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Brain & Behavior > Quiz #4 > Flashcards

Quiz #4 Flashcards

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1
Q

Basal Ganglia Pathways - Summary

A
  1. The “natural” tendency of the direct pathway is to facilitate movement.
  2. The “natural” tendency of the indirect pathway is to decrease movement.
  3. Dopamine facilitates movement:
    •  it activates the direct pathway via D1 receptors
    •  it inhibits the indirect pathway via D2 receptors
  4. Acetylcholine goes with the “natural” tendency of the pathway: •  it activates the direct pathway – facilitating movement •  it activates the indirect pathway – decreasing movement
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2
Q

Neurotransmitters in the BG

A

In Striatum
1. Acetylcholine (ACh) is excitatory to the direct and indirect pathways
2. Dopamine is excitatory through D1 receptors to the direct pathway
3. Dopamine is inhibitory through D2 receptors to indirect pathway
***  Thus, the direct pathway is excited by both ACh and dopamine
and the indirect pathway is excited by ACh and opposed by dopamine

In Pathways (direct and indirect)

  1. Glutamate (GLU) is excitatory
  2. GABA is inhibitory
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3
Q

Key points about BG circuits

A

1.  The connection between the substantial nigra pars compacta and the striatum is dopaminergic.

2.  Both direct and indirect pathways go from the striatum to the globus pallidus pars interna (GPi) and the substantia nigra pars reticulata (SNr).
•  Direct pathway goes there directly (GABAergic neuron)
•  Indirect pathway has interposed: two GABAergic neurons [one to GPe and then to subthalamic nucleus (STN)], and one glutamatergic neuron

  1.   The output from the GPi/SNr is inhibitory to the thalamus (GABA).
  2.   The output from the thalamus is excitatory to the cortex (GLU).
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4
Q

Parkinson’s - mechanism of decreased movement

A

1.  Direct Pathway Effects
•  Without dopamine the direct pathway, which normally favors movement, becomes less active and thus produces less movement
•  ACH acting in the direct pathway as an “activator” can try to compensate, but net effect is a decrease in the activity in the direct pathway

2.  Indirect Pathway Effects
•  Without dopamine the indirect pathway, which favors “no movement”, becomes less inhibited, i.e. more active and thus produces less movement
•  ACH further excites the indirect pathway and the net effect is increased activity in the indirect pathway

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5
Q

levodopa (+/- carbidopa)

A

MOA: precursor of dopamine; carbidopa inhibits peripheral metabolism via dopa decarboxylase

Clinical: most efficacious drug used in Parkinson’s disease (PD)

Kinetics: oral COMT and MAO type B inhibitors can prolong effect; initial honeymoon phase, doses can last around 5 or more hours; afterwards typically 3-4 hours

SEs: GI upset dyskinesias behavioral effects

Notes: on-off phenomena

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6
Q

dopamine agonists:

A

Names:
pramipexole; ropinirole apomorphine–short acting injectable rotigotine (long acting transdermal form)
bromocriptine– NOT used in PD

MOA: D2 agonists (apomorphine bromocriptine, and ropinirole); D3 agonist (pramipexole)

clinical: pramipexole, ropinirole, rotigotine used as sole agents at various stages of PD but side effects may outweigh benefits in later stages s adjunct to L-dopa s apomorphine used as rescue therapy
kinetics: oral
pramipexole: short half-life (tid dosing), renal elimination ropinirole, CYP1A2 metabolism, drug interactions
possible long-acting formulations available
transdermal rotigotine provides 24hr dopamine agonist coverage

SEs: anorexia, nausea, vomiting constipation postural hypotension dyskinesias mental disturbances (psychosis); sudden sleepiness;compulsive behaviors (e.g., shopping & gambling) . . .
Notes: pramipexole and ropinerole being non-ergot agonists, do not have as significant cardiac and GI effects as ergot agonists; still need to monitor for hypotension; few cases of cardiac issues of pramipexole but not clearly defined so still used
bromocriptine is an ergot and not widely used because of ergotism, vasoconstriction, erythromelalgia

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7
Q

MAO inhibitors

A

Names: rasagiline, selegiline

Mech: inhibit MAO type B

clinical: rasagiline/selegiline for mild PD s both drugs adjunctive with L-dopa
kinetics: oral s selegiline has amphetamine metabolite–BID dosing w/ second dose given in early afternoon; rasagiline is given once daily

SEs: typically well tolerated with mild nausea, GI upset or dizziness reported; metabolized in liver; renally excreted

Notes: typically avoid meperdine, tramadol, and dextromethorphan–risk of serotonin syndrome s extremely rare risk of serotonin syndrome with TCA’s and SSRI’S

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8
Q

COMT inhibitors

A

names: entacapone and tolcapone

MOA: block L-dopa metabolism by COMT in periphery (both) and dopamine metabolism by COMT in CNS (tolcapone only)
clinical use: prolong L-dopa actions

kinetics: oral, multiple daily dosing

SEs: relates to increased levels of L-dopa (see above) acute hepatic failure (tolcapone)

Notes: urine can be discolored orange

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9
Q

antimuscarinic agents

A

names: trihexyphenidyl; benztropine

MOA: decrease excitatory actions of cholinergic neurons in striatum by blocking muscarinic receptors

clinical use: improve tremor, rigidity, dystonia

kinetics: multiple daily dosing
tox: typical “atropine-like” side effects: dry mouth, blurry vision, urinary retention, avoid in those with glaucoma
notes: trihexyphenidyl used for PD; benztropine more for druginduced parkinsonism

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10
Q

Amantadine

A

“dirty drug”;

MOA: NMDA receptor antagonist; anticholinergic properties, releases dopamine from nerve terminals

clinical use: good for mild symptoms, dystonia and for dyskinesias s adjunct to L-dopa

kinetics: TID standard dosing; can be used QID
tox: constipation, livedo reticularis, dry mouth, dry eyes, urinary retention, psychosis, fatigue, myoclonus
notes: only drug to treat L-dopa induced dyskinesias but efficacy is not long lasting s originally developed as antiflu medication

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11
Q

Brainstem development & columns

A

Basal Plate: efferent

  • general somatic efferent (GSE) - striated muscles of trunk and limbs, also tongue and eye movements
  • general visceral efferent (GVE) - pregnaglionic parasympathetic neurons (autonomic control),
  • —inneravtes smooth muscles of glands, gut, lungs and cardiac muscles
  • special visceral efferent (branchial arches)

Lateral Plate: afferent

  • general visceral afferent (GVA) - sensory info from thoracic and admonial viscera
  • general somatic afferent (GSA) - sensory info from body wall
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12
Q

Functional Classes of Cranial Nerves

A

Alar - sensory: (lateral)

  • SSA (special somatic afferent): 8
  • GSA (general somatic afferent): 5, 7, 9, 10
  • SVA (special visceral afferent): 7, 9, 10 [taste- to NTS]
  • GVA (general visceral afferent): 9, 10

Basal - motor: (medial)

  • GVE (general visceral efferent): 3, 7, 9, 10
  • SVE ( special visceral efferent): 5, 7, 9, 10, 11
  • GSE (general somatic efferent): 3, 4, 6, 12
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13
Q

Branchial Arches

A

first:
- Nerve: mandibular of trigeminal (V3)
- muscles: mastication, temporaliz, tongue stuff, mylohupid, tensor typani, tensor palatini, ptetygoids

second:

  • nerve: facial nerve (CN7)
  • muscles: facial expression, stylohyoid, platysma

third:

  • nerve: glossopharyngeal (CN 9)
  • muscle: stylopharyngeuous

fourth & sixth:

  • nerve: vagus (CN 10)
  • muscles: larynx and pharynx

fifth dissapeared

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14
Q

Facial Nerve (CN 7)

A

nerve of second cranchial arch
sensory and motor

Functional Components:

  • GSA: sensations from skin of the concha of the auricle, small patch of skin behind ear
  • SVA: taste from anterior 2/3s of tongue
  • SVE: muscles of facial expression, styolohyoid, stapedius
  • GVE: lacrimal, submandibular and sublingual glands - mucus membranes of nose, hard/soft palate
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15
Q

cranial nerve motor/sensory

A

purely motor:
3, 4, 6, 11, 12

purely sensory:
1, 2, 8

both:
5, 7, 9, 10

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16
Q

primary intracranial tumors

A 
38%: meningioma 
30%: neuroepithelial
16%: pituitry craniopharygioma 
8%: cranial nrve sheath 
2%: lymphomas
6% other
17
Q

glial cell development

A 
types of macroglia:
- astrocytes 
- oligodendrocytes
-ependymal cells 
(microglia are resident cells of innate immune system -- not neuroepithelial derived)

tumors from these cells all resemble each other (glial tumors)

18
Q

Glial tumors

A

Astro:

  • PCA: Grade 1, pilocytic astrocytoma (generally cured with srugery), do not progress
  • SEGA: Grade 1, subependymal giant cell tumor
  • Diffuse astrocytoma: Grade 2
  • PXA: Grade 2, pleomorphic xanthatrocytoma
  • PMA: Grade 2, ?
  • anaplastoc astrocytoma: Grade 3
  • glioblastoma (multiforme): Grade 4

Oligo:

  • oligodendroglioma: Grade 2
  • anaplastic oligo-dendroglioma: Grade 3

Epend:

  • SE: grade 1, subependymoma
  • MPE: grade 1, myxopapillaru ependymoma
  • Ependymoma: grade 2
  • anaplastic ependymoma: grade 3

Grade 1: non-infiltrating
Grades 2-4: infiltrating
low grade = grades 1 and 2

19
Q

identifying infiltrative astrocytoma

A

slow growing, relatively little mass effect
subtle infiltration, best stained with IDH1

high grade feature: hypercelluarity and mitotic figure

frontal, temporal common, rarely seen in cerebellum

20
Q

IDH1

A

mutated in many lower grade infiltrating astrocytomas and oligodendrogliomas

  • can be helpful distinguishing between a neoplastic ocondition and a reative one
  • produces and oncometabllite that impacts cellular orcessing
21
Q

oligodendroglioma

A

purple clumps of calcifications
chicken wire - branching capillary vasculature
uniform cells with bland round nuclei and “fried-egg” appearance to cytoplasm (arrtifact)
common 1p/19q co-deletion
- if increased cell density and mitotic figures - anaplastic

mostly in adults 
frontal lobe white matter is common (60%)
often present with seizures 
- median survival ~10 years 
- need IDH mutation AND p1/q19 deletions
22
Q

glioblastoma

A

butterfly shape (impacts corpus callosum)

  • hemorrahage and necrosis
  • palisading necrosis
  • microvascular proliferation
  • IDH mutated is actually good for survival
  • molecular subclass is a better way to segregate groups by urvival than histological criteria alone
23
Q

ependymoma

A

perivacular pseduorosette
true ependymal rosettes
common in kids - posterior fossa (4th ventricle)
- adults: spinal or surpatentorioal (rare in kids)

24
Q

pilocytic astrocytoma

A

cystic mass with mural nodule
biphasic architexture with dense and microcystic areas
- often occurs in children as a cerebellar mass but can occur in adults in other places
- oftne have BRAF alternaions
- pilocytic means hair-like - cells may have hair-like processes, often in bipolar arrangement

25
Q

medulloblastoma

A

small blue cells,
homer wright rosete formation
molecular subtypes: WNT, SHH, C and D
– subgroup prognostics are age dependent (ex: SHH bad in adults but good in infants)
grade 4 most common in kids in the posterior fossa

26
Q

meningioma

A 
extra-axial mass
dural tail
usually grade 1 unless seen to be invading 
WHOLRS
psammoma bodies (bright pink) 
more common in females than males, esp spinal (9:1)
- most common intracranil tumor 
- usually benign
27
Q

mets to brain

A

most common: lung, breast, colorectal, kidney (RCC), melanoma
prostate rare

28
Q

dorsal spinocerebellar tract

A

peri[heral neurons enter below L3 and ascends in fasciculus gracilis then terminates in CLark’es nucleus
(T1-L2), lamina 6
enters via inferior cerebellar peduncle
terminates in intermediate zone of cerebellum (ipsilateral)

(cuneocerebellar – similar but for cervical area)

29
Q

ventral spinocerebellar pathway

A

originates from border cells
crosses midline in anterior white commisure to form the ventro spino tract
enters cerebellum via superior cerebellar peduncle
and then corsses the midline AGAIN within the cerebellar white matter
terminates in vermis and intermediate zone

rostral – similar start in border cells. doesnt do the weird double criossing thing - enters via interfior cerebellar peduncle

30
Q

cell types in cerebellum

A

inputs:

  • mossy fibers –> granular cells
  • climbing fibers –> Purkinje cells

outputs:
- Purkinje cells –> deep cerebellar nuclei

mossy fibers excite granular cells–> these excite purkinje cells
climbing fibers excite Purkinje cells (one to one)
Purkinje cells inhibit deep cerebellar nuceli
stellate, basket and goli cells are all inhibitory

31
Q

Headache disorders

A 
primary:
- migraine 
- tension
- cluster 
secondary:
- brain tumors 
- anuerysms 
- infection 
- hangover
- nose/sinus
- head trauma
32
Q

red flags for headache –imaging

A 
systemic signs - rash, stiff neck
neuro symtpmtoms 
onset - new or changed 
older patient
onset - thunderclap or worst in life 
tinnitus, positional provocations, precipitated by exercise 
side locked
33
Q

migraine

A 
5 or more episodes 
2 of 4 key characterstics:
1. one-sided
2. moderate to severe 
3. throbbing 
4. worse with activity 
associated with at least 2 of these symptoms:
- light and sound sensitivyt 
- nasuea/ vomitting

lasts 4-72 hours
30% have aura (cortical spreading)
regualted by brainstem, vascular control centers
pain centers, trigeminal nerve, anterior cingulate gyrus
migraine generator: raphe nucleus, locus ceruleus, periaquductal grey matter

34
Q

5 phases of migraine attack

A
  1. premonitory: yawn, mood, cravings, fatigue, thirst, stiff neck
  2. aura – visual, dizziness,
  3. headache - pain, light and sound sens, nausea, autonomic
  4. reoslution, pain fades, sleep
  5. postdrome: mood, hungover, hunger, urination
35
Q

migraine treatment

A

abortive treatment:
triptans - serotonin receotpr agonists –vascualr contraindications
NSAIDs and antiemetics

prevention:
- antiepileptics, tricucly depressanrs, SSRIs, botox
supplemtns, gadgets

36
Q

manic episode

A 
for at least one week 
- mood: elevated and expansive, irritable 
- affect: happy, labile 
Cognitive:
- distracted 
- inflated and grandiose
- hyper religious and hyper sexual 
- racing thoughts, flight of ideas 
psychomotor/behavior:
- hypertalkative 
- decreased sleep 
reackless, impulsive 
can be psychotic

treat with mood stablizer - valproate, lithium and maybe also add antidepressant (but never without mood stsbilzer)

37
Q

medications for Tourette’s

A 
alpha 2 agonists: guanfacine 
anti-epileptics: topiramte 
dopamine depletors: tetrabenzine
atypical antipsychoticsL risperidone, aripiprazole 
typical antipsychotics - fluhenazine 
benzodiazepines: clonazepam 
botox
38
Q

corticobulbar pathway

A

supranuclear lesions cause contralateral paralysis of lower face (upper motor neurn type)

lower motor neuron – whole face (still contralteral)

more crossed than uncrossed

contralteral paralysis in genioglossuss - tongue will deviate to contrlateral side of the lesion
if UMN: away from lesion
if LMN: towards lesion

39
Q

auditory pathway

A
  • cohclear division of CN 8–>
  • ventral cochlear nuclei –>
  • dorsal cochlear nuclei –>
  • superior olivary complex –>
  • trapezoid body –>
  • lateral lemniscus –>
  • inferior colliculus –>
  • brachium of inferior colliculus —>
  • medial geniculate nuclei –>
  • primary auditory cortex

Brain & Behavior (6 decks)

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