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Brain and Behavior > Week 2 Lectures > Flashcards

Week 2 Lectures Flashcards

1
Q

What is similar about CN 3, 4, 6, 12?

A

They exit medially/midline –> purely motor

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2
Q

What is similar about CN 5, 7, 8, 9 10?

A

They exit laterally –> both motor and sensory

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3
Q

How many cranial nerves enter/exit the brainstem?

A

9 (except 1, 2, 11)

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4
Q

Which cranial nerves exit the midbrain?

A

3 and 4

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5
Q

Which cranial nerves exit the pons?

A

5, 6, 7, 8

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6
Q

Which cranial nerves exit the medulla?

A

9, 10, 12

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7
Q

The medullary pyramid is….

A

the corticospinal tract/pyramidal tract

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8
Q

What is the only dorsally exiting CN?

A

4 –> under calliculi –> only completely crossed CN –> motor neurons are found on the side of the midbrain opposite to ascent/descent

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9
Q

What structure separates the cerebellum from the pons and medulla?

A

4th ventricle

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10
Q

Corticospinal tract courses _____ and _____ through the brainstem.

A

ventral and medial –> medial brainstem blood supply and lesioned with medium brainstem vascular lesion

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11
Q

What happens if we lesion the corticospinal tract below the brainstem?

A

UMN loss ipsilateral and below

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12
Q

What happens if we lesion the corticospinal tract in the brainstem?

A

UMN loss contralateral and below

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13
Q

What is the role of medial motor systems?

A

bilateral postural control

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14
Q

Medial lemniscus moves from _____ to ______ as it ascends the brainstem?

A

medial to lateral –> change source of blood

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15
Q

What happens if we lesion the corticospinal tract below the brainstem?

A

ipsilateral and below

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16
Q

What happens if we lesion the corticospinal tract above the brainstem?

A

contralateral and below

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17
Q

Where does the anterolateral system course?

A

laterally through the brainstem

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18
Q

T/F the anterolateral system courses straight to the thalamus.

A

F –> projects into other neurons in the brainstem to modulate the pain elicited by the stimulus

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19
Q

What happens if we lesion the corticospinal tract below the brainstem?

A

contralateral and below lesion

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20
Q

What happens if we lesion the corticospinal tract above the brainstem?

A

contralateral and below lesion

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21
Q

What aspect of the brain controls autonomic function?

A

hypothalamus

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22
Q

What system conducts sympathetic control of the face, scalp, and orbit?

A

2 neuron pathway from T1 involving a second neuron in the superior cervical ganglion –> horner’s syndrome

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23
Q

When you lesion descending hypothalamic fibers, what syndrome do patients present with?

A

central horner’s syndrome

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24
Q

When a patient presents with horner’s it is ipsilateral/contralateral to the lesion?

A

ipisilateral ALWAYS

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25
Q

Where do descending hypothalmic fibers run in the brainstem?

A

lateral near the spinothalamic tract –> shared blood supply

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26
Q

When there is interrupted lateral blood supply to the brainstem, which tracts are lesioned?

A

spinothalamic + sympathetic

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27
Q

Medial longitudinal fasciculus

A

links ocular CN nuclei and vestibular system –> conjugate horizontal gaze –> motor CNs 3 and 6 and vestibular system

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28
Q

What will be found in every brainstem section?

A
  1. long tract (corticospinal, dorsal column, spinothalamic, MLF, central tegmental tract)
  2. cranial nerve nucleus or nerve
  3. trigeminal nucleus
  4. cerebellar peduncle or fibers forming one (ICP-medulla, MCP-pons, SCP-midbrain)
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29
Q

LMN in a CN arise from?

A

corticobulbar or corticonuclear axons –> mostly bilateral UMN –> cranial nerve muscles often cross the midline

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30
Q

What would happen if we lesion all the corticobulbar axons emerging from one hemisphere?

A

not much –> still have innervation from opposite size
*exception: LMN in facial nerve have some muscles that are unilaterally innervated (muscles of nose and mouth are only contralateral)

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31
Q

What happens with a lesion of a LMN in the facial nerve?

A

ipsilateral effects –> bell’s palsy

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32
Q

What happens with a lesion of the UMN of the facial nerve?

A

only the muscles for wrinkling forehead and shutting the eyes have dual cortical innervation –> contralateral weakness of the lower face

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33
Q

Embryonic sulcus that separates sensory and motor areas

A

sulcus limitans

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34
Q

Functional columns

A

GSE GVE SVE | SVA/GVA SSA GSA

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35
Q

Motor Functional Columns

A 
GSE = garden variety skeletal muscle (motor only: 3, 4, 6, 11, 12);
GVE = parasympathetics (3 and mixed: 7, 9, 10);
SVE = pharyngeal arch muscle (mixed only: 5, 7, 9 , 10)
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36
Q

What is the only motor cranial nerve that carries autonomics?

A

3- oculomotor

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37
Q

Sensory Functional Columns

A 
GSA = pharyngeal arches (mixed only: 5, 7, 9, 10) --> mostly trigeminal;
GVA = stretch and baroreceptors (9 and 10)
SVA = taste (7, 9, 10)
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38
Q

Functional Columns- garden variety skeletal muscle

A

3 (adduct eye, raise eyelid), 4 (depress eye), 6 (abduct eye), 12 (move tongue), (and 11)–> most medial and motor

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39
Q

Where do the crossed oculomotor nerves go?

A

to the superior rectus and superior oblique on the contralateral side

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40
Q

Functional Columns - preganglionic

A

3 (Edinger Westphal - pupil constriction, near response), 7 (Superior salivatory nucleus - lacrimation), 9 (Inferior salivatory nucleus-parotid), 10 (Dorsal motor nucleus-gut)

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41
Q

Which axons exit the midbrain with the oculomotor nerve and synapse with neurons in the ciliary ganglion and where do they arise?

A

preganglionic parasympathetics from Edinger Westphal nucleus

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42
Q

What are the initial signs of CN3 compression?

A

dilated pupil, loss of lightreflex, and loss of near response on side of lesion

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43
Q

What nucleus gives rise to parasympathetic axons in the facial nerve?

A

Superior salivatory nucleus in the caudal pons –> pterygopalatine, lacrimal, and submandibular

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44
Q

What is the result of a lesion of parasympathetic axons in CN7?

A

loss of lacrimation–> dry ey on side of lesion

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45
Q

Where and what is the nucleus that gives rise to parasympathetics in CN9?

A

inferior salivatory nucleus in the rostral medulla –> otic ganglion –> parotid gland

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46
Q

A lesion of CN9 may result in what?

A

reduction in parotid secretions

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47
Q

What nucleus contains parasympathetics that exit with CNX?

A

dorsal motor nucleus lateral to hypoglossal nucleus in the floor of 4th ventricle –> terminal ganglia in thoracic/abdominal viscera –> slow heart rate, constrict bronchial smooth muscle, promote peristalsis

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48
Q

Where is the motor nucleus of V located?

A

rostral pons –> muscles of mastication and mylohyoid, anterior belly of digastric, tensor tympani, tensor veli palatini

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49
Q

Unilateral lesion of the motor fibers of CN V may cause what?

A

devision of jaw upon protrusion toward side of lesion

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50
Q

The facial motor nucleus is where?

A

caudal pons –> axons form the facial colliculus in the floor of 4th ventricle by wrapping around abducens nucleus –> stapedius, stylohyoid, posterior belly of digastric

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51
Q

With what nerve do facial motor axons run laterally to the genu?

A

sensory and parasympathetic fibers of hte nervus intermedius of the facial nerve

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52
Q

Lesions of the skeletal motor axons in the facial nerve may result in?

A

complete paralysis of muscles of facial expression ipislateral to lesion and hyperacusis due to weakness of stapedius (also weakness in forehead wrinkling, eye shutitng, nostril flaring on the side of lesion)

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53
Q

Which nucleus contains LMN of CN 9 and 10?

A

nucelus ambiguus (some of these neurons contribute to parasympathetic innervation of heart)

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54
Q

A lesion of motor axons from CN 10 from nucleus ambiguus may cause?

A

ipsilateral weakness of soft palate, nasal regurgitation of liquid, deviation of uvula away from side of lesion, weakness of pharygneal muscles/dysphagia, weakness of laryngeal muscles/hoarsness

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55
Q

Where does the accessory nerve arise?

A

accessory nucleus between C1 and C5 –> pass through foramen magnum –> exit jugular foramen –> SCM and trapezius

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56
Q

Where are parasympathetic neurons of 10 located?

A

nucleus ambiguus and dorsal motor nucleus

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57
Q

Which axons loop around the abducens nucleus?

A

Facial nerve axons

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58
Q

Parasympathetics and special pharyngeal arch axons are exiting from a _____ nerve from a _____ position on the brainstem.

A

mixed, ventrolateral

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59
Q

What nucleus conducts visceral sensory fibers for taste and pressure?

A

Solitary nucleus –>medulla (taste= 5,9,10 superior to carotid sinus,body = 9,19)

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60
Q

A bilateral lesion of the solitary nuclei may cause ________.

A

respiratory failure (possibly preceded by ataxic respiration)

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61
Q

The gag reflex utilizes visceral sensory fibers in CN ____ and skeletal motor fibers in CN ____.

A

9 and 10

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62
Q

The cough reflex utilizes both sensory and motor fibers in CN___.

A

10

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63
Q

What do cochlear (CN8) nerve fibers do upon entereing the brainstem at the pontomedullary junction?

A

birfucates and gives rise to processes that synapse in both ventral and dorsal cochlear nuclei

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64
Q

Which ganglion contains the cell bodies of the cochlear nerve fibers?

A

spiral ganglion in cochlea

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65
Q

The ventral cochlear nuclei project bilaterally to neurons in the _______.

A

superior olivary nuclei in the pons

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66
Q

The first auditory nuclei to receive binaural inputs are?

A

the superior olivary nuclei

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67
Q

From which sources does the lateral lemniscus convey auditory input from?

A

cochlear nuclei and superior olivary nuclei to the inferior colliculus in the midbrain

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68
Q

In patients with an ipsilateral sensorineural hearing loss, the lesion is most likely at _____ but not at _____.

A

inner ear, CN8, cochlear nuclei but not at higher levels of central auditory system that receive input from both ears

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69
Q

A lesion to CNS auditory structures in the brain stem above the cochlear nuclei, in the thalamus, or in the cortex may result in…?

A

slight bilateral hearing loss and decreased ability to localize a sound source

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70
Q

The vestibular nerve innervates…?

A

hair cells in the three semicircular ducts and hair cells in the utricular and saccular maculae

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71
Q

The utricle and saccule contain hair cells that respond to…?

A

linear acceleration

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72
Q

The semicircular ducts contain hair cells that respond to…?

A

angular acceleration

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73
Q

Where do central processes of vestibular nerve fibers that enter the brain stem terminate?

A

vestibular nuclei and flocculonodular lobe of cerebellum

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74
Q

4 vestibular nuclei

A

superior, lateral ,medial, inferior

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75
Q

Patients with a vestibular lesion may have?

A

vertigo –> severe in peripheral lesions and mild in central lesions

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76
Q

Patients with Meniere’s may have…?

A

abrupt, recurrent vertigo + tinnitus + ipsilateral sensorineural hearing loss + nausea/vomiting/ear pressure

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77
Q

Axons of vestibular nuclei join what tract?

A

medial longitudinal fasiculus

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78
Q

What does the MLF connect vestibular nuclei to?

A

centers for conjugate gaze and oculomotor, trochlear, and abducens nuclei

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79
Q

Where do axons of CN 5 enter the brainstem?

A

rostral pons

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80
Q

Main, Chief, or Principal Nucleus

A

at entry of CN 5: touch

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81
Q

Mesencephalic Nucleus

A

CN 5: proprioception (superior)

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82
Q

Spinal nucleus

A

CN 5: pain and termperature (inferior)

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83
Q

3 components of spinal nucleus

A
  1. nucleus oralis - face touch
  2. nucleus interpolaris - tooth pulp pain
  3. nucleus caudalis - face pain and temperature
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84
Q

What is the only example of neural crest cells that have migrated into the brainstem?

A

the neurons in the mesencephalic trigeminal nucleus

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85
Q

Facial touch pathway

A

trigeminal ganglion –> ipsilateral principal nucleus of trigeminal complex –> cross over and ascend in medial lemniscus to VPM –> cortex

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86
Q

Forehead face pain and temperature axons enter the pontomedullary junction and ascend/descend to the top/bottom of the nucleus caudalis before crossing over and ascending to the cortex.

A

descend to the bottom

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87
Q

Facial pain and temperature pathway

A

Trigeminal ganglion –> descend in spinal trigeminal tract –> nucleus caudalis –> cross over –> ascend in trigeminothalamic tract to VPM –> cortex

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88
Q

A patient with a lesion of the lower pons may present with?

A

only loss of pain and temperature in face

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89
Q

Which cerebellar peduncle carries ascending information?

A

inferior: spinocerebellar pathways (limb position sense) + inferior olivary nucleus (cerebellar input)

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90
Q

Which cerebellar peduncle carries information from the cortex into the cerebellum?

A

middle

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91
Q

Which cerebellar peduncle carries information from cerebellum to UMN?

A

superior

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92
Q

With regards to vascular insults, ____ CN will be affected in medial tract syndromes.

A

Motor

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93
Q

With regards to vascular insults, ____ CN will be affected in lateral tract syndromes.

A

Mixed

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94
Q

Which artery supplies the posterolateral medulla?

A

PICA from vertebral

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95
Q

Which artery supplies the medial aspect of the medulla?

A

Vertebral artery

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96
Q

Which artery supplies the anteromedial aspect of the medulla?

A

Anterior spinal artery

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97
Q

Which artery supplies the posterior of the midbrain?

A

Quadrigeminal artery

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98
Q

Which artery supplies the lateral aspect of the midbrain?

A

Anterior choroidal artery

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99
Q

Which artery supplies the anterior aspect of the midbrain?

A

Thalamoperforating branches of PCA

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100
Q

Which artery supplies the posterior aspect of the pons?

A

Superior cerebellar artery

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101
Q

Which artery supplies the posterolateral aspect of the pons?

A

AICA from basilar

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102
Q

Which artery supplies the ventrolateral aspect of the pons?

A

Short circumferential branches of the basilar

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103
Q

Which artery supplies the anterior aspect of the pons?

A

paramedian branches of the basilar artery

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104
Q

Most of the diencephalon is composed of?

A

thalamus + hypothalamus

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105
Q

The thalamus is bounded laterally by the ____ and medially by the _____.

A

internal capsule and third ventricle

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106
Q

All connections between cortex and thalamus travel in what structure?

A

internal capsule

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107
Q

5 anatomic thalamic nuclei:

A 
Medial
Lateral
Internal
Intralaminar
Reticularis
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108
Q

Input-output thalamic nuclei:

A

Relay (sensory, motor, limbic); Association (pulvinar, mediodorsal); Non-specific (intralaminar)

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109
Q

Sensory Relay nuclei

A

auditory –> medial geniculate –> auditory cortex; visual –> lateral geniculate –>visual cortex; somatosensory –>ventrobasal –> somatosensory cortex

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110
Q

Motor Relay nuclei

A

basal ganglia and cerebellum –> ventral anterior and ventral lateral –> motor

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111
Q

Limbic Relay nuclei

A

mammillary bodies –> anterior nucleus –> cingulate gyrus (Papez circuit)

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112
Q

Pulvinar Association nuclei

A

parietal-occipital-temporal association cortex

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113
Q

Mediodorsal Association nuclei

A

prefrontal cortex

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114
Q

Intralaminar Non-specific nuclei

A

non-specific projections to widespread area of cortex; receives input from basal ganglia

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115
Q

Basal ganglia

A

participate in parallel anatomical circuits through thalamus and cortex –> each loop with different motor, cognitive, or affective function

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116
Q

Reticular nucleus

A

has no projects outside thalamus

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117
Q

Sensory and motor areas of the cerebral cortex receive inputs from what thalamic nuclei?

A

Relay

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118
Q

Prefrontal and parietal-occipital-temporal cortex receive input from what nuclei?

A

Association

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119
Q

Which thalamic nucleus projects to the basal ganglia?

A

intralaminar nucleus

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120
Q

What kind of cell constitute 80% of all neurons in thalamic nuclei?

A

glutaminergic excitatory projection neurons also called thalamocortical cells

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121
Q

The neurons of the ______ form a thin layer of exclusively _____ inhibitory cells, surrounding the thalamus in its lateral and dorsal aspects and projects to _____.

A

nucleus reticularis, GABAergic inhibitory cells, projects to other thalamic nuclei

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122
Q

T/F only axons from the cortex leave collaterals for the reticular nucleus.

A

F. axons from the cortex and the thalamus do this

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123
Q

T/F thalamocortical cells maintain connections to one another.

A

F

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124
Q

How many layers does the neocortex have?

A

6 (layer 4 = granular)

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125
Q

Agranular cortex lacks what kind of cells?

A

stellate/granule cells

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126
Q

Which area of neocortex contains large pyramidal cells?

A

mainly layer 5

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127
Q

What kind of cortex constitute primary sensory areas?

A

granular cortex = mainly small cells with few large pyramidal cells/few long axons

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128
Q

The study and definition of cortical areas in terms of parameters reveealed by stains of RNA of cell bodies is called_____.

A

Cytoarchitecture (e.g. Broadmann)

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129
Q

The columnar organization probably reflects a general strategy used in the construction of neocortex and suggests that the cortex works as what kind of device?

A

massive parallel processing –> applying similar operations locally to many aspects of the same information

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130
Q

2 types of excitatory cells in the cortex that use glutamate as a neurotransmitter

A

granular/spiny stellate and pyramidal cells

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131
Q

Pyramidal cells

A

80% of neurons in neocortex; excitatory; project to cortex via apical dendrite; system of basal dendrites branch near hte soma in the same layer; giants = betz cells

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132
Q

Granular cells

A

layer 4; receive thalamic input and output to neocortex layers 2 and 3 –> prominent in sensory areas

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133
Q

T/F inhibitory neurons have spines.

A

F

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134
Q

Circuit in thalamus

A

TC –> cortex –> TC with collaterals of each nerve to nucleus reticularis

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135
Q

Circuit in neocortex

A

thalamus –> layer 4/granular excitatory –> layer 2/3/supragranular excitatory–> layer 5/6/infragranular –> out of cortex

*all excitatory inputs also activate local interneurons (gabaergic inhibitory) which inhibit each cell in the pathway and also self-regulate

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136
Q

Supragranular neocortex 2/3 project to ____.

A

other cortical areas

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137
Q

Infragranular neocortex 5/6 project to ____.

A

out of cortex to brainstem, psinal cord, thalamus, superior colliculus

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138
Q

T/F All relay operations are under heavy control of cortical feedback.

A

T

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139
Q

2 Functions of thalamus

A

relay function (specific information transfer to cortex) and gate function (control of the functional state of the forebrain)

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140
Q

Transition between waking and sleep states is modulated by changes in ______.

A

neuromodulation

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141
Q

2 Functions of cortex

A
  1. generate sensory/motor representations of external and internal worlds using a combination of sensory driven activity, internally generated activity, and memory storage
  2. generate consciousness//only a small portion of the activity in corticothalamic networks is accessible to consciousness
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142
Q

T/F The generation of representations and consciousness depends on recurrent loops between cortex and thalamus.

A

T

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143
Q

The _____ is the most useful lab test to help establish the diagnosis of epilepsy and assist in the accurate classification of seizures and specific epileptic syndromes.

A

EEG

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144
Q

The EEG reflects intra/extracellular currents from the summated excitatory and/or inhibitory synaptic potentials of large numbers of cortical neurons.

A

extracellular; excitatory and inhibitory

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145
Q

Low amplitude and high frequency EEG = awake/asleep

A

awake

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146
Q

During waking _____ single thalamic spikes represent the inputs from sensory stimuli. Upon sleep these spikes become _____.

A

irregular; regular and rhythmic

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147
Q

The single most important factor responsible for the change in brain activity in the transition from waking to sleep is _____.

A

the change in thalamic firing mode –> transition from single spike tonic firing in waking to bursting firing mode –> due to hyperpolarization of cells

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148
Q

Bursting in thalamic cells is due to _________ current called ___ that generates an all or none triangular shaped potential with a low threshold called the _____.

A

low threshold calcium current; called It/ T type calcium channel; with a potential called the low threshold spike (LTS)

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149
Q

Which thalamic current is blocked by TTX? Cobalt?

A

TTx = sodium; Cobalt = calcium

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150
Q

T/F Hyperpolarization during sleep brings about the bursting behavior because it allows T channels to be open, resulting in rhythmic thalamic cells that engage the cortex in a rhythmic fashion as well.

A

T

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151
Q

Why is bursting an unreliable response and incompatible with coding of information?

A
  1. it has an all or none intrinsic response that doesn’t relay information about stimuli; 2. rhythmic firing results in a refractory period
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152
Q

Single spike mode shows a ____ and reliable relationship with stimulus intensity while bursting shows a ____ function.

A

linear vs. step

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153
Q

The combination of what three features blocks sensory input form the periphery to the cerebral cortex during sleep.

A

unreliable responses, generation of rhythmic bursting, and large scale synchrony

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154
Q

Why do thalamic neurons become hyperpolarized during sleep?

A

loss of neuromodulatory systems allows Vm closer to the resting K potential.

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155
Q

involuntary coordinated patterns of muscle contraction and relaxation elicited by peripheral stimulation that is stereotyped and modulated by descending inputs.

A

reflex movements

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156
Q

chewing, swallowing, scratching, locomotion, involving central pattern generating (CPG) circuits in spinal cord and brainstem are:

A

rhythmic movement

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157
Q

goal directed, purposeful movements that are generated internally, improve with practice, correct for external perturbations, and involved feedback and feedforward control are:

A

voluntary movements

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158
Q

anticipatory control (for example, for balancing when moving limbs) is called:

A

feedforward

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159
Q

error signals that lead to compensatory change are called:

A

feedback

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160
Q

3 key principles of feed-forward systems

A
  1. essential for rapid action, 2. depends on ability to make prediction, 3. can modify the operation of feedback mechanisms
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161
Q

T/F feedback can override reflexes in voluntary movement.

A

T

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162
Q

The motor areas of the cerebral cortex influence the spinal cord either directily or through the _____ of the brain stem.

A

descending systems

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163
Q

All 3 levels of motor control receive sensory inputs and are under the control of two independent subcortical systems which are:

A
  1. basal ganglia, and 2. cerebellum
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164
Q

The basal ganglia and cerebellum act on cerebral cortex via ___ and ____.

A

VA and VL

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165
Q

Processing of sensory inputs and motor commands is distributed in _______ interconnected areas.

A

hierarchically

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166
Q

motor nuclei in the spinal cord and brainstem are called

A

lower motor neurons

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167
Q

motor control centers in the brainstem are called

A

medial and lateral systems

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168
Q

upper motor neurons are located in _____.

A

cerebral cortex

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169
Q

motor commands and feedback sensory information related to movement is processed in what relationship in various systems.

A

parallel

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170
Q

medial-lateral arrangement of motor nuclei follow what rule

A

proximal-distal

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171
Q

propriospinal neurons are _____ between lateral motor nuclei and _____ for medial nuclei

A

short and long

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172
Q

Visual input travels through the tectospinal tract to the ____ nuclei of the spinal cord and influence axial and proximal muscles.

A

medial –> visually guided postural control

173
Q

Balance signals travel in the ______ tract to the medial nuclei of the spinal cord to influence axial and proximal muscles.

A

Vestibulospinal tract

174
Q

The _______ tract receives many sensory inputs and helps control posture generally.

A

Reticulospinal tract

175
Q

The only lateral brainstem pathway begins at the ______ and extends fibers through the ______ lateral column and terminates in the _______ ventral horn. This system contributes to goal directed movements of the arm and hand (reaching and manipulating).

A

red nucleus; contralateral; contralateral

176
Q

3 medial brainstem pathways

A

tectospinal, reticulospinal, vestibulospinal

177
Q

1/3 of the axons in the corticospinal tract arise in the ______ cortex, 1/3 in _____ and 1/3 in ______.

A

1/3 motor, 1/3 premotor, and 1/3 somatosensory

178
Q

____% of the motor axons in the corticospinal tract cross the midline.

A

75

179
Q

The uncrossed corticospinal axons control what?

A

axial muscles/extensor postural muscles –> medial

180
Q

T/F M1 cells have receptive fields in the periphery and receive proprioceptive inputs from the muscles to which they project and mechnoreceptive information from the overlying skin.

A

T

181
Q

T/F Stimulation of premotor cortex produces movement at a higher threshold. These movements are complex and involve multiple joints and resemble natural coordinated movements.

A

T

182
Q

T/F termination areas of motor and premotor project in spinal cord overlap

A

T

183
Q

Premotor cortex, somatosensory cortex, and association motor cortex project to ______.

A

Motor cortex

184
Q

Parietal area 5 is where visual input converges with _______.

A

somatosensory input

185
Q

Motor cortex projects to basal ganglia and cerebellum via ______.

A

pontine nuclei

186
Q

The activation of any given muscle or set of muscles is carried out by a distributed population of neurons. What is this called?

A

Population encoding

187
Q

T/F As movement becomes more practiced, it is represented more extensively in primary motor cortex.

A

T

188
Q

T/F The firing of the corticospinal neurons is related to the force exerted and not hte displacement of the wrist (in Everton’s expt).

A

T

189
Q

Premotor cortex

A

projects to spinal cord with motor cortex; damage causes more complex motor impairments; involved in in planning and preparation of movement

190
Q

Complex movements initiated internally involve the ______ area.

A

supplementary motor area

191
Q

Movements triggered by external sensory stimuli involve lateral ______ areas.

A

premotor

192
Q

T/F Mental rehearsal invokes premotor areas.

A

T

193
Q

T/F Premotor areas that are active during movement change progressively as performance becomes automatic.

A

T

194
Q

M1 vs SMA vs LatPreM

A

M1 = specific parameters of movement; SMA = specific order of responses based on memory and internally generated plan; LatPreM = sensory motor integration

195
Q

T/F Spinal circuits involved in posture are extensively regulated by descending cortical projections.

A

T

196
Q

Supraspinal projections of the lateral motor system

A
  1. crossed corticospinal tract, 2 rubrospinal tract
197
Q

Supraspinal projections of the medial motor system

A

reticulospinal tract, vestibulospinal tract, and uncrossed corticospinal tract

198
Q

T/F Medial Motor Systems function bilaterally

A

T

199
Q

The primary brainstem regions that influence posture and blaance in the vestibulospinal tract are:

A

vestibular nuclei (lateral and medial)

200
Q

The primary brainstem regions that influence posture and balance in the reticulospinal tract are:

A

pontine and medullary reticular formation motor nuclei

201
Q

In general, the _______ contract during the stance phase and the _____ contract during the swing phase.

A

extensor vs. flexor

202
Q

T/F The muscles of the same type (extensor/flexor) that cause contraction at the three leg joints contract in a temporally overlapping but not simultaneous pattern.

A

T

203
Q

T/F For stability during walking, the opposite limbs show an overlapping pattern only during the swing phase.

A

F –> They overlap during stance to ensure stability

204
Q

CPG

A

central pattern generator is a source of rhythm and pattern of movement

205
Q

The rhythmic motor network (central pattern generator; CPG) that generates locomotion is located in the ____ spinal segments that contain the motor neurons that innervate limb muscles, and it is regulated (e.g. initiated, modulated, terminated) by descending projections, primarily from the ______ (i.e. reticulospinal pathways), as well as by sensory feedback from sensory structures in the limb muscles, joints and overlying skin.

A

same spinal segments that contain the motor neurons that innervate limb muscles and is regulated by descending projections primarily from the brainstem

206
Q

T/F the basic motor pattern for a given behavior (e.g. for locomotion) can continue to be elicited in the completely isolated spinal cord (in animal models), in the absence of both descending (i.e. RST for locomotion) and ascending (i.e. sensory) inputs.

A

T

207
Q

CPG-generated rhythmic motor patterns in the isolated CNS are often termed _________ because the motor pattern is similar to that occurring in the behaving animal but only the CNS is present.

A

fictive behaviors/fictive locomotion

208
Q

The spinal locomotor CPG is a _________ network located in the _____________ zone of the same spinal segments containing the motor neurons that innervate the limbs (i.e. C5 – T1; L2 – S3).

A

bilateral; intermediate

209
Q

One common feature of CPG organization is ______ between functional antagonists.

A

reciprocal inhibition

210
Q

T/F The locomotor CPG is hypothesized to be composed of a flexor CPG module (local circuit) and an extensor CPG module at each joint.

A

T

211
Q

Lecture example of a candidate locomotor CPG

A

HB9

212
Q

Descending control of spinal locomotor CPG

A

cortex –> MLR (mesencephalic locomotor region) –> pontine and medullary reticular formation (brainstem) –> reticulospinal tract–> CPG –> motor neurons –> muscles –> sensory

  • parallel compensatory postural system + visual postural system
213
Q

The spinal locomotor CPG “self-organizes” to generate the appropriate movement pattern based on the _______ of unpatterned input from the mesencephalic locomotor region (MLR).

A

intensity

214
Q

T/F Stepping movements are adapted by visual input that is routed through the motor cortex.

A

T

215
Q

T/F Feed-forward (Anticipatory) Postural Control is initiated by the same set of descending motor cortical signals that drive a voluntary movement.

A

T

216
Q

T/F the feed-forward postural control pathway involves Cortical activation of Reticulopinal and Vestibulospinal Neurons which in turn modify the Medial Spinal Motor System in advance of the onset of the voluntary movement (driven by the Lateral Motor System).

A

T

217
Q

T/F The feedback postural control system utilizes spinal reflex pathways to provide compensatory corrections when necessary.

A

T

218
Q

The Medial Motor System provides voluntary control. The Lateral Motor System enables postural movements.

A

F The Medial Motor System provides postural control. The Lateral Motor System enables voluntary movements.

219
Q

T/F the cerebellum evaluates disparities between intention and action and generates correction signals to cortex and brainstem.

A

T

220
Q

T/F the cerebellum receives efferent copies of every motor command.

A

T

221
Q

What are the consequences of cerebellar lesions?

A
  1. loss of spatial accuracy and temporal coordination of movement, 2. impairment of balance and loss of muscle tone, 3. no loss of sensory thresholds or strength of muscle contraction
222
Q

T/F a cerebellar lesion can result in loss of sensory thresholds or strength of muscle contraction.

A

F –> cerebellum modifies movement but does not directly communicate with motor neurons

223
Q

Cerebellar outputs

A

to brainstem (via spinal descending motor system) and to motor and premotor cortical systems (via thalamus)

224
Q

Key anatomical features of cerebellum

A
  1. gray-white matter organization; 2. folia, 2 transverse fissures, 3 lobes; 4. 3. deep cerebellar nuclei, 4. three white matter bundles;5. 3 mediolateral regions: vermis, and 2 hemispheres
225
Q

To what structure does the cerebellar cortex project?

A

deep cerebellar nuclei

226
Q

2 cerebellar input systems

A
  1. climbing fibers and 2. mossy fiber/parallel fiber system
227
Q

Climbing fibers originate in the _____ and terminate in the ______ of ______ cells.

A

inferior olive and dendrites of purkinje cells

228
Q

Purkinje fibers receive input from _____ climbing fibers whereas one climbing fiber contacts _____ purkinje cells.

A

one and 5-10

229
Q

Mossy fibers originate from nuclei in the ____ and _____ and carry sensory information from the periphery as well as information from the cerebral cortex. They terminate on ______ which send their axons to the _____ layer, forming parallel fibers.

A

spinal cord and brainstem; terminate on granule cells and send axons to the molecular layer

230
Q

Mossy fibers and climbing fibers are 2 _________ excitatory input systems.

A

glutaminergic

231
Q

Climbing fibers originate in the ______ and ascend into the cerebellum via the ______

A

contralateral inferior olive; inferior cerebellar peduncle;

232
Q

Cerebellar output from purkinje cells to DCN is modulated by ______ (neurotransmitter).

A

GABA

233
Q

A parallel fiber is the axon of a ______ cell.

A

Granular

234
Q

Each half of the cerebellum influences movements of _______ limbs.

A

ipsilateral

235
Q

The DCN are _______ cells.

A

excitatory

236
Q

The vestibulocerebellum is the ______ lobe.

A

flocculonodular

237
Q

The spinocerebellum takes inputs from the _______.

A

spinocerebellar tracts and trigeminal

238
Q

The _______ peduncle is formed by _____ fibers from the ______ that are traveling to the cerebellum.

A

mossy; Pontine nuclei

239
Q

The ______ is the only cerebellar component that projects directly out of the cerebellum and goes to the _____.

A

vestibulocerebellum –> vestibular nuclei (balance and eye movements)

240
Q

The purkinje cells in the _____ project to medial DCN (fastigial nucleus) which project to the ________ systems.

A

medial spinocerebellum/vermis –> fastigial –> medial descending systems (motor execution) (axial)

241
Q

Lateral portions of the spinocerebellum project to the _______ nuclei which project through the ________/______.

A

interposed nuclei –> lateral descending systems/red nucleus (contralateral limbs)

242
Q

The cerebrocerebellum projects to the ______ nucleus that projects to the _______ thalamus.

A

dentate –> VA/VL motor

243
Q

Lesion of the vestibulocerebellum

A
  1. inability to control eyes with head movement; 2. difficulty maintaining balance –>vertigo, widespread stance, frequent falls; 3. no problems lying down
244
Q

Lesion of interpositus

A
  1. cerebellar hypotonia, 2. dysmetria (errors in direction and extent of movement); 3. cerebellar ataxia (lack of coordination of joints); 4. terminal tremor; 5. pendular reflexes (oscillations of stretch reflex)
245
Q

Lesion of dentate

A
  1. delay in initiating movement; 2. irregularity in timing of movement components/decomposition of movements; 3. inability to judge elapsed time in tasks
246
Q

Lesion of inferior olive

A

similar to acute destruction of entire contralateral half of cerebellum –> persistent deficit in the motor learning fxns of cerebellum

247
Q

Lesion in right cerebellar hemisphere

A

delays initiation of movement

248
Q

Dysdiadochokinesia

A

irregular pattern of alternating movement

249
Q

The ________ are a collection of subcortical nuclei deep within the brain at its base.

A

basal ganglia

250
Q

Functions of basal ganglia

A
  1. selection, activation, termination of innate and learned motor programs; 2. facilitate learning of appropriate context-dependent motor behavior
251
Q

T/F Pathologic changes in basal ganglia lead to disabling involuntary movements and disorders in balance, muscle tone, and gait.

A

T

252
Q

T/F There is no weakness in basal ganglia pathologies.

A

T

253
Q

T/F Pathologic changes in basal ganglia lead to cognitive changes only.

A

F also affect emotions

254
Q

The basal ganglia contain nuclei of what embryologic origin?

A

telencephalic, diencephalic, mesencephalic

255
Q

Input nuclei of the basal ganglia

A

striatum (caudate and putamen)

256
Q

Output nuclei of the basal ganglia

A

Substantia nigra pars reticularis (SNr), Globus pallidus interna (medial) (GPi)

257
Q

Intrinsic nuclei of the basal ganglia

A

Globus pallidus externa (GPe), Substantia nigra pars compacta (SNc), Subthalamic nucleus (STN)

258
Q

What structure separates the caudate and putamen?

A

Internal capsule

259
Q

Most input to the striatum comes from _____.

A

cortex

260
Q

the putamen is ventral/dorsal to the caudate.

A

ventral

261
Q

The majority of the caudate is more rostral and receives input form the cortical association areas especially the _______ and the ______areas.

A

premotor and supplementary motor

262
Q

3 portions of caudate

A

head, body, tail

263
Q

Role of subthalamic nucleus

A

helps modulate interaction between the globus pallidus externa and interna; lies ventromedial to the pallidum

264
Q

______ is the main NT of the substantia nigra.

A

Dopamine

265
Q

2 components of substantia nigra

A

pars compacta (dopaminergic neurons that project to striatum) and pars reticularis (which receives projection from striatum and forms other ocmponent of direct pathway

266
Q

T/F the basal ganglia only modulates motor outputs from the brain and does not communicate directly with motor neurons.

A

T

267
Q

Basal ganglia pathway

A

Cortex –> striatum –> globus pallidus/substantia nigra reticularis –> cortex via VA and VL

268
Q

What is the recipient of basal ganglia output?

A

frontal lobe –> motor, premotor, supplementary motor, frontal eye fields

269
Q

The _____ pathway is thought to be the most important for the initiation of movement, and for the learning of positive outcomes associated with specific behaviors.

A

direct pathway

270
Q

The ______ pathway is thought to be hte most important for the termination of movement and for the learning of negative outcomes associated with specific behaviors.

A

Indirect

271
Q

Direct pathway

A

excitatory cortex –> striatum –> increase inhibition to internal segment of globus pallidus and substantia nigra pars reticularis (reinforced by dopaminergic input from substantia nigra pars compacta to striatum –> + feedback) –> project to thalamus (pause in inhibition) –> transient disinhibition of thalamic neurons –> increased cortical activity –> excitation of cortex

272
Q

Indirect pathway

A

excitatory signal from cortex –> striatum –> increase inhibition of external segment of globus pallidus –> pause in inhibitory output of the external pallidal segment which terminates on STN –> excitation of internal segment of globus pllidus and substantia nigra pars reticularis –> increased thalamic inhibition –> increased cortical inhibition

273
Q

In the indirect pathway, dopaminergic input from the substantia nigra pars compact is ______, opposite that of the cortical input. In the inhibitory pathway, the dopamine interacts with _____ receptors.

A

inhibitory; D2

274
Q

Which brain structure receives the major output from the basal ganglia?

A

Thalamus

275
Q

Excitatory receptors for dopamine in the striatum of the basal ganglia are ____ receptors.

A

D1 receptors

276
Q

Parkinson’s is due to a slow, progressive brain degeneration related to the accumulation of the protein __________ into cytoplasmic aggregates called ________.

A

alpha synuclein –> Lewy bodies

277
Q

Cardinal signs of Parkinson’s

A

bradykinesia, rigidity, resting tremor, stooped posture (also depression, constipation, urinary symptoms, sleep disorders)

278
Q

Parkinsonian symptoms ultimately result from abnormal ______ of the thalamus.

A

inhibition –> via loss of dopamine in the striatum (knock out the substantia nigra pars compacta)

279
Q

T/F it is believed lack of cortical stimulation causes the symptoms of parkinson’s.

A

T

280
Q

Huntington’s is due to the selective loss of _______ergic neurons of striatum whose output is through the ______ pathway.

A

GABA; indirect

281
Q

Symptoms of Huntington’s

A

chorea, athetosis, mental decline, personality changes

282
Q

Parkinson’s is a ______ disorder while Huntington’s is a _____ disorder.

A

hypo vs hyperkinetic

283
Q

T/F CAG copy number influences severity of Huntington’s.

A

T

284
Q

Neuropathology of Huntington’s is most severe in the _____ and involves reduction in the ________ of thalamic neurons by GPi/SNr.

A

striatum –> reduce inhibition of thalamic neurons –> increased stimulation of cortex

285
Q

Which of the following is not a symptom of Parkinson’s? (weakness, slowness, tremor, stiffness, postural changes)

A

weakness

286
Q

Striatum interneurons communicate with _____ (NT)

A

ACh –> M1 (excitatory) and M4 (inhibitory) receptors

287
Q

Communication between STN and GPi/SNr occurs via ___ (NT).

A

glutamate

288
Q

4 pathways that use dopamine

A
  1. mesocortical (schizophrenia); 2. mesolimbic (reward); 3. nigrostriatal (PD); 4. tuberoinfundibular (prolactin)
289
Q

Side effects of dopamine

A

addictive behaviors and psychosis

290
Q

dopamine is derived from _____

A

tyrosine –> LDOPA (rate limiting enzyme = tyrosine hydroxylase)

291
Q

T/F LDopa can cross the BBB but dopamine can’t.

A

T

292
Q

What is the best therapy for PD?

A

repletion of dopamine using L-dopa

293
Q

L-dopa is converted to dopamine where in the body?

A

intestine, liver, kidney, blood vessel endothelia –> peripheral –> need peripheral inhibitors to prolong breakdown of L-dopa until it enters BBB

294
Q

The inhibitor of dopa decarboxylase (DDC) that is administered with levodopa is_____.

A

carbidopa

295
Q

Symptomatic treatment in Huntington’s can be modulated with ______.

A

dopamine blockade

296
Q

Chorea

A

irregular, rapid random movements that flow from one body part to another

297
Q

Ballism

A

form of chorea with large-amplitude jerking or flinging movement (proximal extremities)

298
Q

Athetosis

A

writhing movements of flexion, extension, pronation, supination of fingers and hands

299
Q

Dystonia

A

sustained muscle contraction producing twisting movements or abnormal postures that are patterned and directional

300
Q

Tremor

A

rhythmic, oscillatory movmenets caused by alternate contraction of opposing muscle groups

301
Q

Tics

A

intermittent repeated, and stereotyped movements or sounds under some voluntary control

302
Q

Myoclonus

A

shock-like or lightning-like contraction or jerk

303
Q

Jerky movements

A

myoclonus, chorea, ballism, tics

304
Q

Non-jerky movments

A

Dystonia, athetosis, tremor

305
Q

Parkinsonism

A

akinesia/bradykinesia and rigidity

306
Q

How to tell PD from Essential tremor

A

ask pt to write –> PD = small writing; ET = jagged, saw tooth script

307
Q

The most common hereditary form of generalized dystonia is due to mutations in the ____ gene.

A

DYT1

308
Q

Free nerve endings are tuned for _____, ______, and ______.

A

pain, temperature, and crude touch

309
Q

T/F Pacinian corpuscles tranduce mechanical deformations and provides tonic information to the CNS.

A

F –> no tonic information. only start and end of a stimulus

310
Q

T/F The pacinian corpuscle is a rapidly adapting receptor.

A

T

311
Q

Where is the start of action potentials in peripheral receptors?

A

The first node of ranvier.

312
Q

T/F A alpha, beta, and delta fibers innervate the skin.

A

F –> there is no A alpha

313
Q

Large diameter axons are more/less vulnerable to anoxia than small diameter axons.

A

More sensitive to anoxia

314
Q

Local anesthetics are more effective on small/large diameter axons.

A

Small diameter is more sensitive

315
Q

Somatosensory receptive field

A

portion of skin which when appropriately stimulated affects the firing of the cell

316
Q

T/F Receptive fields of cutaneous dorsal root axons are round/elliptical in shape and uniform in response to stimuli.

A

T

317
Q

Dorsal root cutaneous axons _______ to synapse with many CNS neurons and each CNS neuron receives ________ from many dorsal root axons.

A

diverge; convergence

318
Q

Surround/lateral inhibition

A

dual process of divergence and convergence results in dilution of signal as it is split among more and more neurons at each level –> addition of inhibitory interneurons narrows the discharge zone on either side of the excitatory region

319
Q

Surround inhibition serves to ______ detection of edges and ________ information about the absolute amount of stimulus energy.

A

enhance or sharpen; reduce

320
Q

VPl and VPm (ventral basal complex) project to the _______ gyrus.

A

postcentral

321
Q

T/F Within any region of S1 cells sharing inputs from a single class of receptors are stacked vertically into cortical columns that extend across all cortical layers.

A

T

322
Q

Columns of stacked receptors within S1 represent either _____ or______ receptor types.

A

rapidly or slowly adapting receptors

323
Q

Components of S1

A

3a (muscle afferents), 3b (cutaneous receptors), 1 (rapidly adapting cutaneous), 2 (deep pressure)

324
Q

_______ of existing connections is the most likely explanation of modifications of cortical maps based on manipulations at receptors.

A

Unmasking

325
Q

What thalamic nucleus provides input to the anterior cingulate gyrus? What is hte major input to this nucleus?

A

anterior nucleus; mammillary bodies

326
Q

T/F Affect is processed in a different region of the brain than S1.

A

T

327
Q

Receptive field changes in adjacent areas after trauma are likely due to _____.

A

temporal correlation

328
Q

The brain receives about _____% of cardiac output.

A

20

329
Q

2 pairs of blood vessels responsible for arterial supply of brain.

A

Vertebrals –> posterior circulation and internal carotids –>anterior circulation

330
Q

T/F the internal carotids and vertebrals have branches in the neck.

A

F

331
Q

1st branch of internal carotid

A

Opthalmic

332
Q

The internal carotid enters the skull at the _________.

A

Foramen lacerum.

333
Q

Oclusion of the opthalmic artery causes ___________ blindness.

A

Ipsilateral monocular blindness

334
Q

Branches of internal carotid

A

Opthalmic, Anterior choroidal, posterior communicating, anterior cerebral and middle cerebral

335
Q

Branches of vertebrals

A

anterior and posterior spinal, posterior inferior cerebellar (PICA)

336
Q

Vertebral artery climbs up the neck via the ________.

A

transverse foramina of cervical vertebrae

337
Q

VA enters the skull via the _____.

A

Foramen magnum

338
Q

Posterior communicating artery connects ______ with ______.

A

ICA and posterior cerebral artery

339
Q

Occlusions of VA and PICA are characterized by _______ syndrome.

A

lateral medullary/Wallenburg syndrome

340
Q

The ____ divides into two major trunks and divides again into 5-7 branches to supply the majority of the lateral hemisphere, frontal lobe, temporal lobe, insular cortex, putamen, and deep white matter.

A

MCA

341
Q

Occlusion of the MCA can result in a clinical syndrome characterized by:

A

contralateral hemiparesis (face, arm, leg), aphasia, neglect, contralateral visual hemifield or quadrant defect, deviation of gaze, cortical sensory deficits

342
Q

The _____ supplies the medial frontal lobe and medial deep structures like the cingulate, corpus callosum, and the caudate nucleus.

A

ACA

343
Q

Occlusion of the ACA is characterized by:

A

contralateral lower extremity weakness

344
Q

Branches of basilar.

A

AICA, SCA, two PCAs

345
Q

Occlusion of the BA results in:

A

Weber Syndrome, Pontine/Locked In Syndrome; generally: crossed facial sensory and body motor signs, diplopia, facial numbness/weakness, vertigo, nausea and vomiting, hearing loss, ataxia, gait abnormality, etc.

346
Q

Occlusion of the PCA can cause:

A

occipital infarction and contralateral visual field loss (hemianopsia)

347
Q

The vertebral arteries supply the ____ and the _____.

A

medulla and cerebellum (PICA)

348
Q

The basilar artery supply the ____ and the _____.

A

pons and cerebellum (AICA)

349
Q

The superior cerebellar arteries supply the _____ and the _____.

A

midbrain and cerebellum (SCA)

350
Q

Tongue and swallowing problems (along with contralateral hemiparesis) may come from occlusion of the ______.

A

vertebral arteries

351
Q

A hallmark of a lower brainstem lesion is:

A

crossed sensory signs: one side of face and opposite side of body

352
Q

Contralateral weakness with eye movement abnormalities is associated with occlusion of _______.

A

distal basilar (midbrain or pontine lesion)

353
Q

Weber Syndrome

A

distal BA occlusion involving proximal PCA and/or circumferential branches –> CN 3 + motor fibers = ipsilateral CN3 palsy + contralateral hemiparesis

354
Q

Locked in/Pontine Syndrome

A

proximal/midbasilar occlusion resulting in pontine infarction –> bilateral damage leading to coma and death or destruction of descending motor pathways but preservation of dorsal pons (consciousness) –> locked in but can’t move

355
Q

Wallenburg Syndrome

A

Occlusion of PICA or VA resulting in lateral medullary symptoms: crossed signs of contralateral pain and temp, ipsilateral loss of pain and temp on face, Horner’s, ataxia, nausea, vertigo etc.

356
Q

Cerebellar infarct

A

usually due to PICA occlusion (but also SCA and AICA) –> ataxia, vertigo, possible hydrocephalus if compression of 4th ventricle

357
Q

Clinical lacunar syndrome

A

Small vessel strokes/lacunes (often of small offshoots of MCA) –> no cortical involvement

358
Q

Which vessel? R face/arm/leg weakness and trouble finding words

A

left MCA

359
Q

Which vessel? R leg weakness and confusion

A

left ACA

360
Q

Which vessel? R face/arm/leg weakness

A

left MCA deep perforator

361
Q

Spontaneous hemorrhages in the brain are usually ____ or _____.

A

Subarachnoid or intraparenchymal

362
Q

______ is usually due to rupture of a macrovascular arterial structure directly in the corresponding space.

A

Subarachnoid

363
Q

SAH presentation

A

worst headache of life + stiff neck + photophobia; with or without focal findings, CT scan + lumbar puncture, bloody and xanthochromic (yellow) CSF, angiography

364
Q

Most important causes of spontaneous SAH

A

rupture berry aneurysm (branch points), arteriovenous malformations (anywhere)

365
Q

The presence of intraparenchymal blood and SAH is likely due to _____

A

AVM rupture.

366
Q

Aneurysm key locations

A

Anterior and posterior communicating arteries + middle cerebral branchpoint

367
Q

One of the major causes of death and disability after aneurysmal SAH is ______ or narrowing of cerebral arteries resulting in ischemic injury.

A

vasospasm

368
Q

Neurologic injury due to vasospasm can be treated with _________.

A

Ca channel blocker –> nimodipine or angioplasty.

369
Q

_______ is a spontaneous hemorrhage into the brain parenchyma.

A

Intracerebral hemorrhage –>CT scan

370
Q

Most ICH is caused by ______ and are atrributed to microscopic ________, which are miniscule vascular outpouchings that occur at 90 degree arteriolar or small penetrating artery branch points.

A

hypertension; Charcot-Bouchard aneurysms

371
Q

Typical sites of ICH branch poitns are _____, ______, ____, ____, and _____.

A

putamen, lobar gray/white jxn, thalamus, pons, cerebellum

372
Q

______ is characterized by multipel cortical hemorrhages.

A

Cerebral Amyloid Angiopathy

373
Q

______ is the MRI sequence most sensitive for detecting old and new blood products.

A

gradient-echo MRI

374
Q

T/F ICH often expands in the first few hours and expansion severely worsens prognosis.

A

T

375
Q

CN _____ runs with the carotid artery

A

VI

376
Q

CN ___, ___, ___ run with the cavernous sinuses.

A

3, 4, 5

377
Q

Fronto-pontine pathway travels in the _______ while the POT pontine pathway travels in the ________.

A

anterior limb of internal capsule vs posterior limb

378
Q

Corticopontocerebellum Frontopontine pathway

A

Frontal lobe –> ALIC –> Crus –> Pons –> crossing pontocerebellar pathway –> MCP –> cerebellar cortex + dentate

379
Q

Corticopontocerebellum POT-pontine pathway

A

POT –> PLIC –> crus –> pons –> crossing pontocerebellar pathway –> cerebellar cortex + dentate

380
Q

Corticopontocerebellum output pathway

A

Purkinje –> dentate –> crossed dentato-rubro-thalamic tract –> through red nucleus –> VL thalamus –> motor cortex

381
Q

Spinocerebellum Input

A

somatosensory receptors –> L2-C8 nucleus dorsalis of Clark –> fasciculus gracilis –> nucleus dorsalis of Clark –> dorsal spinocerebellar pathway –> ICP –> cerebellar cortex –> fastigial nuclei

382
Q

Spinocerebellum Output

A

Purkinje neurons of fastigial nucleus –> vestibular nucleus –> vestibulospinal –> alpha, gamma motor neurons

383
Q

Vestibulocerebellum Input

A

vestibular apparatus –> CN VIII –> ICP –> flocculonodular lobe cortex

384
Q

Vestibulocerebellum Output

A

Purkinje cell –> vestibular nerve –> MLF eye movement + –> lateral vestibulospinal pathway –> alpha and gamma motor neurons

385
Q

The hallmark of cerebellar dysfunction is _____.

A

ataxia

386
Q

_____ cerebellar lesions lead to truncal and proximal limb dysfunction.

A

Midline

387
Q

Disease affecting the cerebellar hemispheres results in ataxia of _____.

A

extremities

388
Q

Nystagmus (jerky) can result from ______ cerebellar lesions.

A

midline

389
Q

Disruption of the metrical structure of speech is called _____.

A

ataxic dysarthria

390
Q

T/F isolated cerebellar syndromes are rare.

A

T

391
Q

Signs of _____ dysfunction are often seen with signs of cerebellar dysfunction.

A

brainstem –> same blood supply and space

392
Q

T/F Recovery from cerebellar damage may be rapid; conversely, with slowly progressive damage, a patient can lose a large volume of cerebellum before signs are apparent.

A

T

393
Q

Normal tone/transient tone with acute cerebellar damage.

A

Transient hypotonia

394
Q

T/F normal tone or hypotonia can occur with chronic cerebellar damage.

A

T

395
Q

Appendicular ataxia is maximal at the ______ endpoint of a motor act.

A

Extreme

396
Q

Cerebellar lesions cause dysfunction on the ipsilateral/contralateral side of the body.

A

ipsilateral –> double crossing

397
Q

Differentiating between sensory and cerebellar ataxia.

A

Romberg sign present with sensory ataxia

398
Q

Differentiating between vestibular dysfunction and cerebellar ataxia.

A

vertigo present with vestibular dysfunction

399
Q

Differentiating between corticospinal tract disease and cerebellar ataxia.

A

UMN signs in corticospinal tract lesion

400
Q

Differentiating between myopathic proximal limb weakness and cerebellar ataxia.

A

weakness present in myopathy

401
Q

T/F autoantibodies from ovarian cancer are often directed at the cerebellum.

A

T –> paraneoplastic cerebellar degeneration

402
Q

Cerebellar symptoms due to antecedent viral infection.

A

Post-infectious cerebellitis

403
Q

Caudal displacement of cerebellar tonsils below foramen magnum.

A

Chiari I malformation

404
Q

Chronic ataxia in the cerebellum can be caused by what drugs?

A

alcohol and phenytoin

405
Q

Chronic ataxia in the cerebellum can be caused by what drugs?

A

alcohol and phenytoin

406
Q

When to consider brainstem as a lesion point.

A
  1. patients have cranial nerve symptoms or 2. patients have cerebellar dysfunction
407
Q

When is brainstem involvement certain.

A
  1. crossed hemiparesis or 2. lesion is on hte side of the cranial nerve palsy or ataxia
408
Q

When should we think about damage AROUND the brainstem?

A
  1. multiple cranial nerve involvement or 2. no crossed motor/sensory signs in the extremities
409
Q

Lesion of the MLF is ipsilateral/contralateral to the eye that doesn’t abduct in INO.

A

ipsilateral

410
Q

Left Afferent Relative Pupillary Defect

A

Eye constricts appropriately when opposite eye is lit but dilates when it is itself lit

411
Q

Anisocoria

A

physiologic –> non disease state with differences in pupil size (consistent size difference in light and dark) vs. abnormal

412
Q

Light stimulation of the pupils produces unilateral/bilateral constriction of the pupils because of 1/2 crosses in ______ area(s).

A

bilateral; 2 crosses; chiasm and pretectal area (edinger-westphal nucleus)

413
Q

When you see an afferent pupil defect, you almost always have a ______ problem.

A

optic nerve

414
Q

Anisocoria is to do with efferents/afferents.

A

Efferents

415
Q

In Horner’s is anisocoria greater in the dark or the light?

A

dark –> dilation lag

416
Q

T/F In Horner’s the eye dilates to cocaine.

A

F

417
Q

Horner’s Syndrome Localizatoin

A

1st order –> brainstem; 2nd order –> brachial plexus/lung apex, 3rd order –> carotid dissection

418
Q

1st order Horner’s

A

brainstem –> miosis, ptosis, anhidrosis (face, arm, leg)

419
Q

2nd order Horner’s

A

brachial plexus/lung apex (e.g. pancoast tumor)-> miosis, ptosis, anhidrosis (face)

420
Q

3rd order Horner’s

A

carotid artery dissection–> miosis, ptosis, anhidrosis (upper face)

421
Q

A lesion of the ciliary ganglion produces a _____ pupil.

A

tonic

422
Q

Adie’s tonic pupil

A

unilaterally large pupil; tonic response to near; segmental reaction of iris; follows ciliary ganglion injury (possible reflexes lost)

423
Q

Argyll Robertson pupil

A

poor light response but brisk near target response –> bilateral

424
Q

3rd nerve palsy is often associated with which aneurysm

A

posterior communicating artery

425
Q

Which Horner’s syndrome is painful?

A

3rd

426
Q

T/F An afferent pupillary defect may also be seen in chiasmal and optic tract lesions, but not in pathological processes that affect the visual pathway posterior to the lateral geniculate body.

A

T

427
Q

T/F

A

Patients with cataracts and functional visual loss as a cause for their visual loss will not have an afferent pupillary defect.

428
Q

T/F The most common central cause of Horner’s syndrome is a dorsolateral medullary infarction.

A

T

429
Q

T/F Birth trauma and occult neuroblastoma are the most important causes of Horner’s syndrome to recognize in childhood.

A

T

Brain and Behavior (5 decks)

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