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Neuro > FA Neurology - Anatomy and Physiology > Flashcards

FA Neurology - Anatomy and Physiology Flashcards

1
Q

What are ependymal cells?

A

Inner lining of ventricles, make CSF

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2
Q

What parts of the nervous system come from neuroectoderm?

A

CNS neurons, ependymal cells, oligodendroglia, astrocytes

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3
Q

What parts of the nervous system come from the neural crest?

A

Schwann cells, PNS neurons

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4
Q

What parts of the nervous system come from the mesoderm?

A

Microglia, like Macrophages, original from Mesoderm.

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5
Q

What is Nissl substance and where is it?

A

Nissl substance (RER) in cell body and dendrites but NOT the axon.

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6
Q

What is Wallerian degeneration?

A

Axon injury –> neuron degeneration distally, axonal reaction (cellular swelling, dispersal of Nissl substance) proximally.

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7
Q

What do astrocytes do/?

A

Physical support, repair, potassium metabolism, removal of excess neurotransmitter, maintenance of blood-brain barrier. Reactive gliosis in response to injury. Astrocyte marker - GFAP.

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8
Q

What are microglia? What happens to microglia in HIV?

A

CNS phagocytes. Mesodermal origin. Not readily discernible in Nissl stains. Have small irregular nuclei and relatively little cytoplasm. They are the scavenger cells of the CNS. Respond to tissue damage by differentiating into large phagocytic cells.

HIV-infected microglia fuse to form multi-nucleated giant cells in the CNS.

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9
Q

What is myelin?

A

CNS - oligodendrocytes; PNS - Schwann cells.

Insulates axons: increase space constant and conduction velocity.

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10
Q

How many CNS axons are myelinated by one oligodendocyte?

A

Up to 30!

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11
Q

What do oligodendrocytes look like on H&E and Nissl stains?

A

On H&E, like fried eggs. In Nissl stains, they appear as small nuclei with dark chromatin and little cytoplasm. They are the predominant type of glial cell in white matter.

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12
Q

What types of cells are destroyed in MS?

A

Oligodendrocytes

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13
Q

How many PNS axons are myelinated by Schwann cells?

A

1:1.

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14
Q

What do Schwann cells do?

A

Promote axonal regeneration and increase conduction velocity via saltatory conduction between nodes of Ranvier, where there are a high concentration of Na channels.

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15
Q

What diseases are associated with Schwann cells?

A

Destroyed in Guillain-Barré; Acoustic neuroma is a type of schwannoma that is typically located in the internal acoustic meatis (CNVIII).

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16
Q

Type of fibers in free nerve endings

A

C - slow, unmyelinated fibers; a-delta - fast, myelinated fibers.

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17
Q

Location of free nerve endings

A

All skin, epidermis, and some viscera

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18
Q

What do free nerve endings sense?

A

Pain and temperature

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19
Q

What fibers are in Meissner’s corpuscles?

A

Large, myelinated fibers

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20
Q

Where are Meissner’s corpuscles located?

A

Glabrous (hairless) skin

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21
Q

What do Meissner’s corpuscles sense?

A

Position, dynamic fine touch (e.g. manipulation), adapt quickly.

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22
Q

What type of fibers in Pacinian corpuscles?

A

Large, myelinated

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23
Q

Where are Pacinian corpuscles located?

A

Deep skin layers, ligaments, and joints

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24
Q

What do Pacinian corpuscles sense?

A

Vibration and pressure

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25
Q

What type of fibers in Merkel’s disks?

A

Large, myelinated

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26
Q

Where are Merkel’s disks located?

A

Hair follicles

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27
Q

What do Merkel’s disks sense?

A

Position sense, static touch (e.g., shapes, edges, textures), adapt slowly

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28
Q

What are the layers of the peripheral nerve? What does each layer do?

A

Endoneurium: invests single nerve fiber layers (inflammatory infiltrate in Guilliain Barré
Perineurium (Permeability barrier): surrounds a fascicle of nerve fibers. Must be rejoined in microsurgery for limb reattachment.
Epineurium: dense connective tissue that surrounds entire nerve (fascicles and blood vessels).

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29
Q

Where is norepinephrine synthesized?

A

Locus ceruleus (pons)

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30
Q

Where is dopamine synthesized?

A

Ventral tegmentum and SNc (midbrain)

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31
Q

Where is 5-HT synthesized?

A

Raphe nucleus (pons)

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32
Q

Where is acetylcholine synthesized?

A

Basal nucleus of Meynert

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33
Q

Where is GABA synthesized?

A

Nucleus accumbens (where the caudate and putamen come together)

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34
Q

What is associated with the locus ceruleus?

A

Stress and panic

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35
Q

What is associated with the nucleus accumbens and septal nucleus?

A

Reward center, pleasure, addiction, fear.

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36
Q

How does NE change in disease?

A

increased in anxiety, decreased in depression

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37
Q

How does dopamine change with disease?

A

Increased in schizophrenia, decreased in Parkinson’s and depression

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38
Q

How does 5-HT change with disease?

A

Decreased in both anxiety and depression

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39
Q

How does ACh change with disease?

A

Decreased in Alzheimer’s and Huntington’s. (Increased with REM sleep).

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40
Q

How does GABA change with disease?

A

Decreased in anxiety and Huntington’s

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41
Q

Of what three structures is the blood-brain barrier formed?

A
  1. Tight junctions between non-fenestrated capillary endothelial cells
  2. Basement membrane
  3. Astrocyte processes
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42
Q

What can cross the blood-brain barrier?

A

Non-polar/Lipid soluble substances cross rapidly via diffusion.
Hypothalamic inputs and outputs permeate.
Glucose and amino acids cross slowly by carrier-mediated transport mechanism.
A few specialized brain regions with fenestrated capillaries and no blood brain barrier allow molecules in the blood to affect brain function (e.g., area postrema - vomiting after chemo, OVLT - osmotic sensing) or neurosecretory products to enter circulation (e.g., posterior pituitary - ADH release)

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43
Q

Name three barriers in the body

A
  1. Blood-brain
  2. Blood-testis
  3. Maternal-feltal blood barrier of placenta
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44
Q

What happens if infarction and.or neoplasm destroys the endothelial tight junctions of the BBB?

A

Vasogenic edema

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45
Q

What does the hypothalamus do?

A

The hypothalamus wears TAN HATS!

Thirst and water balance (produces ADH)
Adenohypophysis control
Neurohypophysis releases hormones from H

Hunger
Autonomic regulation
Temperature regulation
Sexual urges

Makes ADH (supraoptic) & oxytocin (paraventricular)

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46
Q

Name two inputs to the hypothalamus (areas not protected by BBB)

A 
OVLT (senses change in osmolarity)
area postrema (responds to emetics)
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47
Q

What part of the hypothalamus makes ADH?

A

The supraoptic nucleus!

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48
Q

What part of the hypothalamus makes oxytocin?

A

Paraventricular nucleus

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49
Q

With what is the lateral nucleus of the hypothalamus associated?

A

Hunger!

Destruction –> anorexia, failure to thrive (infants). Inhibited by leptin.

If you zap your lateral nucleus, you shrink laterally.

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50
Q

With what is the ventromedial nucleus of the hypothalamus associated?

A

Satiety!

Destruction (e.g. craniophayngioma) –> hyperphagia. Stimulated by leptin.

If you zap your ventromedial nucleus, you grow ventrally and medially.

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51
Q

With what is the anterior hypothalamus associated?

A

Cooling (parasympathetic)

Anterior nucleus = cool off. A/C = anterior cooling

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52
Q

With what is the posterior hypothalamus associated?

A

Heating (sympathetic)

Posterios nucleus = get fired up (heating, sympathetic). If you zap your posterior hypothalamus, you become a Poikilotherm (cold-blooded, like a snake).

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53
Q

With what is the suprachiasmatic nucleus of the hypothalamus associated?

A

Circadian rhythm.

You need sleep to be charismatic (chiasmatic).

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54
Q

What does the posterior pituitary (neurohypophysis) do?

A

Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei.

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55
Q

What is the thalamus?

A

It is the major relay for all ascending sensory information except olfaction.

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56
Q

VPL Input, info, and destination

A

Spinothalamic and dorsal columns/medial leminiscus

Pain and temperature; pressure, touch, vibration, and propioception;

primary somatosensory cortex

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57
Q

VPM input, info, and destination

A

Trigeminal and gustatory pathway

Face sensation and taste
(Makeup goes on the face!)

Primary somatosensory cortex

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58
Q

LGN input, info, and destination

A

CN II

Vision

Calcarine sulcus

Lateral = Light! (LGN for vision)

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59
Q

MGN input, info, and destination

A

Superior olive and inferior colliculus of tectum

Hearing

Auditory cortex of temporal lobe

Medial = Music! (MGN for hearing)

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60
Q

To what part of the thalamus does AL and DC information go?

A

VPL

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61
Q

To what part of the thalamus does Trigeminal and gustatory pathway (face sensation and taste) go?

A

VPM

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62
Q

To what part of the thalamus does vision go?

A

LGN (Lateral geniculate nucleus)

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63
Q

To what part of the thalamus does hearing go?

A

MGN (medial geniculate nucleus)

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64
Q

To what part of the thalamus does the spinothalamic tract go?

A

VPL (Ventral posterolateral nucleus)

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65
Q

To what part of the thalamus does the trigeminal nerve go?

A

VPM (Ventral posteromedial nucleus)

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66
Q

To what part of the thalamus does the dorsal column go?

A

VPL

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67
Q

To what part of the thalamus does the gustatory pathway go?

A

VPM

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68
Q

Where is the auditory cortex?

A

Temporal lobe

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69
Q

Where is the primary visual cortex concentrated?

A

Calcarine sulcus of the occipital lobe

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70
Q

Trace the route of the spinothalamic through the thalamus and cerebrum

A

VPL –> primary somatosensory cortex (postcentral gyrus of the parietal lobe)

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71
Q

Trace the route of the trigeminal through the thalamus and cerebrum

A

VPM –> primary somatosensory cortex

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72
Q

What is the limbic system?

A

Includes cingulate gyrus, hippocampus, fornix, mammillary bodies, and septal nucleus

Responsible for the 5Fs: feeding, fleeing, fighting, feeling, and sex

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73
Q

What does the lateral cerebellum do?

A

Voluntary movement of extremities

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74
Q

What does the medial cerebellum do?

A

Balance, truncal coordination, ataxia; when injured, propensity to fall toward injured (ipsalateral) side.

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75
Q

If someone starts falling to his left, what might you suspect?

A

Injury in the LEFT medial cerebellum

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76
Q

If someone starts falling to her right, what might you suspect?

A

Injury to the RIGHT medial cerebellum

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77
Q

What are the deep nuclei of the cerebellum?

A

From lateral to medial, Don’t Eat Greasy Foods.

Dentate,
Emboliform,
Globose,
Fastigial

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78
Q

The cerebellum receives contralateral cortical input via WHAT?

A

The middle cerebellar peduncle

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79
Q

The cerebellum receives ipsilateral proprioceptive information via WHAT?

A

The inferior cerebellar peduncle

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80
Q

What are the input nerves to the cerebellum?

A

Climbing and mossy fibers (WHAT?)

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81
Q

What kind of input does the cerebellum receive from the MIDDLE cerebellar peduncle?

A

Contralateral cortical input

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82
Q

What kind of input does the cerebellum receive from the INFERIOR cerebellar peduncle?

A

Ipsilateral proprioceptive input

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83
Q

Name the two types of input that the cerebellum receives

A

Contralateral cortical and ipsilateral proprioceptive

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84
Q

To modulate movement, the cerebellum provides stimulatory feedback to the XXXX cortex.

A

CONTRAlateral

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85
Q

What does the cerebellum do?

A

Provides stimulatory feedback to contralateral cortex to modulate movement

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86
Q

If you injure your medial cerebellum, you fall towards the XXXXX (same or opposite) side of the body as the injury.

A

Same

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87
Q

What are the output nerves of the cerebellum?

A

Purkinje fibers output to deep nuclei of cerebellum, which in turn output to cortex via SUPERIOR cerebellar peduncle.

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88
Q

What is going through the superior, middle, and inferior cerebellar peduncles?

A

Superior (OUTPUT): Purkinje fibers deep nuclei to cortex

Middle (INPUT): Contralateral cortical input

Inferior (INPUT): ipsilateral proprioceptive input

89
Q

What does the basal ganglia do?

A

Important in voluntary movements and making postural adjustments

Receives cortical input, provides negative feedback to cortex to modulate movement

90
Q

The cerebellum provides XXX feedback to the cortex to modulate movement.

The basal ganglia provides XXX feedback to the cortex to modulate movement.

A

Stimulatory (to contralateral)

Negative (to WHAT SIDE?)

91
Q

Striatum = ?

A

The putamen (motor) and the caudate (cognitive)

92
Q

Lentiform = ?

A

Putamen (motor) + globus pallidus (???)

93
Q

What is the excitatory pathway of the basal ganglia?

A

Cortical inputs stimulate the striatum, stimulating the release of ACh, which disinhibits the thalamus via the GPi (globus pallidus internus)/SNc (sunstantia nigra pars compacta) (INCREASES motion)

94
Q

What neurotransmitter is part of the excitatory pathway of the basal ganglia?

A

GABA = inhibitory and Glutamate = excitatory

95
Q

What is the inhibitory pathway of the basal ganglia?

A

Cortical inputs stimulate the striatum, which disinhibits the STN (subthalamic nucleus) via GPe (globus pallidus externus), and then STN stimulates the globus pallidus internus (GPi) to inhibit the thalamus (DECREASES motion)

96
Q

What is the role of dopamine in the basal ganglia?

A

Dopamine binds to D1, stimulating the excitatory pathway, and to D2, inhibiting the inhibitory pathway. Both of these work to INCREASE motion.

97
Q

What happens when dopamine binds to D1?

A

Stimulates the excitatory pathway –> increased motion

98
Q

What happens when dopamine binds to D2?

A

Inhibits the inhibitory pathway –> increasid motion

99
Q

What is Parkinson’s disease?

A

Degenerative disorder of CNS associated with Lewy bodies (composed of alpha-synclein - intracellular inclusion) and loss of dopaminergic neurons (i.e. depigmentation) of the substantia nigra pars compacta

TRAP (you are TRAPped in your body)

Tremor (at rest, e.g., pill-rolling tremor)
cogwheel Rigidity
Akinesia
Postural instability

100
Q

Lewy bodies are associated with what disease?

A

Parkinson’s

101
Q

What are Lewy bodies?

A

Intracellular inclusions composed of alpha-synuclein that are associated with Parkinson’s

102
Q

Depigmentation of the substantia nigra is associated with what disease?

A

Parkinson’s

103
Q

What type of neurons in the substantia nigra are lost in Parkinson’s?

A

Dopaminergic

104
Q

What neurotransmitter is affected in Parkinson’s?

A

Dopamine

105
Q

What are the symptoms of Parkinson’s?

A

TRAP (you are TRAPped in your body)

Tremor (at rest, e.g., pill-rolling tremor)
cogwheel Rigidity
Akinesia
Postural instability

106
Q

Tremor at rest makes you think …

A

Parkinson;s

107
Q

Postural instability makes you think …

A

Parkinson’s

108
Q

Cogwheel rigidity makes you think …

A

Parkinson’s. Cogwheel rigidity is increased tension in the extensors of a joint when it is passively flexed, giving way suddenly on exertion of further pressure.

109
Q

What should you think when you see increased tension in the extensors of a joint when it is passively flexed, giving way suddenly on exertion of further pressure.

A

Parkinson’s (Cogwheel rigidity)

110
Q

Sudden, wild flailing of ONE arm +/- ONE leg makes you think?

A

Hemiballismus

111
Q

What is hemiballismus?

A

Half ballistic, as in throwing a baseball.

Hemiballismus, sometimes called ballism, is a very rare movement disorder, classified by a decrease in activity of the subthalamic nucleus of the basal ganglia, resulting in decreased suppression of undesired movements.

Caused by loss of inhibition of thalamus through the globus pallidus.

112
Q

What causes hemiballismus?

A

Contralateral subthalamic nucleus lesion (e.g., lacunar stroke in a patient with a history of hypertension) –> loss of inhibition of thalamus through globus pallidus.

113
Q

Hemiballismus might result from a subthalamic nucleus lesion on the XXX side as the flailing arm.

A

OPPOSITE (contralateral)

114
Q

Lacunar stroke in a patient with a history of HTN might cause …?

A

Hemiballismus

115
Q

Loss of inhibition of the thalamus through the WHAT might cause hemiballismus?

A

Globus pallidus

116
Q

With Parkinson’s, what gross changes in morphology could you see?

A

Depigmentation of the substantia nigra (on autopsy I presume - check)

117
Q

With Huntington’s, what gross changes in morphology could you see on imaging?

A

Atrophy of striatal nuclei (main inhibitors of movement)

118
Q

Chorea is characteristic of a lesion where?

A

In the basal ganglia

119
Q

What is chorea?

A

Sudden, jerky, purposeless movement. Characteristic of basal ganglia lesion (e.g., Huntington’s).

Chorea = dancing (Greek). Think choreography.

120
Q

What is athetosis?

A

Slow, writhing movements, especially of fingers. Characteristic of basal ganglia lesion (e.g., Huntington’s).

Athetos = not fixed (Greek). Think snake-like.

121
Q

Chorea makes you think …

A

Huntington’s

122
Q

Athetosis makes you think …

A

Huntington’s

123
Q

Sudden, jerky, purposeless movements are called …

A

chorea

124
Q

Slow, writhing movements, especially of the fingers are called …

A

athetosis

125
Q

Sudden, brief muscle contraction, like a jerks or hiccups, are called …

A

Myoclonus

126
Q

Sustained, involuntary muscle contractions,, like writer’s cramp or blepharospasm are called …

A

Dystonia

127
Q

How do you treat an essential tremor?

A

Beta-blockers

128
Q

Intention tremor is associated with …

A

Cerebellar dysfunction

129
Q

What is the genetic cause of Huntington’s?

A

Expansion of CAG repeats (anticipation). It is autosomal dominant.

CAG: Caudate loses ACh and Gaba.

130
Q

What are the symptoms of Huntington’s?

A

Chorea, aggression, depression, and dementia. It is sometimes initially mistake for substance abuse.

131
Q

What molecular changes underlie the symptoms of Huntington’s?

A

Neuronal death via NMDA-R binding and glutamate toxicity –> atrophy of striatal nuclei.

132
Q

The caudate loses what neurotransmitters in Huntington’s?

A

CAG: Caudate loses ACh and GABA.

133
Q

Neuronal death via NMDA-R binding and glutamate toxicity causes …

A

Huntington’s.

134
Q

What is Huntington’s?

A

An autosomal-dominant trinucleotide repeat disorder.

135
Q

Jerks and hiccups are more formally called …

A

myoclonus

136
Q

Writer’s cramp and blepharospasm are more formally called …

A

Dystonia

137
Q

What is myoclonus?

A

Sudden, brief muscle contraction

138
Q

What is dystonia?

A

Sustained, involuntary muscle contractions

139
Q

An essential/posteral tremor is an action tremor that worsens when …

A

holding posture.

140
Q

An essential/posteral tremor is …

A

an action tremor that worsens when holding posture. It is autosomal dominant (often with positive family history). Essential tremor patients often self-medicate with alcohol, which decreases tremors. You should treat it with beta-blockers.

141
Q

A resting tremor is most noticeable …

A

distally.

142
Q

Resting tremor makes you think …

A

Parkinson’s.

143
Q

What is an intention tremor?

A

Slow, zigzag motion when pointing toward a target; associated with cerebellar dysfunction.

144
Q

What do you call a slow, zigzag motion when pointing towards a target?

A

Intention tremor

145
Q

What do you call a tremor that worsens when holding posture?

A

Action/essential/postural tremor

146
Q

What do you call a tremor at rest, like a pill-rolling tremor?

A

Resting tremor

147
Q

Name three types of tremors.

A

Action, Resting, Intention

148
Q

Lower extremity deficit in sensation or movement may indicate involvement of what artery?

A

Anterior cerebral.

149
Q

Patient presents with hypersexuality, disinhibited behavior, and hyperorality

A

Kluver-Bucy syndrome (lesion on the amydala). Note: Associated with HSV-1.

150
Q

Patient presents with disinhibition and deficits in concentration, orientation, and judgement and may have the reemergence of primitive reflexes.

A

Lesion in the frontal lobe.

151
Q

The patient only dresses half of his body (or paints half of a self-portrait). You think …

A

Parietal lobe lesion, which causes spatial neglect syndrome (agnosia of the contralateral side of the world). Note: lesion in RIGHT parietal lobe causing LEFT-sided neglect is more common.

Hemispatial neglect results most commonly from brain injury to the right cerebral hemisphere, causing visual neglect of the left-hand side of space. Right-sided spatial neglect is rare because there is redundant processing of the right space by both the left and right cerebral hemispheres, whereas in most left-dominant brains the left space is only processed by the right cerebral hemisphere.

152
Q

Patient is in a coma. It might be damage to the …

A

Midbrain (reticular activating system).

153
Q

Patient presents with confusion and confabulation.

A

Wernicke-Korsakoff syndrome resulting from lesion in the mamillary bodies (bilateral).

154
Q

What is Wernicke-Korsakoff syndrome?

A 
Wernicke = confusion + ophthalmoplegia + ataxia
(ophthalmoplegia = weakness in 1 or more extra-ocular muscles).

Korsakoff = memory loss + confabulation + personality changes.

155
Q

Patient presents with tremor at rest, chorea, or athetosis. It could be a lesion in the …

A

Basal ganglia

156
Q

The patient presents with intention tremor or limb ataxia. It could be a lesion in the …

A

Cerebellar hemisphere.

157
Q

The patient falls to the right.

A

Lesion in the right cerebellar hemisphere.

Cerebellar hemispheres are LATERALLY located, so they affect LATERAL limbs.

Cerebellum –> SCP –> contralateral cortex –> corticospinal decussation = ipsilateral

158
Q

The patient has right limb ataxia.

A

Lesion in the right cerebellar hemisphere.

159
Q

Why does cerebellar injury result in ipsilateral deficit?

A

Cerebellum –> SCP –> contralateral cortex –> corticospinal decussation = ipsilateral

160
Q

The patient presents with truncal ataxia and dysarthria.

A

Lesion in the cerebellar vermis.

The vermis is CENTRALLY located, so it affects CENTRAL body.

161
Q

The patient presents with right hemiballismus

A

Damage to left subthalamic nucleus.

162
Q

The patient can’t make new memories.

A

Anteroretrograde amnesia could be caused by a lesion in the hippocampus.

163
Q

The patient keeps looking to the right.

A

It could be a lesion in the LEFT paramedian pontine reticular formation (PPRF, eyes look away from side of the lesion) or a lesion in the RIGHT frontal eye field (eyes look towards the lesion).

164
Q

What happens if you have a lesion in the amygdala?

A

Hyperorality, hypersexuality, dishinitbted behavior (Kluver-Bucy syndrom, associated with HSV-1)

165
Q

What happens if you have a lesion in the frontal lobe?

A

Disinhibition and deficits in concentration, orientation,and judgement; may have reemergence of the primitive reflexes.

166
Q

Differential for disinhibition.

A

Frontal lobe lesion, amygdala lesion, substance use/abuse, psychiatric diagnosis, (CNS syphilis –> damage to XXX lobe), Alzheimer’s, other dementia, progressive supranuclear palsy.

167
Q

What happens if you have a lesion in the right parietal lobe?

A

Left sided neglect

168
Q

What happens if you have a lesion in the reticular activating system (midbrain)?

A

Reduced levels of arousal and wakefulness, e.g., coma

169
Q

What happens if you have a lesion in the mammillary bodies?

A

Wernicke-Korsakoff

170
Q

What happens if you have a lesion in the basal ganglia?

A

Chorea, tremor at rest, athetosis.

171
Q

What happens if you have a lesion in the right cerebellar hemisphere?

A

intention tremor,right limb ataxia (fall to right)

172
Q

What happens if you have a lesion in the cerebellar vermis?

A

Truncal ataxia and dysarthria

173
Q

What happens if you have a lesion in the LEFT subthalamic nucleus?

A

RIGHT hemballismus

174
Q

What happens if you have a lesion in the hippocampus?

A

Anteroretrograde amnesia.

175
Q

What happens if you have a lesion in the paramedian pontine reticular formation (PPRF)?

A

Eyes look away from the side of the lesion.

176
Q

What happens if you have a lesion in the frontal eye fields?

A

Eyes look towards the lesion.

177
Q

Rapid correction of hyponatremia can cause …

A

Central pontine myelinolysis

178
Q

Patient presents with acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness.

A

Central pontine myelinolysis (abnormal increased signal in the pons)

179
Q

Symptoms of central pontine myelinolysis

A

Acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness.

180
Q

What is Broca’s aphasia?

A

Nonfluent aphasia with intact comprehension. Broca’s area is in the inferior frontal gyrus.

Broca’s Boken Boca: person can understand but can’t speak

181
Q

What is aphasia?

What is dysarthria?

A

Higher-order inability to speak.

Motor inability to speak.

182
Q

What do you call a motor inability to speak?

A

Dysarthria

183
Q

What is Wernicke’s aphasia?

A

Fluent aphasia with impaired comprehension. Wernicke’s area is in the superior temporal gyrus.

Wernicke’s is Wordy but makes no sense. Wernicke’s = what?

184
Q

What is global aphasia?

A

Nonfluent aphasia with impaired comprehension. Both Broca’s and Wernicke’s areas affect.

185
Q

What is conduction aphasia?

A

Poor repetition but fluent speech, intact comprehension. Arcuate fascicles - connects Broca’s, Wernicke’s areas.

Can’t repeat phases such as, “No ifs, ands, or buts.”

186
Q

What is supplied by the anterior cerebral artery?

A

Anteromedial surface of the brain.

Specifically, motor and sensory lower limb.

187
Q

What is supplied by the middle cerebral artery?

A

The lateral surface of the brain.

Specifically, motor and sensory upper limb and face, as well as Wernicke’s and Broca’s areas.

188
Q

What is supplied by the posterior cerebral artery?

A

The posterior and inferior superior surface of the brain.

Specifically, occipital and visual cortex.

189
Q

Where are the watershed zones in the brain? What happens if you have severe hypotension?

A

Between ACA/MCA and PCA/MCA.

Damage in severe hypotension –> upper leg/upper arm weakness, defects in higher-order visual processing.

190
Q

Patient presents with upper leg/upper arm weakness and defects in higher-order visual processing.

A

It could be damage to watershed zones caused by severe hypotension.

191
Q

How is cerebral perfusion regulated?

A

Normally driven by PCO2, but also by PO2 with severe hypoxia.

Therapeutic hyperventilation (decrease PCO2) helps decrease ICP in cases of acute cerebral edema (stroke, trauma).

192
Q

What helps decrease ICP in cases of acute cerebral edema (stroke, trauma)?

A

Therapeutic hyperventilation (decrease PCO2)

193
Q

What supplies the anterior circulation? What is the anterior circulation composed of?

A

Internal carotid.

ACA, lateral striate, MCA

194
Q

What supplies the posterior circulation? What is the posterior circulation composed of?

A

Subclavian

AICA, PICA, anterior spinal artery (ASA), basilar, vertebral, PCA

195
Q

What are the symptoms of a stroke in the MCA?

A

Contralateral paralysis and/or loss of sensation in the arm and/or face. Hemineglect if lesion affects nondominant (usually right) side.

196
Q

What are the symptoms of a stroke in the ACA?

A

Contralateral paralysis and/or loss of sensation in contralateral leg.

197
Q

What are the symptoms of a stroke in the lateral striate artery?

A

Contralateral hemiparesis/hemiplegia.

Note that is is a common location of lacunar infarcts secondary to unmanaged HTN.

198
Q

What are the symptoms of a stroke in the anterior spinal artery?

A

Contralateral hemiparesis of the lower limbs. Decreased contralateral proprioception
Ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally).

199
Q

What are the symptoms of a stroke in PICA?

A

Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia).

Vomiting, vertigo, nystagmus.
Decreased pain and temperature sensation in the limbs and face.
Dysphagia, hoarseness, and decreased gag reflex.
Ipsilateral Horner’s syndrome
Ataxia, dysmetria.

200
Q

What are the symptoms of a stroke in AICA?

A

Facial droop means AICA’s pooped.

Vomiting, vertigo, nystagmus.
Paralysis of face,
Decreased lacrimation, salivation, taste from anterior two-thrids of tongue, corneal reflex.
Decreased pain and temperature sensation in the face and ipsilateral hearing loss. Ipsilateral Horner’s syndrome.

201
Q

What are the symptoms of a stroke in the PCA?

A

Contralateral hemianopsia with macular sparing.

202
Q

What happens if you have an aneurysm in AComm?

A

Visual field defects

203
Q

What happens with a berry aneurysm in PComm?

A

Third nerve palsy (only SO and LR work), so the eye is down and out.

204
Q

Berry aneurysms occur at the bifurcations in the circle of Willis. What is the most common site?

A

The bifurcation of the anterior communicating after.

205
Q

What is the most common complication of berry aneurysm in the anterior communicating?

A

Rupture leads to hemorrhagic stroke.subarachnoid hemorrhage.

206
Q

With what diseases is berry aneurysm associated?

What are the other risk factors?

A

ADPKD, Ehlers-Danlos, and Marfan’s

Advanced age, HTN, smoking, race (higher in blacks)

207
Q

What are Charcot-Bouchard microaneurysms?

A

Associated with chronic HTN, affects small vessels (e.g. in the basal ganglia or thalamus)

208
Q

Epidermal hematoma is caused by rupture of the …

A

middle meningeal artery (branch of maxillary), often secondary to fracture of the temporal bone.

209
Q

Rupture of the middle meningeal artery causes ..

A

Epidermal hematoma

210
Q

Subdural hematoma is caused by rupture of the …

A

bridging veins.

211
Q

Rupture of the bridging veins causes …

A

subdural hematoma.

212
Q

Subarachoid hemorrhage is caused by rupture of an aneurysm OR …

A

An AVM (arteriovenous malformation)

213
Q

What kind of aneurysm is most commonly associated with subarachnoid hemorrhage?

A

Berry aneurysm in Marfan’s, Ehlers-Danlos, ADPKD

214
Q

What happens in an epidural hematoma?

A

there’s a lucid interval, then rapid expansion under systemic arterial pressure –> transtentorial herniation, third nerve palsy (eye down and out).
CT shows biconvex disk not crossing suture lines. it can cross falx and tenorium.

215
Q

What happens in a subdural hematoma?

A

Slow venous bleeding –> crescent-shaped hemorrhage that crosses suture lines. Midline shift. Gyri are presrved, since pressure is distributed equally. Cannot cross falx or tentorium.

216
Q

Subdural hematoma is seen most commonly in:

A

elderly, alcoholics, blunt trauma, shaken baby (pre-disposing factors – brain atrophy, shaking, whiplash.

217
Q

What is the bbb for?

A

Helps prevent bacterial infxn from spreading to brain. (Also restricts drug delivery to brain.)

218
Q

What area is associated with vomiting after chemo?

A

Area postrema (roof of fourth ventricle)

219
Q

Name examples of specialized brain regions with fenestrated capillaries and no bbb.

A

Area postrema & OVLT

Neuro (14 decks)

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