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Neuro > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Somatic motor of CN nuclei

A

Modality: GSE
Function(s): extraocular mm., intrinsic tongue mm.
Brainstem nuclei: oculomotor, trochlear, abducens, hypoglossal
CNs: III, IV, VI, XII

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2
Q

Branchial motor of CN nuclei

A

Modality: SVE
Function(s): mm. of mastication, facial expression, middle ear, pharynx, larynx, SCM, upper portion of trap
Brainstem nuclei: motor nucleus of CN V, facial nucleus, nucleus ambiguus, accessory spinal nucleus
CNs: V, VII, IX, X, XI

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3
Q

Parasympathetic of CN nuclei

A

Modality: GVE
Function(s): parasympathetic innervation of head and thoracoabdominal viscera above splenic flexure
Brainstem nuclei: Edinger-Westphal nucleus, superior salivatory nucleus, inferior salivatory nucleus, dorsal motor nucleus of CN X
CNs: III, VII, IX, X

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4
Q

Visceral sensory of CN nuclei (special)

A

Modality: SVA
Function(s): taste
Brainstem nuclei: nucleus solitarius (rostral portion, gustatory nucleus)
CNs: VII, IX, X

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5
Q

Visceral sensory of CN nuclei (general)

A

Modality: GVA
Function(s): inputs for control of cardio-respiratory and digestive function
Brainstem nuclei: nucleus solitarius (caudal portion, cardiorespiratory nucleus)
CNs: IX, X

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6
Q

General somatic sensory of CN nuclei

A

Modality: GSA
Function(s): touch, pain, temp, position, and vibration sense for face, sinuses, and meninges
Brainstem nuclei: trigeminal nuclei
CNs: V, VII, IX, X

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7
Q

Special somatic sensory of CN nuclei

A

Modality: SSA
Function(s): olfaction, vision, hearing, vestibular sensation
Brainstem nuclei: cochlear nuclei, vestibular nuclei (olfaction and vision do not have sensory nucleus)
CNs: CN VIII

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8
Q

Common symptoms of brain stem lesions

A
  1. Double vision
  2. Vertigo
  3. Nausea
  4. Incoordination
  5. Gait imbalance
  6. Numbness of the face
  7. Hoarseness
  8. Difficulties with swallowing and speaking
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9
Q

Common signs of brain stem lesions

A
  1. Multiple cranial nerve dysfunctions
  2. Gaze palsies
  3. Nystagmus
  4. Sympathetic dysfunction (Horner’s syndrome)
  5. Hearing loss
  6. Dysphagia
  7. Dysarthria
  8. Dysphonia
  9. Tongue deviation or atrophy
  10. Paresis or dysesthesia of face with contralateral motor or sensory deficits in the body
  11. Unilateral hemiparesis with ataxia
  12. Significant bilateral brain stem lesions produce altered mental status or coma
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10
Q

DCML pathway

A

Function: pressure, vibration, fine touch, proprioception
Primary afferent: sensory nerve ending»bypasses pseudounipolar cell body in DRG»enters spinal cord»ascends ipsilaterally in dorsal columns
First synapse: nucleus gracilis, nucleus cuneatus in ipsilateral medulla
Secondary afferents: decussates in medulla»ascends contralaterally as the medial lemniscus
Second synapse and projections: VPL in thalamus»sensory cortex

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11
Q

Spinothalamic tract

A

Function: pain, temperature
Primary afferent: sensory nerve ending (Adelta and C fibers)»bypasses pseudounipolar cell body in DRG»enters spinal cord
First synapse: ipsilateral gray matter in spinal cord
Secondary afferents: decussates in spinal cord as anterior white commissure»ascends contralaterally
Second synapse and projections: VPL in thalamus»sensory cortex

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12
Q

Lateral corticospinal tract

A

Function: voluntary movement of contralateral limbs
Primary efferents: UMN: cell body in primary motor cortex»descends ipsilaterally through posterior limb of internal capsule, most fibers decussate at caudal medulla in pyramids»descends contralaterally
First synapse: cell body of lateral ventral horn of spinal cord
Secondary efferents: LMN: leaves spinal cord
Second synapse and projections: NMJ»muscle fibers

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13
Q

CN III GVE nucleus, ganglia, and end-organs

A

Edinger-Westphal

CIliary ganglion»pupillary constrictor and ciliary mm

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14
Q

CN VII GVE nucleus, ganglia, and end-organs

A

Superior salivatory
Pterygopalatine ganglion»lacrimal gland and nasal pharynx
Submandibular ganglion»submandibular and sublingual salivary glands

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15
Q

CN IX GVE nucleus, ganglia, and end-organs

A

Inferior salivatory

Otic ganglion»parotid salivary gland

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16
Q

CN X GVE nucleus, ganglia, and end-organs

A

Dorsal motor nucleus

Ganglia in end-organs»heart, lung, digestive tract to level of splenic flexure

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17
Q

CN IX and X GVA nucleus

A

Nucleus solitarius
Chemo- and baroreceptors of carotid body (IX) and aortic arch (X)»cardiorespiratory system and digestive tract (X) caudal portion

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18
Q

Anterior nuclei

A

part of the limbic circuitry and receive input from the hippocampus/hypothalamus and project to the cingulate gyrus

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19
Q

Medial nuclei

A

thalamic relay nuclei for the association cortex in the frontal lobe
Lesions result in deficits in working memory

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20
Q

Ventral anterior nuclei

A

receive input from the basal ganglia, substantia nigra, and cerebellum and project to all areas of motor cortex
Movement planning

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21
Q

Ventral lateral nuclei

A

receive input from the basal ganglia, substantia nigra, and cerebellum and project to primary motor cortex
Movement planning and control

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22
Q

Ventral posterior nuclei (VPL/VPM)

A

receive input from DCML and spino/trigeminothalamic systems and project to somatosensory cortex
Touch, Proprioception

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23
Q

Lateral nuclei

A

relay nuclei to association cortices in the parietal and temporal lobes and function in sensory integration for vision, hearing, and eye movement control

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24
Q

Extra-intralaminar nuclei

A

Diffuse projection nuclei

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25
Q

Lateral geniculate nucleus

A

visual info to visual cortex

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26
Q

Medial geniculate nucleus

A

auditory info to auditory cortex

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27
Q

Pulivar nucleus

A

parieto-occipital cortex; eye and head control with movement

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28
Q

Hypothalamus

A

plays a primary role in the regulation and release of hormones from the pituitary gland, maintenance of body temperature, and organization of goal seeking behaviors such as feeding, drinking, mating and aggression
Primary center for control of autonomic function

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29
Q

Epithalamus

A

Includes the Pineal Gland known as the ‘tranquilizing organ’

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30
Q

Pinealocytes

A

Secrete serotonin and melatonin (circadian rhythms)

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31
Q

Anterior cerebral artery covers what area of the cerebral cortex?

A

Frontal lobe; right down the center of where hemispheres meet

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32
Q

Middle cerebral artery covers what areas of the cortex?

A

Parietal and upper temporal lobes

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33
Q

Broca’s area

A

Within frontal lobe responsible for speech production»lesion results in aphasia

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34
Q

Wernicke’s area

A

Within temporal lobe responsible for language reception and comprehension

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35
Q

Frontal lobe

A

Motor and voluntary movement; prefrontal cortex = executive brain, higher-order thinking and problem-solving

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36
Q

Parietal lobe

A

Somatosensory cortex (pain, temp, touch, pressure) and spatial processing and manipulation

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37
Q

Occipital lobe

A

Vision

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38
Q

Temporal lobe

A

Auditory and language

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39
Q

Assymetries of the brain

A
  • Left parieto-occipital region wider and extends further posteriorly than right
  • frontal lobe larger on right and more anterior
  • Broca’s and Wernicke’s larger on left
  • blood flow greater on right in infants»dominance shifts from right to left with left parietal dominance and right-handedness emerging
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40
Q

Why have hemispheric lateralization?

A

Allows certain functions to be processed mainly within one hemisphere, eliminating delays caused by long callosal transmission times

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41
Q

Dominant hemisphere

A

Left

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42
Q

Non-dominant hemisphere

A

Right

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43
Q

WADA test

A

Anesthetize the brain with sodium amytal and look to see what function is left

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44
Q

Hemineglect syndrome

A

Neglect left side with lesions on right because right parietal lobe is pretty much monitoring the environment of both sides - often seen with strokes or neurosurgery; short-lived, but can be seen in aging

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45
Q

Right hemisphere

A

Visuo-spatial skills

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46
Q

Left hemisphere

A

Language, praxis (motor formulation)

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47
Q

Prefrontal cortex

A

Restraint
Initiative
Order

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48
Q

Frontal lobe lesion symptoms

A
  • Contralateral hemiparesis, facial weakness
  • Broca’s aphasia: motor, expressive aphasia (dominant)
  • Primitive reflexes: grasp and sucking
  • Apraxia of gait
  • Incontinence
  • Paralysis of contralateral eye movement and head turning (favoring gaze away from the lesion)
  • Behavioral changes: social disinhibition, loss of initiative and interest, inability to solve problems, loss of abstract thought, impaired concentration and attention without intellectual or memory decline
49
Q

Parietal lobe lesion symptoms

A
  • Contralateral discriminatory, vibratory sensory impairment
  • Visual field defect: contralateral lower homonymous quadrantanopia
  • Dominant syndromes: Gerstmann’s syndrome, bilateral ideomotor and ideational apraxia
  • Non-dominant syndromes: constructional apraxia, dressing apraxia, contralateral sensory inattention (neglect)
50
Q

Temporal lobe lesion symptoms

A
  • Wernicke’s aphasia: sensory, receptive aphasia (dominant)
  • Auditory agnosia: inability to recognize sounds (non-dominant)
  • Visual field defect: contralateral upper homonymous quandrantanopia
  • Learning difficulties: auditory (dominant) and visual (non-dominant) information
  • Memory impairment
  • Emotional disturbances: aggression, rage -Hypersexuality
  • Olfactory and gustatory hallucinations
  • Vestibular dysfunction
51
Q

Occipital lobe lesion symptoms

A
  • Contralateral homonymous hemianopia
  • Cortical blindness
  • Visual agnosia
  • Visual illusions
52
Q

Bones derived from neural crest (ectoderm)

A

Frontal, sphenoid, ethmoid nasal, lacrimal, zygomatic, maxilla, incisive, mandible, squamous temporal bone, hyoids

53
Q

Bones derived from somites (mesoderm)

A

Parietal, petrous temporal, occipitals, body of sphenoid

54
Q

Endochondral ossification in head

A

Skull base elongates and facial bones grow inferiorly and enlarge

55
Q

Intramembranous ossification in head

A

Mesenchyme forms models that ossify via intramembranous ossification.
Bones enlarge radially until they meet.
Thereafter bone resorption allows growth.

56
Q

Early cranial base bones

A

-Basioocipital»occipital bone anterior to foramen magnum
-Basisphenoid and presphenoid»body of sphenoid bone
Mesethmoid»ethmoid

57
Q

Neoteny

A

Persistence of child-like features in adults

58
Q

Achondroplasia

A

Early closure of growth plates due to FGFR mutation

  • Large head
  • Mid-facial hypoplasia
  • Prominent forehead
  • Short limbs
59
Q

What regulates the interaction of bony spicules during growth of the calvarium?

A

Dura mater and periosteum

60
Q

Suture formation (week 6-8)

A
  1. Signals from bone fronts prevent suture obliteration.
  2. Once fronts overlap, signals from dura stabilize suture while other signals thicken cranial bones.
  3. The suture sends signals back to dura to stop osteogenic signals.
  4. If no signals from the bone edges or underlying dura mater, sutures will fuse too early.
61
Q

Early closure of metopic suture

A

Synostotic trigonocephaly (Stewie shaped head; triangle; frontal and occipital bulges A/P)

62
Q

Early closure of bicoronal suture

A

Synostotic brachycephaly (round, short head, frontal and temporal bulges L/R)

63
Q

Early closure of unicoronal suture

A

Synostotic anterior plagiocephaly (slanting head; expands away from fused suture, temporal)

64
Q

Deformational posterior plagiocephaly (positional plagiocephaly)

A

Happens when the baby lays on their back too much; looks like a rhombus; ear anterior

65
Q

Early closure of lamboid suture

A

Synostotic posterior plagiocephaly (slanting; skull expands away from fused suture, occpital; ear on fused side is posterior)

66
Q

Early closure of sagittal suture

A

Synostotic scaphocephaly (boat; looks like an oval, frontal and occpiptal bulge A/P)

67
Q

Premature closure of the coronal and lambdoidal sutures causes the skull to expand superiorly to a point

A

Oxocephaly

68
Q

Premature closure of the coronal and lambdoidal sutures causes the skull to expand superiorly but it doesn’t come to a point

A

Turricephaly

69
Q

Least to most complex sutures

A

Metopic»squamous»coronal»sagittal»lambdoid

70
Q

Where are wormian bones most commonly seen?

A

Lambdoid suture

71
Q

Development of sinuses

A

Maxillary - before birth
Ethmoid air cells - 2
Sphenoid sinus - begins at 2
Frontal sinus - 7

72
Q

Sonic hedgehog

A

Facial epithelium and initiates changes that will lead to a typical cranio-facial appearance

73
Q

Pharyngeal grooves derived from

A

Ectoderm

74
Q

Pharyngeal pouches derived from

A

Endoderm

75
Q

1st pharyngeal pouch forms

A

Auditory tube and primitive tympanic cavity

76
Q

1st pharyngeal groove forms

A

External auditory meatus

77
Q

2nd pharyngeal pouch forms

A

Tonsilar bed where palatine tonsil will sit

78
Q

3rd pharyngeal pouch forms

A

Inferior parathyroid gland and thymus

79
Q

4th pharyngeal pouch forms

A

Superior parathyroid gland and ultimobranchial body (C cells of thyroid gland)

80
Q

How does the auricle develop

A

from six auricular hillocks that fuse, migrate and eventually form the mature auricle.

81
Q

Malformation of external ears can be indicative of problems with…

A

1st and 2nd arches (hillocks come from 1 and 2)

82
Q

Failure of the cervical sinus to obliterate can result in

A

Branchial fistulae or cysts

83
Q

Branchial fistulae

A

openings from the skin (external) or oral region (internal) that extend to a cervical cyst.

84
Q

Branchial cysts

A

Fluid-filled sacs along anterior border of SCM

85
Q

Thyroid gland descends inferiorly and leaves a pit called… and is connected to the tongue via the…

A

foramen cecum; thyroglossal duct

86
Q

Thyroglossal duct cyst

A

Thyroid tissue lodges along the path of the thyroglossal duct. Separate from the thyroid gland

87
Q

Holoprosencephaly

A

there is midline narrowing, which in an extreme form has the eyes (or eye) form so close to the midline that the frontonasal prominence is unable to descend, leaving a proboscis in the forehead.

88
Q

Unilateral cleft lip

A

Unilateral failure of medial nasal prominence to fuse with maxillary process

89
Q

Oblique facial cleft

A

Failure of medial and lateral nasal prominences to fuse with the maxillary prominence.

90
Q

Bilateral cleft lip

A

Bilateral failure of medial nasal prominences to fuse with maxillary processes

91
Q

Philtrum is connected to…which contributes the 4…to the maxilla and fuses with the rest of the hard palate

A

Incisive bone; incisors

92
Q

Crouzon syndrome

A
  • caused by a mutation affecting the FGFR2 gene/protein.
  • often manifests as first pharyngeal arch malformations, a flattened face, malformations of the palate, exophthalmos, and premature suture fusion.
93
Q

Pharyngeal grooves 2-4 form

A

Cervical sinus temporarily

94
Q

1st arch

A
  • Maxilla, mandible, malleus, and incus
  • Muscles of mastication, tensor veli palatini, tensor tympani, mylohyoid, anterior belly of digastric muscle.
  • Innervated by CN V
95
Q

2nd arch

A
  • Stapes, styloid, and part of hyoid bone
  • Muscles of facial expression, stapedius, stylohyoid, posterior belly of digastric muscle
  • Innervated by CN VII
96
Q

3rd arch

A
  • Body & greater horn of hyoid bone
  • One pharyngeal muscle – stylopharyngeus m.
  • Innervated by CN IX
97
Q

4th and 6th arches

A
  • Laryngeal cartilages
  • Pharyngeal and Laryngeal muscles: swallowing & phonation
  • 4th arch innervated by CN X
  • 6th arch innervated by recurrent laryngeal nerve from CN X.
98
Q

Corticonuclear tracts

A

Origin: lateral motor cortex
Decussation: at or near target nucleus
Target: motor neurons in cranial motor nuclei V, VII, IX, X, XI, and XII

99
Q

Which inputs into the nuclei are bilateral?

A

motor nucleus of V, facial motor nucleus to forehead and upper face, nucleus ambiguus (IX and X), except for neurons innervating soft palate and uvula, hypoglossal except genioglossus

100
Q

Which inputs into the nuclei are unilateral?

A

facial motor nucleus to rest of face is contralateral, IX and X are contralateral to soft palate and uvula, accessory motor nucleus is contralateral for upper trapezius and ipsilateral to SCM, hypoglossal to genioglossus contralateral

101
Q

Mesencephalic nucleus of V

A

primary afferent neurons conveying proprioceptive info from muscles of mastication and periodontal ligament

102
Q

Pseudobulbar palsy

A
  • Degeneration of corticobulbar pathways to V, VII, X, XI, XII
  • LMN signs absent
  • gag reflex +/exaggerated
  • jaw jerk +
  • spastic tongue
  • spastic dysarthria
  • dysphagia
  • lack of facial expressions
  • difficulty chewing
  • emotional lability
  • bilateral UMN
103
Q

Bulbar palsy

A
  • Disturbeances to X, XI, XII, sometimes VII rather than tracts
  • LMN signs present
  • gag reflex -
  • wasted tongue, fasciculations
  • jaw jerk (n)
  • nasal speech
  • normal emotions
  • LMN
  • progressive dysarthria/dysphagia
104
Q

LMN lesion of accessory motor nucleus

A

Ipsilateral weakness of shoulder shrug or arm elevation and weakness of head turning AWAY from lesion

105
Q

UMN lesions of accessory motor nucleus

A

Contralateral weakness of shoulder shrug or arm elevation

Weakness of head turning away from lesion

106
Q

LMN lesion of XII

A

tongue deviates toward lesion

107
Q

UMN lesion of XII

A

tongue deviates away from lesion

108
Q

Chief sensory nucleus of V

A

Fine touch and vibration»trigeminal lemniscus pathway»VPM in thalamus (nucleus is homologue of DCML nuclei - gracilis and cuneatus)

109
Q

Mesencephalic nucleus of V

A

Proprioception

110
Q

Spinal nucleus of V

A

Pain, temp, dull touch»trigeminothalamic tract pathway»VPM in thalamus (analogous to dorsal horn of spinal cord)

111
Q

Trigeminal lemniscal pathway

A

Primary neuron: pseudounipolar neurons with cell bodies in cranial ganglion of trigeminal nerve
Secondary neuron: neurons in chief sensory nucleus of V
Decussate immediately on leaving chief sensory nucleus of V to join contralateral trigeminal lemniscus
Tertiary neuron: VPM nucleus of thalamus
Travel in posterior limb of internal capsule to postcentral gyrus of parietal lobe

112
Q

Trigeminothalamic pathway

A

Trigeminal pain and temp fibers descend caudally in spinal tract of V to enter and synapse on secondary neurons in spinal nucleus of V
-Fibers from spinal nucleus of V decussate and join the ascending spinothalamic tract as the trigeminothalamic pathway

113
Q

Blink reflex

A

Early phase- input from A-beta fibers in V from the cornea synapse on neurons in the chief sensory nucleus which in turn synapse on motor neuron in VII motor nucleus
Late phase- input of A-delta and C-fibers in V from the cornea enter the Spinal Tract of V and synapse on neurons in the Spinal Nucleus of V which project and synapse bilaterally on motor neurons in VII.
The side that is directly stimulated is called the DIRECT corneal reflex while that on the opposite side is called the CONSENSUAL corneal reflex.

114
Q

Gag reflex

A
  1. Irritant stimulates IX afferent fibers in posterior tongue
  2. Spinal nucleus of V
  3. Nucleus ambiguus
  4. Branchial motor efferent nerves stimulated
  5. Elevation of soft palate, closure of glottis, contraction of pharyngeal wall
115
Q

Glossopharyngeal neuralgia

A

Pain begins in posterior tongue or pharyngeal wall and radiates to the ear (triggered by swallowing or talking)
-when drugs don’t work, transection of dorsomedial portion of spinal tract of V can offer relief

116
Q

CN III parasympathetic nucleus

A

Edinger-Westphal

  • Ciliary ganglion
  • pupillary constrictor muscle and ciliary muscle
117
Q

CN VII parasympathetic nucleus

A

Superior salivatory

  • pterygopalatine ganglion
  • lacrimal gland and nasopharynx
  • submandibular ganglion
  • submandibular and sublingual glands
118
Q

CN IX parasympathetic nucleus

A

Inferior salivatory

  • otic ganglion
  • parotid salivary gland
119
Q

CN X parasympathetic nucleus

A

Dorsal motor nucleus

  • ganglia in end-organs
  • heart, lung, digestive tract to level of splenic flexure

Neuro (6 decks)

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