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USMLE1 - Neurology > 1. Anatomy and Physiology > Flashcards

1. Anatomy and Physiology Flashcards

1
Q

CNS/PNS origins: Neuroectoderm (gives rise to what?)

A

CNS neurons Ependymal cells (inner lining of ventricles, make CSF) Oligodendrocytes Astrocytes

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2
Q

CNS/PNS origins: Neural Crest (gives rise to what?)

A

Schwann cells PNS neurons

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3
Q

CNS/PNS origins: Mesoderm (gives rise to what?)

A

M icroglia, like M acrophages, originate from M esoderm

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4
Q

Neurons: location, division and morphology

A

Comprise nervous system. Permanent cells – do not divide in adulthood. Large cells w/ prominent nucleoli.

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5
Q

Nissl substance. What are they and were do you find them?

A

RER found in cell body and dendrites, but not axon of neurons.

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6
Q

Astrocytes. What are their functions? What happen if they are injured?

A

Physical support, repair, K+ metabolism, removal of excess NT. Maintenance of BBB. Reactive gliosis in response to injury.

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7
Q

Astrocyte marker?

A

GFAP

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8
Q

Microglia. What are they and what are their origins? Can you Nissle stain them? Morphology?

A

CNS phagocytes. Mesodermal origin. Not readily discernible in Nissle stains. Have small, irregular nuclei and relatively little cytoplasm.

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9
Q

What happens to microglia in the presence of tissue damage?

A

Microglia –(tissue damage)–> differentiate into large ameboid phagocytic cells

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10
Q

What happens to HIV-infected microglia?

A

HIV-infected microglia fuse to form multinucleated giant cells in the CNS

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11
Q

Oligodendria. What are they and what do they do? Can you nissle stain them? Morphology?

A

Each oligodendrocyte myelinates multiple CNS axons (up to 30 each). In Nissle stains, they appear as small nuclei with dark chromatin and little cytoplasm.

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12
Q

What is the predominant type of glial cell in white matter?

A

Oligodendrocytes.

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13
Q

What cells are destroyed in multiple sclerosis?

A

Oligodendrocytes.

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14
Q

What do oligodendrocytes look like on H&E?

A

Fried Eggs

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15
Q

Schwann cells. Where are they and what do they do? What are they derived from?

A

Each Schwann cell myelinates only 1 PNS axon. Also promote axonal regeneration. Derived from neural crest.

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16
Q

What are the cells that are destroyed in Guillain-Barré syndrome?

A

Schwann cells.

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17
Q

An acoustic neuroma is a type of…? Where is it located?

A

Acoustic neuroma is a type of Schwannoma. It is typically located in internal acoustic meatus (CN VIII)

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18
Q

Sensory receptors/corpuscles: Free nerve endings (C, A-delta fibers) Location? Senses?

A

In all skin, epidermis, some viscera. Senses pain and temperature.

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19
Q

Sensory receptors/corpuscles (location and senses): In all skin, epidermis, some viscera. Senses pain and temperature. Which is this?

A

Free nerve endings (C, A-delta fibers)

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20
Q

Sensory receptors/corpuscles: Meissner’s corpuscles Location? Senses?

A

In glabrous (hairless) skin. Senses dynamic fine touch (e.g., manipulation), adapt quickly.

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21
Q

Sensory receptors/corpuscles (location and senses): In glabrous (hairless) skin. Senses dynamic fine touch (e.g., manipulation), adapt quickly. Which is this?

A

Meissner’s corpuscles

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22
Q

Sensory receptors/corpuscles: Pacinian corpuscles Location? Senses?

A

In deep skin layers, ligaments, and joints. Sense vibration, pressure.

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23
Q

Sensory receptors/corpuscles (location and senses): In deep skin layers, ligaments, and joints. Sense vibration, pressure. Which is this?

A

Pacinian corpuscles

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24
Q

Sensory receptors/corpuscles: Merkel’s disks Location? Senses?

A

(cup-shaped, unencapsulated) In hair follicles. Sense static touch (e.g., shapes, edges, textures), adapt slowly.

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25
Q

Sensory receptors/corpuscles (location and senses): (cup-shaped, unencapsulated) In hair follicles. Sense static touch (e.g., shapes, edges, textures), adapt slowly. Which is this?

A

Merkel’s disks

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26
Q

Peripheral nerve layers: Endoneurium

A

Invests a single nerve fiber (Endo = inner)

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27
Q

Peripheral nerve layers: Perineurium

A

(P erineurium is the P ermeability barrier) Surrounds a fascicle of nerve fibers. (Peri = around) Must be rejoined in microsurgery for limb reattachment.

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28
Q

Peripheral nerve layers: Epineurium

A

Dense connective tissue that surrounds entire nerve (fasicles and blood vessels) (Epi = outer)

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29
Q

Neurotransmitters: NE Change in dz? Location of synthesis?

A

Increased in anxiety, decreased in depression. Made in the locus ceruleus.

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30
Q

Increased in anxiety, decreased in depression. Made in the locus ceruleus. What NT is this?

A

NE

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31
Q

Neurotransmitters: Dopamine Change in dz? Location of synthesis?

A

Increased in schizophrenia, decreased in Parkinson’s. Made in the ventral tegmentum and SNc

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32
Q

Increased in schizophrenia, decreased in Parkinson’s. Made in the ventral tegmentum and SNc What NT is this?

A

Dopamine

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33
Q

Neurotransmitters: 5-HT Change in dz? Location of synthesis?

A

Decreased in anxiety, depression. Made in the raphe nucleus

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34
Q

Decreased in anxiety, depression. Made in the raphe nucleus What NT is this?

A

5-HT

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35
Q

Neurotransmitters: ACh Change in dz? Location of synthesis?

A

Decreased in Alzheimer’s, Huntington’s. Made in the basal nucleus of Meynert. Upregulated in REM sleep

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36
Q

Decreased in Alzheimer’s, Huntington’s. Made in the basal nucleus of Meynert. What NT is this?

A

ACh

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37
Q

Neurotransmitters: GABA Change in dz? Location of synthesis?

A

Decreased in anxiety, Huntington’s. Made in nucleus accumbens.

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38
Q

What 3 structures form the blood-brain barrier (BBB)?

A

1.) Tight junctions btw nonfenestrated capillary endothelial cells 2.) Basement membrane 3.) Astrocyte processes

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39
Q

Besides the BBB, what are 2 similar barriers?

A

1.) Blood-testis barrier 2.) Maternal-fetal blood barrier of placenta

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40
Q

What happens at the BBB w/ infarction?

A

Infarction destroys endothelial cell tight junctions, leading to vasogenic edema

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41
Q

How do glucose and amino acids cross the BBB?

A

Cross slowly by carrier-mediated transport mechanism.

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42
Q

How do nonpolar/lipid-soluble substances cross the BBB?

A

Cross rapidly via diffusion.

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43
Q

What is the function of specialized brain regions w/ fenestrated capillaries and no BBB?

A

Allow molecules in the blood to affect brain function (e.g., area postrema - vomiting center after chemo, OVLT - osmotic sensing) or neurosecretory products to enter circulation (e.g., neurohypophysis - ADH release)

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44
Q

Hypothalamus functions

A

The hypothalamus wears TAN HATS : T-hirst and water balance A-denohypophysis control N-eurohypophysis releases hormones from hypothalamus H-unger A-utonomic regulation T-emperature regulation S-exual urges

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45
Q

Inputs to the hypothalamus

A

OVLT (senses change in osmolarity) Area postrema (responds to emetics)

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46
Q

Supraoptic nucleus of the hypothalamus

A

Area that makes ADH.

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47
Q

Area that makes ADH.

A

Supraoptic nucleus of the hypothalamus

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48
Q

Paraventricular nucleus of the hypothalamus

A

Area that makes oxytocin.

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49
Q

Area that makes oxytocin.

A

Paraventricular nucleus of the hypothalamus

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50
Q

Lateral area of the hypothalamus

A

Controls hunger: destruction leads to anorexia. (“If you zap the lateral nucleus, you shrink laterally “) Inhibited by leptin.

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51
Q

Ventromedial area of the hypothalamus

A

Controls satiety: destruction leads to hyperphagia. (“If you zap your ventromedial nucleus, you grow ventrally and medially .”) Stimulated by leptin.

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52
Q

Anterior hypothalamus

A

Cooling (Anterior = cooling, or A/C). A nterior is pA rasympathetic.

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53
Q

Posterior hypothalamus

A

Heating (posterior = get fired up / heating). Sympathetic. If you zap your P osterior hypothalamus, you become a P oikilotherm (cold-blooded, like a snake)

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54
Q

Septal nucleus of the hypothalamus

A

area responsible for sexual urges

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55
Q

area responsible for sexual urges

A

Septal nucleus of the hypothalamus

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56
Q

Suprachiasmatic nucleus of the hypothalamus

A

Circadian rhythm. (“You need to sleep to be charismatic [chiasmatic]”).

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57
Q

Posterior pituitary (neurohypophysis)

A

Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei. Oxytocin: oxys = quick; tocos = birth.

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58
Q

Anterior pituitary aka…?

A

A nterior pituitary = A denohypophysis

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59
Q

What is the main function of the thalamus?

A

Major relay for ascending sensory information that ultimately reaches the cortex.

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60
Q

Blood supply to the thalamus

A

posterior communicating, posterior cerebral, and anterior choroidal arteries.

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61
Q

Lateral geniculate nucleus (LGN) of thalamus

A

(hint: “L ateral for L ight”) area of thalamus for visual information.

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62
Q

area of thalamus for visual information.

A

Lateral geniculate nucleus (LGN) of thalamus (hint: “L ateral for L ight”)

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63
Q

Medial geniculate nucleus (MGN) of the thalamus

A

(hint: M edial for M usic) Area of the thalamus responsible for auditory information

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64
Q

Area of the thalamus responsible for auditory information

A

Medial geniculate nucleus (MGN) of the thalamus (hint: M edial for M usic)

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65
Q

Ventral posterior nucleus, lateral part (VPL) – of thalamus

A

part of the thalamus responsible for body sensation (proprioception, pressure, pain, touch, vibration via dorsal columns, spinothalamic tract).

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66
Q

part of the thalamus responsible for body sensation (proprioception, pressure, pain, touch, vibration via dorsal columns, spinothalamic tract).

A

Ventral posterior nucleus, lateral part (VPL) – of thalamus

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67
Q

Ventral posterior nucleus, medial part (VPM) – of the thalamus

A

(hint: you put M akeup on your face, and sensory info is relayed through the VPM ) Area of thalamus responsible for facial sensation (via CN V)

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68
Q

Area of thalamus responsible for facial sensation (via CN V)

A

Ventral posterior nucleus, medial part (VPM) – of the thalamus (hint: you put M akeup on your face, and sensory info is relayed through the VPM )

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69
Q

Motor and sensory locations in the thalamus

A

Motor is anterior to sensation in the thalamus, just like the cortex.

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70
Q

Limbic system: Includes what? Responsible for what?

A

Includes cingulate gyrus, hippocampus, fornix, and mammillary bodies. Responsible for F eeding, F leeing, F ighting, F eeling, and sex (….) (The famous 5 F’s )

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71
Q

Input to the cerebellum

A

Receives contralateral cortical input via middle cerebellar peduncle and ipsilateral proprioceptive information via inferior cerebellar peduncle. Input nerves = climbing and mossy fibers.

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72
Q

Output from the cerebellum

A

Provides stimulatory feedback to contralateral cortex to modulate movement. Output nerves = Purkinje fibers output deep to nuclei of cerebellum, which in turn output to cortex via superior cerebellar peduncle.

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73
Q

Deep nuclei of the cerebellum

A

Lateral to medial: D entate, E mboliform, G lobose, F astigial (“D on’t E at G reasy F oods”)

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74
Q

Lateral cerebellum

A

area of the cerebellum responsible for voluntary movement of extremities

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75
Q

area of the cerebellum responsible for voluntary movement of extremities

A

Lateral cerebellum

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76
Q

Medial cerebellum

A

Area of cerebellum responsible for balance, truncal coordination.

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77
Q

Area of cerebellum responsible for balance, truncal coordination.

A

Medial cerebellum

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78
Q

Basal ganglia (overall function)

A

Important in voluntary movements and making postural adjustments. Receives cortical input, provides negative feedback to cortex to modulate movement.

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79
Q

Important in voluntary movements and making postural adjustments. Receives cortical input, provides negative feedback to cortex to modulate movement.

A

Basal ganglia (overall function)

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80
Q

Excitatory pathway of the basal ganglia

A

Substantia Nigra pars compacta’s (SNc’s) dopamine binds to D1 receptros in the excitatory pathway, stimulating the excitatory pathway (incr motion). Therefore, loss of dopamine in Parkinson’s inhibits the excitatory pathway (decr motion).

Cortex ->(+) Caudate/Putamen -> (-) GPi -> (-) VA/VL thalamus -> (+) Cortex

Key: Grey = stimulatory || Black = inhibitory SNc = Substantia nigra pars compacta GPe = Globus pallidus externus GPi = Globus pallidus internus STN = Subthalamaic nucleus D1 = Dopamine D1 receptor (excitatory) D2 = Dopamine D2 receptor (inhibitory)

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81
Q

Inhibitory pathway of the basal ganglia

A

SNc’s dopamine binds to D2 receptros in the inhibitory pathway, inhibiting the inhibitory pathway (incr motion). Therefore, loss of dopamine in Parkinson’s dz excites (i.e., disinhibits) the inhibitory pathway (decr motion).

Cortex -> (+) Caudate/Putamen -> (-) GPe/subthalamic nucleus -> (-) GPi -> (-) VA/VL thalamus -> (+) Cortex

Key: Grey = stimulatory || Black = inhibitory SNc = Substantia nigra pars compacta GPe = Globus pallidus externus GPi = Globus pallidus internus STN = Subthalamaic nucleus D1 = Dopamine D1 receptor (excitatory) D2 = Dopamine D2 receptor (inhibitory)

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82
Q

Parkinson’s disease. Clinical Presentation, Histologic findings, Drug-related

A

Degenerative disorder of CNS associated w/ Lewy bodies (composed of alpha-synuclein) and depigmentation of the substantia nigra pars compacta (loss of dopaminergic neurons).

Rare cases have been linked to exposure to MPTP, a contaminant in illicit street drugs.

(“TRaP = T remor (at rest), cogwheel Rigidity, a nd Postural instability. You are TRaPped inside your body.”)

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83
Q

Degenerative disorder of CNS associated w/ Lewy bodies (composed of alpha-synuclein) and depigmentation of the substantia nigra pars compacta (loss of dopaminergic neurons). Rare cases have been linked to exposure to MPTP, a contaminant in illicit street drugs. (“TRaP = T remor (at rest), cogwheel R igidity, a nd P ostural instability. You are TRaP ped inside your body.”)

A

Parkinson’s disease

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84
Q

Hemiballismus. Classic Presentation, Etiology

A

Sudden, wild flailing of 1 arm. Characteristic of contralateral subthalamic nucleus lesion. Loss of inhibition of thalamus through globus pallidus. (“Hemiballismus = Half ballistic – like throwing a baseball”)

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85
Q

Huntington’s dz. Genetics, Pathology, Clinical Presentations, Age

A

Autosomal-dominant trinucleotide repeat expansion (CAG, anticipation). Chromosome 4. Atrophy of caudate nucleus (loss of GABAergic neurons) leads to enlarged lateral ventricles on CT. Neuronal death through NMDA-R receptor binding and glutamate toxicity.

Chorea, depression, progressive dementia. Sx manifest in affeccted indvls btw ages 20-50. (Expansion of CAG repeats: “C audate loses A Ch and G ABA”)

86
Q

Autosomal-dominant trinucleotide repeat d/o. Chromosome 4. Atrophy of caudate nucleus (loss of GABAergic neurons) leads to enlarged lateral ventricles on CT. Chorea, depression, progressive dementia. Sx manifest in affeccted indvls btw ages 20-50. (Expansion of CAG repeats: “C audate loses A Ch and G ABA”)

A

Huntington’s dz

87
Q

Chorea. What is it and which dz is it associated with?

A

Sudden, jerky, purposeless movements. Characteristic of basal ganglia lesion (e.g., Huntington’s disease) (Chorea = dancing (Greek). Think choral dancing or choreography)

88
Q

Athetosis. What is it and which dz is it associataed with?

A

Slow, writhing movements, especially if fiingers. Characteristic of basal ganglia lesion (e.g., Huntington’s dz) (Athetos = not fixed (Greek). Think snakelike.)

89
Q

Myoclonus. What is it and give an example.

A

Sudden, brief muscle contraction. Jerks, hiccups

90
Q

Dystonia. What is it and give two examples.

A

Sustained, involuntary muscle contractions. Often with athetosis. Writer’s cramp, blepharospasm.

91
Q

Essential/postural tremor. Characteristics, Genetics, and Medications

A

Action tremor (worsen when holding posture), autosomal dominant. Essential tremor pts often self-medicate w/ alcohol, which decreases the tremor. Tx: beta-blockers.

92
Q

Resting tremor. Presentation and Disease.

A

Most noticeable distally. Seen in Parkinson’s (“pill-rolling” tremor)

93
Q

Intention tremor. Presentations and Disease

A

Slow, zigzag motion when pointing twd a target; associated w/ cerebellar dysfunction.

94
Q

Cerebral cortex: where are the Sylvian fissure vs. Central sulcus?

A

A: Sylvian fissure is above temporal lobe; central sulcus divides frontal and parietal lobes.

95
Q

Cerebral cortex: What is the arcuate fasciculus?

A

Connection between Associative auditory cortex (Wernicke’s area; dominant hemisphere) and Motor speech area (Broca’s area; dominant hemisphere)

96
Q

Cerebral cortex: Where is the primary auditory cortex (Heschel’s gyrus)? The primary motor area? The primary sensory area? The premotor area (part of extrapyramidal circuit)?

A
97
Q

Frontal lobe functions

A

Executive functions Planning, inhibition, concentration, orientation, language, abstraction, judgment, motor regulation, mood. Lack of social judgment is most notable in frontal lobe lesion. (“D amage = D isinhibition” - e.g., Phineas Gage)

98
Q

Homonculus: What is it? What is it used for? What reaches into the Sylvian fissure? The longitudinal fissure?

A

Topographical representation of sensory and motor areas in the cerebral cortex. Used to localize lesion (e.g., in blood supply) leading to specific defects. For example, lower extremity deficit in sensation or movement indicates involvement of anterior cerebral artery.

99
Q

Brain lesion in: Broca’s area

A

(hint: BRO ca’s is BRO ken speech.) Consequence: Motor (nonfluent/expressive) aphasia w/ good comprehension.

100
Q

Motor (nonfluent/expressive) aphasia w/ good comprehension. Where is the lesion?

A

Broca’s area (hint: BRO ca’s is BRO ken speech.)

101
Q

Brain lesion in: Wernicke’s area

A

(hint: W ernicke’s is W ordy but makes no sense.) Consequence: Sensory (fluent/receptive) aphasia w/ poor comprehension, neologisms.

102
Q

Sensory (fluent/receptive) aphasia w/ poor comprehension, neologisms. Where is the lesion?

A

Wernicke’s area (hint: W ernicke’s is W ordy but makes no sense.)

103
Q

Brain lesion in: Arcuate fasciculus (connects Wernicke’s to Broca’s area)

A

Consequence: Conduction aphasia; good comprehension, fluent speech, but poor repetition.

104
Q

Conduction aphasia; good comprehension, fluent speech, but poor repetition. Where is the lesion?

A

Arcuate fasciculus (connects Wernicke’s to Broca’s area)

105
Q

Brain lesion in: Amygdala (bilateral)

A

Consequence: Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior)

106
Q

Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior) Where is the lesion?

A

Amygdala (bilateral)

107
Q

Brain lesion in: Frontal lobe

A

Consequence: Personality changes and deficits in concentration, orientation, and judgment; may have reemergence of primitive reflexes.

108
Q

Personality changes and deficits in concentration, orientation, and judgment; may have reemergence of primitive reflexes. Where is the lesion?

A

Frontal lobe

109
Q

Brain lesion in: Right parietal lobe

A

Consequence: Spatial neglect syndrome (agnosia of the contralateral side of the world)

110
Q

Spatial neglect syndrome (agnosia of the contralateral side of the world) Where is the lesion?

A

Right parietal lobe

111
Q

Brain lesion in: Reticular activating system (midbrain)

A

Consequence: Reduced levels of arousal and wakefulness (e.g., coma)

112
Q

Reduced levels of arousal and wakefulness (e.g., coma) Where is the lesion?

A

Reticular activating system (midbrain)

113
Q

Brain lesion in: Mammillary bodies (bilateral)

A

Consequence: Wernicke-Korsakoff syndrome (Wernicke-confusion, ophthalmoplegia, ataxia; Korsakoff-memory loss, confabulation, personality changes) - Thiamine deficiency in alcoholics.

114
Q

Wernicke-Korsakoff syndrome (Wernicke-confusion, ophthalmoplegia, ataxia; Korsakoff-memory loss, confabulation, personlity changes). Where is the lesion?

A

Mammillary bodies (bilateral)

115
Q

Brain lesion in: Basal ganglia

A

Consequence: May result in tremor at rest, chorea, or athetosis

116
Q

May result in tremor at rest, chorea, or athetosis Where is the lesion?

A

Basal ganglia

117
Q

Brain lesion in: Cerebellar hemisphere

A

(hint: cerebellar hemispheres are laterally located, so they affect the lateral limbs) Consequence: Intention tremor, limb ataxia; Damage to the cerebellum results in ipsilateral deficits; Fall toward side of lesion (cerebellum -> SCP -> contralateral cortex -> corticospinal decussation=ipsilateral)

118
Q

Intention tremor, limb ataxia; Damage to the cerebellum results in ipsilateral deficits; Fall toward side of lesion (cerebellum -> SCP -> contralateral cortex -> corticospinal decussation=ipsilateral). Where is the lesion?

A

Cerebellar hemisphere (hint: cerebellar hemispheres are laterally located, so they affect the lateral limbs)

119
Q

Brain lesion in: Cerebellar vermis

A

(hint: vermis is centrally located, so it affects the central body) Consequence: Truncal ataxia, dysarthria.

120
Q

Truncal ataxia, dysarthria. Where is the lesion?

A

Cerebellar vermis (hint: vermis is centrally located, so it affects the central body)

121
Q

Brain lesion in: Subthalamic nucleus

A

Consequence: Contralateral hemiballismus

122
Q

Contralateral hemiballismus Where is the lesion?

A

Subthalamic nucleus

123
Q

Brain lesion in: Hippocampus

A

Consequence: Anterograde amnesia – inability to make new memories

124
Q

Anterograde amnesia – inability to make new memories Where is the lesion?

A

Hippocampus

125
Q

Brain lesion in: Paramedian pontine reticular formation (PPRF)

A

Consequence: Eyes look away from side of lesion

126
Q

Eyes look away from side of lesion Where is the lesion?

A

Paramedian pontine reticular formation (PPRF)

127
Q

Brain lesion in: Frontal eye fields

A

Consequence: Eyes look toward lesion.

128
Q

Eyes look toward lesion. Where is the lesion?

A

Frontal eye fields

129
Q

Central Pontine Myelinolysis. Clinical Presentation, Etiology, Imaging

A

Acute paralysis, dysarthria, dysphagia, diplopia and loss of consciousness. Commonly caused by very rapid correction of hyponatremia. T1-weighted MRI shows abnormal increased signal in the pons.

130
Q

Aphasia (definition) vs. Dysarthria (definition)

A

Aphasia is a higher-order inability to speak. vs. Dysarthria is a motor inability to speak.

131
Q

Broca’s aphasia

A

Nonfluent aphasia w/ intact comprehension. Broca’s area – inferior frontal gyrus. (“Bro ca’s Bro ken Boca “ [boca = mouth in Spanish])

132
Q

Wernicke’s aphasia

A

Fluent aphasia with impaired comprehension. Wernicke’s area – superior temporal gyrus. (“W ernicke’s is W ordy but makes no sense.” or “W ernicke’s = W hat?”)

133
Q

Global aphasia

A

Nonfluent aphasia w/ impaired comprehension. Both Broca’s and Wernicke’s areas affected.

134
Q

Conduction aphasia

A

Poor repetition but fluent speech, intact comprehension. Arcuate fasciculus – connects Broca’s and Wernicke’s areas.

135
Q

Anterior cerebral artery: what areas of cortex does it supply?

A

Supplies anteromedial surface of brain

136
Q

Middle cerebral artery: what areas of cortex does it supply?

A

Supplies lateral surface of brain

137
Q

Posterior cerebral artery: what areas of cortex does it supply?

A

Supplies posterior and inferior surfaces

138
Q

What normally regulates cerebral perfusion? What regulates cerebral perfusion in severe hypoxia?

A

Normally driven by P CO2, but also by P O2 with severe hypoxia. Therapeutic hyperventilation (decreased P CO2 helps decrease ICP in cases of acute cerebral edema (stroke, trauma)

139
Q

Anterior cerebral artery: Where is it? What does it supply? What deficits are associated with ACA infarct?

A

Supplies medial surface of the brain, leg-foot area of motor and sensory cortices. Contralateral paralysis and loss of sensation of upper limb and face. Hemineglect if lesion affects non dominant (usually right) side.

140
Q

Middle cerebral artery: Where is it? What does it supply?

A

Supplies lateral aspect of brain, trunk-arm-face area of motor and sensory cortices, Broca’s and Wernicke’s speech areas (on dominant hemisphere), optic radiations.

141
Q

What deficit occurs w/ problems in the middle cerebral artery?

A

Contralateral face and arm paralysis and sensory loss, aphasia (dominant sphere), hemineglect if lesion affects nondominant (usually right) side.

142
Q

Posterior cerebral artery: Where is it? What does it supply?

A

Supplies the occipital cortex, visual cortex.

143
Q

What deficit is associated with problems in the posterior cerebral artery?

A

Contralateral homonymous hemianopia with macular sparing.

144
Q

Anterior communicating artery: Where is it? What is associated with this artery?

A

Common site of saccular (berry) aneurysm -> impingement on cranial nerves. Lesions are typically aneurysms, not strokes. Visual field defects.

145
Q

Posterior communicating artery: Where is it? What is associated with this artery?

A

Common site of saccular (berry) aneurysm; Lesions are typically aneurysms, not strokes. CN III palsy - eye is “down and out”.

146
Q

Lateral striate: Where are they? What do they supply?

A

Divisions of the middle cerebral artery that supply the internal capsule, caudate, putamen, and globus pallidus.

147
Q

What deficit is associated with the lateral striate?

A

Arteries of stroke; infarct of internal capsule causes pure motor hemiparesis; contralateral hemiparesis/hemiplegia. Common location of lacunar infarcts, secondary to unmanaged HTN

148
Q

Watershed zones of the circle of Willis

A

Between anterior cerebral/middle cerebral, posterior cerebral/middle cerebral arteries. Damaged in severe hypotension –< upper leg/upper arm weakness, defects in higher-order visual processing.

149
Q

Posterior Inferior Cerebellar Artery (PICA): Where is it? What deficits are associated with an infarct here?

A

Lateral medulla (vestibular nuclei, lat ST tract, STri nucleus, Nucleus ambiguus, symp fibers, inf. cerebellar peduncles).Infarcts cause Wallenberg’s syndrome (aka lateral medullary syndrome) (nystagmus, ipsilateral ataxia, nausea, vomiting, Horner’s syndrome); vomiting, vertigo; decrease pain/temp sensation; dysphagia, horaseness, decrease ag reflex; ip horner, ataxia, dysmetria

150
Q

Basilar artery: Where is it? What would an infarct here cause?

A

Infarct causes locked-in syndrome.

151
Q

In general, strokes of the anterior circle of Willis vs. the posterior circle of Willis

A

stroke of the anterior circle : General sensory and motor dysfunction, aphasia. stroke of the posterior circle : Cranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia)

152
Q

Anterior spinal artery: Where is it? What defects are associated?

A

Medial medullary syndrome: contralateral hemiparesis (lower extremities), medial lemniscus (decr proprioception), ipsilateral paralysis of hypoglossal nerve

153
Q

Anterior Inferior Cerebellar Artery (AICA) Where is it located? What deficits are associated?

A

Lateral pons (vest nuclei, facial nuclei, STri nucleus, cochlear nucleus, symp fibers, middle/inf. cerebellar peduncles).

Lateral inferior pontine syndrome. vomiting, vertigo, nystagmus. Paralysis of face (droop). decrease lacrimation, salivation, taste from ant 2/3, corneal reflex. decrease face pain/temp. ips hearing and horner.

154
Q

Berry aneurysms: Where do they occur? What is the most common complication?

A

Occur at the bifurcations in the circle of Willis. Most common site is bifurcation of the anterior communicating artery. Rupture (most common complication) leads to hemorrhagic stroke/subarachnoid hemorrhage.

155
Q

Berry aneurysms: associated with? other risk factors?

A

Associated with: Adult polycystic kidney dz Ehlers-Danlos syndrome Marfan’s syndome Risk factors: Advanced age HTN Smoking Race (higher risk in blacks)

156
Q

Charcot-Bouchard microaneurysms: Associated with? What do they affect?

A

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

157
Q

Epidural hematoma

A

Rupture of middle meningeal artery (branch of maxillary artery), often secondary to fracture of temporal bone. Lucid interval. CT shows “biconvex disk” not crossing suture lines. Can cross falx, tentorium.

158
Q

Subdural hematoma

A

Rupture of bridging veins. Venous bleeding (less pressure) with delayed onset of Sx’s. Seen in elderly individuals, alcoholics, blunt trauma, shaken baby. Crescent-shaped hemorrhage that crosses suture lines. Cannot cross falx, tentorium.

159
Q

Factors predisposing to a subdural hematoma

A

Brain atrophy, shaking, whisplash: elderly, alcoholics, blunt trauma, shaken baby

160
Q

Subarachnoid hemorrhage

A

Rupture of aneurysm (usually berry aneurysm) or an AVM. Pts complain of “worst headache of my life.” Bloody or yellow (xanthochromic) spinal tap. 2-3 days afterward, there is a risk of vasospasm (Tx w/ Ca2+ channel blockers).

161
Q

Parenchymal hematoma

A

Caused by HTN, amyloid angiopathy [see below], DM, and tumor. Typically occurs in basal ganglia and internal capsule.

162
Q

How long after lack of perfusion to th brain would you have rireversible damage?

A

5 min

163
Q

Hemorrhagic stroke

A

Intracerebral bleeding, often due HTN, anticoagulation and cancer (abnormal vessels can bleed). May be secondary to ischemic stroke following reperfusion (incr vessel fragility)

164
Q

Ischemic stroke

A

Emboli block large vessels; etiologies include: atrial fibrillation, carotid dissection, patent foramen ovale, endocarditis. Lacunar strokes block small vessels, are secondary to HTN. Tx: tPA w/in 4.5 hours (so long as patient presents within 3 hours of onset).

165
Q

Transient Ischemic Attack (TIA)

A

Brief, reversible episode of neurologic dysfunction due to focal ischemia. Typically, symptoms last less than 24h.

166
Q

What do you see on MRI and CT for stroke?

A

Bright on diffusion-weighted MRI in 3-30 minutes, remains bright for 10 days
Dark noncontrast CT inn 24h. Bright areas on noncontrast CT indicate hemorrhage (tPA contraindicated)

167
Q

What areas are the most vulnerable for brain infarcts?

A

Hippocampus, neocortex, cerebellum, watershed areas

168
Q

Give the sequence of events in a brain infarct (5 steps)

A

Red neurons (12-48 hours)
Necrosis + neutrophils (24-72 hours)
Macrophages (3-5 days)
Reactive gliosis and vascular proliferation (1-2 weeks)
Glial scar (> 2 weeks)

169
Q

Dural venous sinuses: Where do they run? What is the sequence?

A

Venous sinuses run in the dura mater where its meningeal and periosteal layers separate. Cerebral veins –> venous sinuses –> internal jugular vein

170
Q

Where is the supereior sagittal sinus? The confluence of the sinuses? The Occipital sinus? The Transverse and sigmoid sinuses?

A

The superior sagittal sinus (main location of CSF return via arachnoid granulations) is along the superior/median border of the brain. The confluence of the sinuses is posterior, bringing together the occipital sinus (inferiorly), sagittal sinus (superiorly), transverse sinuses (laterally), and straight sinus (ventrally)

171
Q

Where is the inferior sagittal sinus? The Great cerebral vein (of Galen)? The Straight sinus?

A

The inferior sagittal sinus runs deep to the superior sagittal sinus in the median line. The great cerebral vein runs inferior to that, and the two sinuses meet at the straight sinus, which feeds into the confluence of the sinuses posteriorly.

172
Q

What is one vein that feeds into the dural venous sinuses?

A

The Superior ophthalmic vein feeds into the cavernous sinus, which reaches the sup. sagittal sinus and the transverse sinus by way of the Sphenoparietal sinus.

173
Q

Where is CSF made? Where is reabsorbed?

A

CSF is made by ependymal cells lining the ventricles; it is reabsorbed by venous sinus arachnoid granulations.

174
Q

What connects the lateral to the 3rd ventricle?

A

Ventricular foramen of Monro

175
Q

What connects the 3rd and 4th ventricles?

A

The cerebral aqueduct

176
Q

What connects the 4th ventricle and the subarachnoid space?

A

Foramina of L uschka = L ateral Foramen of M agendie = M edial

177
Q

What is hydrocephalus? What are the types of hydrocephalus?

A

Accumulation of excess CSF in ventricular system leading to increased intracranial pressure; ventricular dilation.
Normal pressure, Communicating, Non-communicating (Obstructive), and Hydrocephalus ex vacuo (appearance of increased CSF)

178
Q

What are symptoms of increased intracranial pressure?

A

Nausea, vomitting, headache, nuchal rigidity, mental status change, bilateral papilledema, increased open pressure on LP, loss of venous pulsations

179
Q

Normal pressure hydrocephalus. Symptoms and Etiology.

A

“Wet, wobbly and wacky”. Does not result in increased subarachnoid space volume. Expansion of ventricles distorts fibers of corona radiatia and leads to clinical traid of dementia, ataxia and urinary incontinence (reversible cause of dementia in elderly).

180
Q

Communicating Hydrocephalus. Symptoms and Etiology

A

Decreased CSF absorption by arachnoid villi, which can lead to increased intracranial pressure, papilledema, and herniation (e.g. arachnoid scarring post-meningitis)

181
Q

Obstructive (non-communicating) hydrocephalus

A

Caused by structual blockage of CSF circulation w/in the ventricular system (e.g., stenosis of the aqueduct of Sylvius)

182
Q

Hydrocephalus ex vacuo

A

Appearance of increased CSF in atrophy (e.g. Alzheimer’s, advanced HIV, Pick’s disease). Intracranial pressure normal, triad not seen.

183
Q

Total # of spinal nerves? Per section?

A

There are 31 spinal nerves. (“31 like the 31 flavors at Baskin-Robbins”) 8 Cervical 12 Thoracic 5 Lumbar 5 Sacral 1 Coccygeal

184
Q

Numbering of cervical spinal nerves

A

Nerves C1-C7 exit via intervertebral foramina above the corresponding vertebra. All other nerves exit below .

185
Q

Where does vertebral disk herniation usually occur?

A

Vertebral disk herniation (nucleus pulposus herniates through annulus fibrosus) usually occurs btw L5 and S1.

186
Q

How far does the spinal cord extend in adults? The subarachnoid space? Where do you perform a lumbar puncture?

A

In adults, the spinal cord extends to the lower border of L1-L2; subarachnoid space extends to lower border of S2.
Lumbar puncture is usually performed in L3-L4 or L4-L5 interspaces, at the level of the cauda equina. (“To keep the cord alive, keep the spinal needle btw L3 and L5 “)

187
Q

Where do you get CSF from in a lumbar puncture?

A

CSF is obtained from lumbar subarachnoid space btw L4 and L5 (at the level of iliac crests)

188
Q

Structures pierced in a lumbar puncture (in order)

A

Skin -> Superficial Fascia -> Deep Fascia -> Supraspinatous ligament -> Interspinous ligament -> Interlaminar region (lumbar) -> epidural space -> dura -> arachnoid -> subarachnoid space -> CSF
Pia is not pierced.

189
Q

What do the dorsal columns of the spinal cord relay?

A

Pressure, vibration, touch, proprioception.

190
Q

How are the dorsal columns of the spinal cord organized?

A

Medially: fasciculus gracilis (lower body, extremities) Laterally: fasciculus cuneatus (upper body, extremities) (“Dorsal column is organized as you are, with hands at sides. Arms outside, legs inside.”)

191
Q

What do the lateral corticospinal tract and spinothalamic tract relay? Where are they located? How are they organized?

A

Lateral corticospinal tract relays voluntary motor information, is located in the lateral spinal cord. Spinothalamic tract relays pain and temperature, is located antero-laterally. (“L egs are L ateral in L ateral corticospinal, spinothalamic tracts”)

192
Q

What arteries follow the spinal cord?

A

2 Posterior spinal arteries, 1 anterior spinal artery

193
Q

Where are the intermediate horn sympathetics found?

A

The lateral gray matter of the thoracic [only] spinal cord

194
Q

Ascending spinal tracts and synapsing

A

They synapse then cross.

195
Q

Spinal tract: Dorsal column – medial lemniscal pathway: Function

A

Ascending pressure, vibration, touch, and proprioceptive sensation

196
Q

Ascending pressure, vibration, touch, and proprioceptive sensation what spinal tract is this?

A

Dorsal column – medial lemniscal pathway

197
Q

Spinal tract: Spinothalamic tract. Function

A

Ascending pain and temperature sensation

198
Q

Ascending pain and temperature sensation what spinal tract is this?

A

Spinothalamic tract

199
Q

Spinal tract: Lateral corticospinal tract. Function

A

Descending voluntary movement of contralateral limbs

200
Q

Descending voluntary movement of contralateral limbs what spinal tract is this?

A

Lateral corticospinal tract

201
Q

Spinal tract: Dorsal column – medial lemniscal pathway.

A
  • *First order neuron**: sensory nerve endings Ad/C fibers, cell body in dorsal root ganglion -> enters spinal cord and ascends ipsilaterally in dorsal column
  • *Synpase 1:** at ipsilateral nucleus cuneatus or gracilis in medulla -> decussates in medulla -> ascends contralaterally in medial lemniscus
  • *Synapse 2:** VPL of thalamus -> sensory cortex
202
Q

Which spinal tract synapse at nucleus cuneatus/gracilis and decussates at medulla?

A

Dorsal column – medial lemniscal pathway

203
Q

Spinal tract: Spinothalamic tract Pathway

A

1st order neuron: Sensory nerve ending (A-delta and C fibers), cell body in dorsal root ganglion -> enters spinal cord
Synpase 1: ipsilateral gray matter (spinal cord); decussates at anterior white commissure -> ascends contralaterally
Synapse 2: VPL of thalamus to sensory cortex

204
Q

Which spinal tract synapse at gray matter in spinal cord and decussates at anterior white commissure?

A

Spinothalamic tract

205
Q

Spinal tract: Lateral corticospinal tract

A

Upper motor neuron: cell body in primary motor cortex -> descends ipsilaterally through internal capsule until decussating at caudal medulla (pyramidal decussation) -> descends contralaterally
Synapse 1: Cell body of anterior horn (spinal cord), lower motor neuron leaves spinal cord to neuromuscular junction

206
Q

Which spinal tract decussates at caudal medulla and descends contralaterally?

A

Lateral corticospinal tract

207
Q

Spinal tract: Dorsal column – medial lemniscal pathway. What is the first synapse?

A

What is the 1st synapse? Ipsilateral nucleus cuneatus or gracilis (medulla)

208
Q

Ipsilateral nucleus cuneatus or gracilis (medulla) This is the 1st synapse in which spinal tract?

A

Dorsal column – medial lemniscal pathway

209
Q

Ipsilateral gray matter (spinal cord) This is the 1st synapse in which spinal tract?

A

Spinothalamic tract

210
Q

What is the most common congenital aqueductal stenosis?

A

Maternal infection (CMV, toxo)

211
Q

What is pseudotumor cerebri?

A

Benign intracranial hypertension: increased resistance to outflow, increased ICP, slit-like ventricles, papilledema, headaches, visual changes; young obese women
Amiodarone, Lupus, Oral Cont, Tetracycline, Vit. A in high dose, Steroids

USMLE1 - Neurology (4 decks)

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