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Flashcards in 01a: Basics Deck (53)
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1
Q

Which NTs are considered catecholamines?

A

NE, DA, Epi

2
Q

Anterograde transport in neurons carried out by (X). And retrograde transport by (Y).

A
X = kinesin
Y = dynein
3
Q

DA is (short/long)-range NT originating from which areas in brainstem?

A

Long;

Substantia nigra and VTA (ventral tegmental area)

4
Q

List the three major distribution pathways of dopamine.

A
  1. Mesostriatal
  2. Mesolimbic
  3. Mesocortical
5
Q

(X) dopaminergic pathway regulates movement via (exciting/inhibiting) (X) regions (caudate, putamen).

A

X = mesostriatal

Exciting
X = extra-pyramidal

6
Q

(X) dopaminergic pathway regulates affect, reward, emotion by projecting to (Y).

A

X = mesolimbic

Y = Medial temporal lobe, cingulate cortex, amygdala

7
Q

(X) dopaminergic pathway regulates cognition (working memory) by distributing to (Y).

A
X = mesocortical
Y = neocortex (prefrontal cortex exclusively)
8
Q

T/F: Dopamine synthesized from NE.

A

False - vice versa

9
Q

(DA/NE/ACh/Glu) important in attention and maintaining wakefulness.

A

NE

10
Q

T/F: Both DA and NE synthesized from Tryptophan.

A

False - from Tyrosine

SA is derived from Tryptophan

11
Q

Raphe nuclei responsible for (X) neurons and are found in (lateral/midline) brainstem.

A

X = serotonergic

Midline

12
Q

Rostral raphe nuclei project to (X) to control (Y).

A
X = forebrain
Y = mood and emotion
13
Q

Caudal raphe nuclei project to (X) to control (Y).

A
X = cerebellum, medulla, SC
Y = pain perception
14
Q

Histamine is found in (X) location in brain and projects to (Y).

A
X = hypothalamus (tuberomamillary nucleus)
Y = forebrain, cerebellum, pons
15
Q

(X) biogenic amine (NT) has important long-range projections to forebrain to maintain alert state.

A

X = His

16
Q

Opioid-producing cells mainly found in (X) region(s) of brain/SC.

A

X = PAG and posterior horn of SC

17
Q

Axons in periphery: collections of nerve fibers are bundled together in fascicles and surrounded by (X), composed of multiple layers of:

A

X = perineurium

Perineurial cells interconnected with tight junctions (blood-nerve barrier)

18
Q

Which cells are allowed in the peripheral nerve fascicle? Star the most abundant of these.

A
  1. Schwann cells* (90%)
  2. Mast cells
  3. Fibroblasts
  4. Macrophages
19
Q

List the connective tissue elements present in peripheral nerve fascicle.

A
  1. Basal (external) laminae around Schwann cells

2. Endoneurial fibers (collagen) - bind basal laminae together

20
Q

T/F: Anterograde (Wallerian) degeneration causes axonal/terminal disintegration a few days post-injury.

A

False - within first 24 hours

21
Q

List the morphological changes in cell body after axonal transection.

A
  1. Peripheral movement of nucleus
  2. Dissolution of Nissl bodies
  3. Stripping of synapse from dendrites/cell body
22
Q

Peripheral neuron recovery from injury involves growth factors secreted by (X) that attract sprouting axons.

A

X = Schwann cells of new distal tube

23
Q

Peripheral neuron recovery from injury: the tips of the neuritic sprouts LOVE (X).

A

X = laminin (major glycoprotien of external lamina)

24
Q

Peripheral neuron recovery from injury: traumatic neuroma occurs if…

A

Sprouting axon (from proximal segment) can’t reach Schwann cell tubes (at distal segment)

25
Q

Regeneration of central nerves is extremely rare due to lack of:

A

ECM (external lamina) to guide axon sprouts

26
Q

Regeneration of central nerves is extremely rare due to presence of:

A

Central myelin (potent inhibitor of axonal growth)

27
Q

(X) cells in CNS clear myelin (quicker/slower) than peripheral macrophages do, thus contributing to poor central nerve regeneration.

A

X = microglial

Slower

28
Q

(X) cells in CNS wall off injured area, contributing to poor regeneration.

A

X = astrocytes

29
Q

Consciousness, the components of which include (X) and (Y), depends on integrity of physio mechanisms that originate in which part of brain?

A
X = arousal
Y = attention

Reticular formation (and other structures between hypothalamus and mid-pons)

30
Q

Patient with Sx of indifference, abulia (low willpower), apathy likely has damage to (X) part of frontal lobe.

A

X = dorsolateral convexity and medial frontal lobes

31
Q

Patient with Sx of disinhibition, irritability, lability, poor judgement likely has damage to (X) part of frontal lobe.

A

X = orbitofrontal area (ex: Phineas Gage)

32
Q

Presence of inappropriate reflexes (grasp, rooting, glabellar, etc) in adult is referred to as (X) sign and reflects (focal/diffuse) cerebral disturbance.

A

X = frontal release

Diffuse (throughout frontal lobes)

33
Q

Broca’s usually result of (X) affecting (Y) artery territory.

A
X = stroke
Y = MCA
34
Q

(X) aphasia may be accompanied by “pie in the sky” visual field cut.

A

X = Wernicke’s

35
Q

T/F: Wernicke’s aphasia commonly a result of embolic stroke.

A

True

36
Q

(X) aphasia characterized by prominent repetition deficit with relatively normal spontaneous speech/comprehension. Where is the lesion?

A

X = conduction

Arcuate fasciculus (white matter connecting Wernicke’s to Broca’s

37
Q

(X) aphasia characterized by intact repetition with marked reduction in amount/complexity of spontaneous speech. Where is the lesion?

A

X = transcortical

Cortex surrounding Wernicke’s and/or Broca’s

38
Q

Transcortical aphasia: reading comprehension (lost/preserved) and auditory comprehension (lost/preserved).

A

Both relatively preserved

39
Q

T/F: Transcortical sensory aphasia is characterized by impaired auditory comprehension and preserved repetition.

A

True

40
Q

Anomia is inability to (X).

A

X = generate names (common symptom in all forms of aphasia)

41
Q

Alexia with agraphia is seen without aphasia when the lesion is located at:

A

Temporal-parietal region (esp angular gyrus)

42
Q

Alexia without agraphia is seen when the lesion is located at:

A

L (dominant) visual cortex and splenium of CC

43
Q

Alexia without agraphia: which visual defect is present?

A

R homonymous hemianopsia (entire R visual field blank)

44
Q

Alexia without agraphia: patients can see words via (R/L) hemisphere, which reaches (R/L) visual cortex. So why can’t they read?

A

L; R

Can’t cross over (damaged CC splenium) to L cortex (needed to process language)

45
Q

Korsakoff’s syndrome clinical features:

A
  1. Anterograde and “patchy” retrograde amnesia

2. Confabulation

46
Q

T/F: EtOH toxicity directly causes Korsakoff’s.

A

False - vit B deficiency in alcoholics

47
Q

Location of lesions seen in Korsakoff’s syndrome.

A

Diencephalon and frontal lobes (bilateral with atrophy of mammillary bodies)

48
Q

Wernicke’s encephalopathy is associated with (X) deficiency and lesions in (Y).

A
X = thiamine (vit B1)
Y = medial hypothalamus and mammillary bodies
49
Q

Wernicke’s encephalopathy triad:

A
  1. Confusional state
  2. Oculomotor dysfxn
  3. Ataxia
50
Q

What’s apraxia?

A

Inability to perform movement despite intact sensory and motor function

51
Q

What’s agnosia?

A

Failure to recognize/ID stimulus

52
Q

What’s astereognosis?

A

Failure of tactile recognition (associated with parietal lesions of contralateral hemisphere)

53
Q

What’s prosopagnosia?

A

Inability to recognize faces (temporal or occipital lesions, usually bilaterally)