID2
  2. Produces excitation via D1 receptors on striatal neurons of the direct pathway- ED1
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29
Q

Substantia Nigra Pars Compacta promotes

A

Thalamic excitation by activating the direct pathway and inhibiting the indirect pathway

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30
Q

Substantia Nigra Pars Compacta is inhibited by

A

Striatal GABAnergic input

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31
Q

Substantia Nigra Pars Compacta is excited by

A

Cholinergic input from pedunculo-pontine nucleus (PPN).

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32
Q

The pedunculo-pontine n is a brainstem n that contributes to the

A

Pontine reticulospinal tract and produces descending excitation of spinal LMN.

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33
Q

Motor loop is associated with the regulation of what type of movement?

A

Voluntary movement.

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34
Q

Where does the motor loop arise from? 

A

Supplementary motor cortex & other cortical areas

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35
Q

What are the functions of the motor loop?

A

Regulate VA/VL thalamic and motor cortex excitability via connections through the Putamen & GPi (direct pathway) and GPe and subthalamus (indirect pathway).

  • Preparation, organization and execution of action
  • Initiated by the intention to act
  • Endogenous generation of responses when environmental stimuli fail to provoke responses
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36
Q

The oculomotor channel (loop) is associated with regulation of

A

eye movements.

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37
Q

Where does the oculomotor loop begin?

A

In the SMA & Posterior parietal cortex

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38
Q

The oculomotor loop projects via- CGS

A

via caudate nucleus, GPi & SNpr to regulate excitability of the VA and MedioDorsal / dorsomedial thalamic nuclei.

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39
Q

Area of cortex where thalamic output of the oculomotor loop project to

A

Prefrontal areas - vicinity of frontal eye fields.

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40
Q

Functions of the oculomotor channel include: 

A

Higher-order control of eye movements -orientation of eyes towards specific objects in the environment and is implicated in visual exploration and visual learning

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41
Q

The prefrontal channel is associated with

A

Cognition.

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42
Q

Part of the prefrontal channel where the cortical input to the head of the caudate is primarily from?

A

The dorsolateral pre-frontal cortex.

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43
Q

In the prefrontal channel, the caudate influences the GPi & SNpr to regulate

A

Excitability of the VA and mediodorsal (MD) thalamic nuclei. These nuclei in turn project to the prefrontal cortex (PFC)

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44
Q

Functions of the prefrontal channel

A
  • Processing information about fairness of decision-making,
  • Trusting in “fair” decisions & those who make them
  • ‘Altruistic punishment’ – the desire to punish violations of social norms even when we have not been personally wronged
  • Regulation of ‘worry’
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45
Q

The limbic channel is associated with regulation of

A

Emotions and motivational drives

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46
Q

The limbic channel Input from temporal cortex, hippocampus & amygdala into the basal nuclei is via the . NVC

A
  • Nucleus accumbens
  • Ventral putamen &
  • Caudate.
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47
Q

Nucleus accumbens, ventral putamen & caudate connect to the .

A

GPi for output to the mediodorsal thalamic nucleus

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48
Q

The dorsomedial thelamic nucleus projects to the which cortex? AO

A

Anterior cingulate cortex & orbitofrontal cortex

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49
Q

Functions of the limbic channel

A
  • Evaluation of personal actions and environmental resources
  • Social, behavioral and affective self-regulation of behaviors.
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50
Q

The limbic channel is the channel implicated in excessive gambling seen in which disorder?

A

Parkinson’s patients on L-Dopa & dopamine agonists

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51
Q

What is Parkinson’s Disease?

A

A progressive degenerative disease caused by death of dopaminergic (DA) neurons primarily in the SNpc.

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52
Q

What does the time course of Parkinson’s Disease begin with?

A

Loss of noradrenergic input into the dorsal motor nucleus of X & the noradrenergic neurons of the locus coeruleus.

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53
Q

What neurotransmitter is depleted / lost in Parkinson’s disease?

A

Dopaminergic neurons seen in SNpc with normal aging (50% decrease ages 20 to 60)

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54
Q

True/false - aging may be a major factor in the accelerated development of PD

A

True

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55
Q

Patients with parkinson’s disease shows progressive decline in DA in areas of the Mesolimbic system including projections from the

A
  • Ventral tegmental area (VTA) to the amygdala
  • Nucleus accumbens
  • Prefrontal cortex
  • Hippocampus via medial forebrain bundle (MFB)
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56
Q

Progression of Parkinson’s Disease causes continued decline & loss of connections in which parts of the cortex?

A
  • Prefrontal cortex / brain
  • Limbic cortex &
  • Hippocampus.
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57
Q

Continued development of Parkinson’s Disease produces loss in

A
  • Cognitive skills,
  • Memory and
  • Higher associative cognitive functioning
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58
Q

Cardinal signs of Parkinson’s Disease includes: BRRP

A
  • Bradykinsesia
  • Resting tremor 
  • Rigidity 
  • Postural instability.
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59
Q

Resting Tremor

A

4-6 Hz resting “pill-rolling” tremor. Begins in peripheral extremities but extends proximally as the disease progresses

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60
Q

Name the three components of Bradykinesia- HAB

A
  • Hypokinesia-paucity of movement 
  • Akinesia – problem initiating movement
  • Bradykinesia – slowed movement 
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61
Q

Non-motor impairments include: CHAP2S

A
  • Cognitive decline (up to 80%) 
  • Hallucinations 
  • Autonomic changes
  • Postural hypotension 
  • Pain
  • Sleepiness & Fatigue 
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62
Q

Etiology of Parkinson disease

A
  • No known cause of degeneration / apoptosis of dopaminergic neurons
  • Some cases environmental or genetic causes are implicated - Combination of factors
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63
Q

What are some pharmacological approaches to the management of Parkinson’s patients: BRAVeD 

A
  • Blocking the enzymatic breakdown of dopamine
  • Replacement therapy
  • Anticholinergic interventions
  • Various other approaches
  • Dopamine agonists
64
Q

What is the medication used to supplement the loss of dopamine?

A

Levodopa (L-DOPA)

65
Q

What is L Dopa co-administered with to minimize peripheral metabolism

A

Carbidopa

66
Q

What does carbidopa do?

A

Blocks DOPA Decarboxylase and does not cross the BBB.

67
Q

What is the combination of L-DOPA and carbidopa called?

A

SinemetTM

68
Q

True/false- L-DOPA use requires intact dopaminergic neurons therefore as apoptosis of dopaminergic neurons continues, the use of L-DOPA is less effective with the progression of the disease

A

True

69
Q

True/false- Patients on L-DOPA therapy may exhibit sudden ON-OFF shifts of symptoms late in therapy

A

True

70
Q

Sudden ON-OFF shifts of symptoms late in therapy due to L-DOPA use may be due to

A

Apoptosis of dopaminergic neurons and the relatively short half-life of L-DOPA

71
Q

How long does L-Dopa lasts?

A

 about 90 minutes

72
Q

What helps to extend the action of L-DOPA?

A

Sustained release Sinemet-CR.

73
Q

Patients on L-DOPA often suffer considerably from this disorder

A

Dyskinesias - may be an effect of dosing of the drug and its rapid metabolism.

74
Q

True / false- there is some evidence that L-DOPA may accelerate DA neuron cell death secondary to increased free radicals or metabolic stress. So many neurologists suggest shifting to other medications early in the progression of the disease to minimize these effects.

A

true

75
Q

Since dopamine cannot cross blood-brain barrier, what is the metabolic precursor that must be used to help it across?

A

Levorotatory 3, 4 dihydroxyphenylalanine (L-DOPA).

76
Q

Why is L-DOPA rapidly metabolized peripherally?

A

Because large numbers of dopaminergic neurons are in the enteric nervous system (n surrounding the gut),

77
Q

What is the newest approach to treatment of Parkinson’s patients? DoRA

A

Dopamine receptor agonists

78
Q

What does dopamine receptor agonist do?

A

Mimics the effect of DA at DA receptors.

79
Q

Advantages of dopamine receptor agonist over L-DOPA therapy include: MoL2eS2

A
  • More selective action (D1 or D2 agonists)
  • Longer effect over the course of the disease
  • Less dyskinesias
  • Slower rate of metabolism so longer half-life of effectiveness
  • Slows SNpc cell death
80
Q

Similar adverse reactions of dopamine agonists & L-Dopa?

A

Both increase the action on DA receptors either by:

  • Iincreasing DA or
  • Mimicking the effects of DA.
81
Q

Adverse reactions of dopamine agonists & L-Dopa include: CHA2 D

A
  • Constipation – due to action on DA neurons of enteric nervous system
  • Hallucinations
  • Addictive behaviors – excessive gambling
  • Abnormal thinking – hold onto false beliefs
  • Dyskinesias – choreoform movements
82
Q

Inhibitors of dopamine metabolism:

A

Monoamine oxidase (MAO) inhibitors and Catechol-O-methyl transferase (COMT) inhibitors

83
Q

Oldest therapies for Parkinson’s Disease before L-DOPA AA

A

Anticholinergic agents

84
Q

Blocking ____________receptors could reduce some of the symptoms of Parkinsons disease

A

Muscarinic receptors

85
Q

Other drugs used to treat Parkinson’s patients include: NA2

A

Amantadine – Antiviral may also have effects on catecholamine pathways but has little efficacy

Anti-depressants – other than MAO inhibitors probably have no direct effect per se but used for depression symptoms.

NMDA receptor antagonists -Newest Tx, may slow cell degeneration (apoptosis).

86
Q

Surgical Interventions for Parkinson’s Disease: PVD

A
  • Pallidotomy or lesion of the globus pallidus internus
  • Ventrolateral thalamotomy
  • Deep brain stimulation.
87
Q

What is Pallidotomy or lesion of the globus pallidus internus?

A

Common approach involving use of a stereotaxic device to localize GP & stabilize patients. Pallidotomy reduces tremor & rigidity but not other symptoms.

88
Q

What is Ventrolateral thalamotomy –

A

Lesioning of the VL nucleus- done with similar results to GPi lesions

89
Q

Deep brain stimulation-

A

Implantation of leads to different brain regions along with an implanted pacemaker unit. Common targets for DBS are the thalamus, subthalamic nucleus, and GPi

90
Q

True / False- Fetal nigral transplantation- has had Little efficacy despite positive MRI results. In addition Substantial adverse reactions noted in young patients

A

True

91
Q

Huntington’s Disease is also know as

A

Huntington’s Chorea

92
Q

What is Huntington’s disease?

A

An Inherited neurodegenerative disease.

93
Q

T / F- Children of Huntington Disease patients have a 50% risk of developing the disease.

A

True

94
Q

Test for Huntington disese

A

Genetic testing to identify gene or not.

95
Q

Huntington’s Disease causes Gross atrophy of

A

The striatum (caudate and putamen)

96
Q

What is Huntingtin?.

A

An autosomal dominant mutation in either of an individual’s two copies of a gene

97
Q

Characteristics of Huntington’s Disease CPM

A
  • Cognitive decline -leading to dementia
  • Psychiatric disorders- paranoid and psychosis behaviors
  • Motor changes – choreoathetosis
98
Q

Typical age of onset of Huntington disease?

A

40–50 years

99
Q

Most Huntington patients progress to a vegetative state within

A

10–15 years and die

100
Q

Medical Management of Huntington disease? FeD2S

A
  • Fetal transplantation (unsuccessful)
  • Dopamine antagonists
  • Deep brain stimulation
  • Surgical ablation of the GPi all without much value
101
Q

Hemiballismus

A

Wild, unpatterned, flinging movements of an entire extremity. 

102
Q

Cause of Hemiballismus?

A

A discrete lesion of the subthalamic nucleus contralateral to symptoms which reduces activity of the indirect pathway and thus reduces the inhibition of movement.

103
Q

Hemiballismus most commonly results from vascular disorder of which artery?

A

Penetrating branch of the posterior cerebral artery (PCA)

104
Q

Three main Connections of the cerebellum to the Brainstem SIM

A
  • Superior peduncle
  • Inferior peduncle
  • Middle peduncle
    *
105
Q

Inferior cerebellar peduncle contains

A

Both cerebellar afferents and efferents

106
Q

Inferior cerebellar afferents (cerebellopetal fibers) contains the foll. tracts? DROVe C

A
  • Dorsal, Cuneo & Rostral spinocerebellar tracts
  • Olivocerebellar tract
  • Vestibulocerebellar tract
107
Q

Nuclei of the Inferior cerebellar efferent (cerebellofugal fibers) contain? VR

A
  • Vestibular nuclei
  • Reticular nuclei
108
Q

Middle cerebellar peduncle tract and fibers

A

Pontocerebellar tract which are afferent or cerebellopetal fibers

109
Q

Superior cerebellar peduncle contains

A
  • Some affferent fibers - Ventral spinocerebellar tract,
  • Primarily efferent corticofugal fibers from cerebellum which terminate in the red nucleus and the VL motor nucleus of the thalamus
110
Q

What fibers are the most numerous form of input into the cerebellum?

A

Mossy fibers

111
Q

Each parallel mossy fiber excites

A

>500 Purkinje cells and from 100-300,000 parallel fibers excite a single Purkinje cells (glutamate).

112
Q

What type of synapses does Mossy fibers form?

A

Glutaminergic excitatory synapses with glutaminergic mediated EPSPs.

113
Q

Where does EPSPs of Mossy fibers end?

A
  • On granule cells (of the granule cell layer), whose axons form parallel fibers which ascend up into the molecular layer of the cerebellar cortex to synapse with glutaminergic excitatory endings on the dendrites of Purkinje cells.
114
Q

Mossy fibers originate from- VSC

A
  • Vestibular primary afferent fibers via inferior peduncle
  • Vestibular nuclei via inferior peduncle
  • Spinal cord (spinocerebellar tracts) via mostly inferior peduncle (ventral SCT via superior peduncle)
  • Cerebral cortex via pontine nuclei & pontocerebellar fibers (middle peduncle)
  • End also on Golgi cells – inhibitory interneurons
115
Q

Most climbing fibers direct to- P

A

Purkinje cells

116
Q

Climbing fibers originate from

A

Contralateral inferior olivary nucleus

117
Q

Climbing fibers end with

A

Excitatory aspartate synapses directly on Purkinje cells

118
Q

Climbing fibers produces

A

Large EPSPs which produce bursts of Purkinje cell action potention activity

119
Q

Each Purkinje cell receives .

A

Single climbing fiber

120
Q

Each climbing fiber innervates only

A

1-3 Purkinje cells

121
Q

What type of signal does climbing fibers provide?

A

Feed forward signals

122
Q

Feed forward signals from climbing fibers travel from the cerebral cortex to the cerebellum via COOC

A

Cortico-olivary and olivocerebellar fibers

123
Q

Mossy fibers provide feedback signals from SVO

A

spinal, vestibular & other inputs

124
Q

Cerebellar Interneurons are what type of cells? GBS

A

Golgi cells, Basket and Stellate cells

125
Q

Golgi cells are innervated / excited by what fibers? MP

A

Mossy & parallel fibers

126
Q

T/F- Golgi cells are inhibitory interneurons of the granule cell layer

A

True

127
Q

Golgi cell Inhibitory action (GABA) on granule cell dendrites produces FF& FB

A

Both feed forward (via mossy fibers) and feedback (via parallel fibers) inhibition to granule cells

128
Q

Basket & stellate cells produces GI

A

GABAminergic Inhibitory action on Purkinje cells

129
Q

Basket and stellate cells produce a prolonged inhibition related to

A

Associative learning in cerebellum

130
Q

Outflow from cerebellar cortex is via

A

Purkinje neurons

131
Q

T / F- Output from cerebellar cortex is excitatory, 

A

False it is inhibitory (GABA)

132
Q

Purkinje neurons project to which nuclei?

A

Deep cerebellar nuclei

133
Q

Vestibulocerebellum Purkinje cells project directly to which nuclei?

A

vestibular nuclei

134
Q

T / F- With just a few Purkinje cells leaving the cerebellum the principle outputs from cerebellum are from the deep cerebellar nuclei.

A

True

135
Q

T / F- Mossy & climbing fibers create an inhibitory drive which is sculpted by the inhibitory influence of the Purkinje neurons

A

False it produces an excitatory drive

136
Q

Where does vestibular afferents project to?

A

Cortex of vestibulocerebellum Fastigial nucleus through the inferior cerebellar peduncle

137
Q

Vestibular afferents Influence TENT

A
  • Tone in limbs
  • Extraocular eye muscles,
  • Neck
  • Trunk
138
Q

Visual systems project indirectly to vestibulocerebellum through

A

Climbing fibers of the inferior olivary nucleus.

139
Q

Input from which cerebellar peduncle assists in regulating the vestibular ocular reflex (VOR)

A

Inferior cerebellar peduncle

140
Q

Vestibulocerebellum outputs go to. BVn

A

Brainstem Vestibular nuclei.

141
Q

Vestibulocerebellum outputs to Projections influence

A

Extraocular motor neurons via the medial longitudinal fasciculus

142
Q

Vestibulocerebellum outputs to the brainstem end in nuclei of the

A

Reticular formation which send both descending fibers forming the reticulospinal tracts and ascending fibers to extraocular motor nuclei

143
Q

Role of vestibulocerebellum outputs to the vestibular nuclei

A

Influence body and limb tone and responses via the vestibulospinal tracts

144
Q

Functions of the vestibulocerebellum (Flocculonodular lobe) include: 

A
  • Balance in sitting, standing & gait
  • Plasticity of vestibulo-ocular reflex
  • Nodule function- sensitivity to motion sickness (ablated this makes subject immune to motion sickness)
145
Q

Regions of the cerebellum.

A
  • Pontocerebellum
  • Spinocerebellum &
  • vestibulocerebellum.
146
Q

The Pontocerebellum / Neocerebellum belongs to which zone of the cerebellum?

A

Lateral zone- including the more lateral regions of anterior & posterior lobes

147
Q

The Spinocerebellum / paleocerebellum belongs to which zone of the cerebellum?

A

Intermediate zone - includes medial aspects of both lobes, cerebellar tonsils and vermis

148
Q

Vestibulocerebellum / archicerebellum

A

Most medial part of the cerebellum and

Includes the flocculonodular lobe

149
Q

4 pairs of deep nuclei in the cerebellum

A
  • Fastigial
  • Globose & Emboliform or interposed nuclei
  • Dentate nucleus
150
Q

The Fastigial nucleus

A

The most medial -associated with primarily the vestibulocerebellum but also relays projections from the spinocerebellum

151
Q

Interposed Nuclei (Globose & Emboliform)

A

As their name implies are interposed between the fastigial and dentate nuclei - associated with spinocerebellum

152
Q

The Dentate nucleus

A

Most lateral & largest of the deep cerebellar nuclei -associated with pontocerebellum

153
Q

Three distinct layer of the cerebellar cortex:

A
  • Molecular layer
  • Purkinje cell layer and
  • Granule cell layer.
154
Q

The Molecular Layer

A
  • Most Superficial layer.
  • Low neuron cell body density
  • Types of inhibitory neurons: stellate & basket cells.
  • Contain large dendritic arborizations of Purkinje cells- dendritic arborizations lie in a single plane which is perpendicular to long axis of folia, which are the gyri of the cerebellar cortex.
155
Q

Two sets of afferent fibers in the Molecular Layer of the cerebellar cortex:

A
  • Parallel fibers- Unmyelinated Granule cell axons, each runs 5 mm along (parallel to) long axis of folium activating hundreds of Purkinje cells
  • Climbing fibers – wraps around individual Purkinje cell dendritic trees
156
Q

Purkinje Cell Layer

A

Middle layer of the cerebellar cortex - composed of cell bodies of Purkinje neurons. Neurons are Inhibitory (GABA mediated) to the deep nuclei and some axons will exit the cerebellum

157
Q

Granular Layer

A
  • Innermost layer of the cerebellar cortex- tightly packed with granule cells.
  • Many inhibitory interneurons in this layer called Golgi cells.
  • Axons of granule cells ascend into molecular layer to form parallel fibers.
  • Parallel fibers run about 5 mm along the cortex activating with excitatory (glutamate) endings with each parallel fiber ending on >500 Purkinje cells

neuro final exam (10 decks)

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