Download Neuroanatomy 18 [4-20

Chapter 18; pp. 820-838
Limbic System
1.
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Mesocortex
= limbic cortex
Cingulate gyrus, parahippocampal gyrus, temporal pole
Transition from 3- to 6-layered cortex
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Allocortex (Archicortex and Paleocortex)
Hippocampus, 3-layered
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3.
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Corticoid Areas
Amygdala, no consistent layering
i.
There are four parts to the amygdala, including bed nucleus of stria terminalis
4.
Review MRI sections!!! (don’t worry about gross vertical slices)
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Pathways by which the hippocampus talks to the thalamus:
fornix
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Pathways by which the amygdala communicates with hypothalamus:
Stria terminalis & ventral amygdalofugal pathways
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Olfaction pathway:
Olfactory nerve => mitral and tufted cells => primary olfactory cortex (piriform & amygdaloid cortices) and amygdala => orbitofrontal olfactory area
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Components of the hippocampal formation:
Dentate gyrus, hippocampus, and subiculum
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Intrinsic Hippocampal formation circuit:
Entorhinal cortex =perforant pathway=>
i.
Also E.C. =alvear pathway=> CA1 & CA3
Dentate gyrus (granule cell layer) =mossy fibers=>
CA3 =Schaffer collaterals=>
i.
Also CA3 => fornix
CA1 =>
Subiculum =>
i.
Also subiculum => fornix
Entorhinal cortex
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In which part of the above circuit does long-term potentiation occur?
LTP occurs in the perforant pathway and Schaffer collaterals
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What is the Hebb Rule?
The Hebb Rule can be paraphrased as: “Fire together, wire together” ---synaptic strength increases due to a growth change or metabolic process occurs in neurons when a presynaptic cell repeatedly stimulates the postsynaptic neuron
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What kind of neurons from the medial septal nucleus and diagonal band nucleus are modulatory inputs to the hippocampus?
These neurons release acetylcholine
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10.
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Inputs to hippocampus:
frontal, parieto-occipital, temporal association cortices
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Output from hippocampus via entorhinal cortex:
Multimodal association cortex
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Output from hippocampus via subiculum (and then fornix):
Diencephalon and septal nuclei
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17.
[emotional end of the line]
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Parts of fornix, inferior/~anterior to superior/posterior:
Hipppocampal formation => fimbria => crura =(commissure)=> body=> columns =>
=> postcommisural fornix => medial and lateral mamillary nuclei,
=> precommisural fornix => lateral septal nuclues,
=> or anterior thalamic nucleus
Papez Circuit:
Fornix => => Anterior thalamic nucleus =internal capsule=> cingulate gyrus => back to hippocampal formation
Holguin sez:
Know CT/MRI, but not vertical slice
Doesn’t really test olfaction
Star hippocampus and dementia
Hebb Rule
Choline modulates memory
Memory Disorders
18. Although unilateral lesions of the medial temporal or diencephalic lobes do not produce severe
amnesia, what happens after a lesion in the dominant side? Nondominant?
 Verbal memory defecits
[think Wernicke’s and Broca’s areas]
 Visual-spatial memory
[remember hemineglect from nondominant lesion in Ch. 10]
19. What part of the brain is important for habit learning?
 Caudate nucleus
20. How is information consolidated in the neocortex?
 (Through rehearsal?) by the medial temporal and diencephalic strucures (thalamus)
i. Gradually shifts location to neocortex over the course of years
21. What arteries suply the medial thalami?
 PCA branches: paramedian thalamoperforator arteries
i. Sometimes there is only one: “artery of Percheron”
 So lesions at the top of the basilar artery cause bilateral or unilateral infarcts
22. Describe transient global amnesia:
 Lasts 4-12 hours, abrupt global amnesia, afterwards permanent loss of memory for a few
hours before and after the event, usually nevere happens again
23. Which nucleus of the amygdala has direct and indirect connections all over the brain? Which is
connected to the olfacotry bulb and forebrain areas controlling appetite? Which is important in
autonomic control (hypothalamus and brainstem)?
 Basolateral
 Corticomedial
[think: mead-ial]
 Central
24. What syndrome appears after bilateral lesions of the amygdala?
 Kluver-Bucy syndrome
25. How does the amygdala connect to the medial orbitofrontal and cingulate cortices?
 Via the uncinate fasciculus
26. What are the two pathways from the amygdala to subcortical regions? What do they transmit?
How does the amygdala talk to the brainstem?
 Stria terminalis – transmits olfactory information to hypothalamus in order to modulate
appetite
 ventral amygdalofugal pathway – emotion, motivation, cognitive function, homeostasis
i. connects nucleus basalis, septal nuclei, ventral striatum, and thalamus
 medial forebrain bundle – amygdala & hypothalamus  brainstem
27. How does an auditory cortex seizure manifest? Auditory association cortex? Differences btw.
Sides?
 Positive or negative signs, contralateral
 Voices or music, sometimes speech
 Musical hallucinations are more common in nondominant hemisphere seizure
28. Todd’s paresis =
 Focal weakness post-ictal
29. Frontal motor association cortex seizure can cause:
 Fencing posture or other complex posturing
30. What is a complex partial seizure?
 Loss of conciousness, plus the motor/somatosensory/autonomic/psychic symptoms of a
simple partial seizure
 Or secondary generalization
31. How do you localize a temporal lobe partial seizure, with side 1 exhibiting automatisms
(repetetive behaviours), and side 2 showing dystonia or immobility?
 Side 1 (movement) is ipsilateral to focus
 The basal ganglia contralateral to paralysis get fried
32. Absence seizure EEG shows:
 3-4 hertz spike and wave discharges
33. What are the three top causes of seizure in the elderly? What electrolyte abnormalities cause
seizure?
 Cerebrovascular disease, tumors, and neurodegenerative disorders
 Hypoglycemia, hyponatremia, hypernatremia, hypocalcemia, and hypomagnesmia
34. How can a febrile seizure cause temporal lobe epilepsy? How does it develop in time?
 Complex febrile seizure (longer than 15 minutes or multiple in a day) cause medial temporal
sclerosis or hippocampal sclerosis
 Latent period of up to a few years before onset of complex partial seizures
35. What is Rolandic epilepsy? What appears on EEG?
 Focal, nocturnal seizures in children, remits by 15 years, AD inheritance
 EEG shows centrotemporal spikes
36. What is a Wada test?
 Injection of sodium amytal is used to sedate one half of the brain, after which language skills
are tested in order to determine the dominant hemisphere
 In patients with a nonfunctional medial temporal lobe, injection of the good side causes
severe memory difficulties
i. Since common carotid is injected (and PCA continues to supply the medial
temporal lobe) we think loss of input causes memory issues
37. When is callosotomy done?
 To stop generalization from occuring during a seizure, used to prevent falls in injury-prone
patients
38. Defects associated with Schizophrenia? OCD? Depression?
 Small amygdala, hippocampus, parahyppocampal gyrus ,and basal ganglia; low DA
neurotransmission
 Increased activity in the caudate nucleus, low 5-HT
 Decreased noradrenaline and 5-HT; increased cortisol, some other NTs