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Neuro/Behavior I > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Nanocircuits

A

Within neurons: constitute biochemical machinery, for key neuronal properties such as learning and memory, and genesis of neuronal rhythmicity

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2
Q

MicrocircuitS

A

Between a few neurons: perform complex tasks, such as reflexes, sensing, locomotion, and learning/memory

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3
Q

Macrocircuits

A

Among multiple microcircuits: mediate higher brain functions, such as object recognition and cognition

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4
Q

Alzheimer’s disease

A

Loss of cognitive function and memory due to neurodegeneration, particularly cholinergic neurons in the CNS

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5
Q

Epilepsy

A

Brain seizure due to uncontrolled recruitment of electrical activity of neurons

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6
Q

Huntington’s disease

A

Neurodegenerative diseases associated with abnormal involuntary movements due to repeated mutation in Huntington gene

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7
Q

Myasthenia gravis

A

Autoimmune disease associated with muscular weakness due to loss of acetylcholine receptors at the neuromuscular synapse

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8
Q

Parkinson’s disease

A

Movement disorder due to degeneration of dopamine neurons in the substantia nigra-basal ganglia pathway

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9
Q

Schizophrenia

A

Delusions and hallucinations due to imbalance in the dopamine and glutamate neurotransmitter systems

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10
Q

Stroke

A

Loss of specific functions do to occlusion of blood supply to a specific brain region

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11
Q

Core mechanisms of neurological function

A

1.) genes
2.) neuronal structures: myelin, synapse
3.) Neurotransmitters and receptors: dopamine
4.) neural circuits: basal ganglia

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12
Q

Vesicular fusion is more likely when:

A

Release of calcium in presynaptic neuron is high— causing sodium release

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13
Q

Multipolar neurons

A

1.) motor neurons
2.) pyramidal neurons
3.) Purkinje cells

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14
Q

Bipolar neurons

A

In the sensory system

1.) retinal neuron
2.) olfactory neuron

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15
Q

Unipolar neurons

A

1.) dendrites and axons, touch and pain sensory neurons

2.) anaxonic neuron: amacrine cell, dendrites only

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16
Q

Who stained pyramidal, and Purkinje neurons?

A

Cajal

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17
Q

Electrical signals in a neuron

A
  1. Resting membrane potential
  2. Synaptic potential
  3. Action potential

Depolarization= increase in positive charge

Hyperpolarization= increase in negative charge (AP less possible)

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18
Q

Ion transporters

A

• actively move ions against concentration gradient
• create ion concentration gradients
• one molecule at a time

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19
Q

Ion channels

A

• allow ions to diffuse down a concentration gradient
• cause selective permeability to certain ions
• opens entire channel, free flow

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20
Q

Electrical signals are generated by:

A

1.) concentration differences of ions across the membrane (transporters)
2.) selective permeability of membrane to certain ions (channels)

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21
Q

Resting membrane potential is set by:

A

Equilibrium potential for potassium (K)

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22
Q

Resting and action potentials rely on permeability to:

A

Different ions:

• resting potential= k»na
• action potential= na»k
• repolarization= k»na

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23
Q

Hodgkin and Huxley model

A

Action potential depend on three time and voltage sensitive processes:

1.) activation of sodium channels
2.) activation of potassium channels
3.) inactivation of sodium channels

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24
Q

How do sodium and potassium channel blockers affect an action potential?

A

Sodium: amplitude of the AP
Potassium: width of the AP

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25
Q

Tetrodotoxin

A

TTX blocks sodium channels resulting in paralysis. Produced by bacteria that live in pufferfish

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26
Q

Procaine and lidocaine

A

Clinical application of sodium channel antagonist for local anesthesia— decreases AP, sensory neurons not sending signal to brain

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27
Q

Halothane treatment

A

Clinical application of potassium channel agonists, for general anesthesia— hyperpolarization makes APs difficult to generate

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28
Q

What makes APs different in each area of the body/brain?

A

Non-uniform distribution of ion channels (example: dopamine neuron is 20x wider than Purkinje neuron AP)

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29
Q

Developmental shortening

A

Mature neurons have a much more narrow AP

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30
Q

Activity dependent modulation

A

Inactivity of sodium and potassium channels can cause a larger gap/width of AP

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31
Q

Spike initiation site

A

Usually axon hillock, but sometimes dendrites

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32
Q

Spike propagation

A

Forward into axon and backward into dendrites

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33
Q

Spike conduction requires both:

A

Active and passive current flow

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34
Q

Saltatory action potential

A

Jumping from node to node of Ranvier when axon is myelinated. Nodes of Ranvier boost, electrical signal by opening channels. Myelination conducts 100x faster

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35
Q

Electronic synapse

A

Gap junctions: allow ions to flow through their gap junction channels from one neuron to the next

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36
Q

Chemical synapse

A

Vesicular synapsing: allow neurotransmitter release, and ions flow through postsynaptic channels

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37
Q

Excitatory chemical synapses

A

Glutamate: inflow of sodium (cation), depolarization, EPSP (excitatory, postsynaptic potential)

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38
Q

Inhibitory synapse

A

GABA: inflow of chloride ions (anion), hyperpolarization, IPSP (inhibitory postsynaptic potential)

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39
Q

Postsynaptic potential relies on

A

Temporal and spatial summation (excitatory versus inhibitory, and the time it occurs at)

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40
Q

Feedforward excitation

A

Pre excites post

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41
Q

Feedforward inhibition

A

Pre excites inhibitory interneuron, inhibitory interneuron inhibits post

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42
Q

Lateral inhibition

A

Pre excites to inhibitory interneurons, which inhibit neighboring cells

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43
Q

Feedback/recurrent inhibition

A

Pre excites post, post excites inhibitory interneuron, inhibitory interneuron inhibits pre

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44
Q

Feedback/recurrent excitation

A

Pre excites post, which excites interneuron, which excites pre

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45
Q

Example of feedforward circuitry

A

Knee-jerk reflex: pre excites post, pre excites inhibitory interneuron which inhibits post at the same time

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46
Q

Divergence

A

One sensory neuron—> many motor neurons (great force)

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47
Q

Convergence

A

Many sensory—> one motor (guarantees movement)

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48
Q

Circadian rhythm

A

Feedback inhibition of PER generates circadian rhythm

TIM plus PER= inhibition of period gene

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49
Q

SCALP

A

Skin, connective tissue, aponeurosis, loose connective tissue, Pericranium

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50
Q

Pathway of cranial veins

A

Superficial veins in connective tissue connect to dural venous sinuses (superior sagittal sinus) via diploic veins, and emissary veins

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51
Q

Superficial artery, vein, and nerve of face and scalp

A

Superficial temporal artery, by ear, pulse point

Auriculotemporal nerve (sensory branch of mandibular division of CN V— trigeminal nerve)

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52
Q

Trigeminal nerve, CN V

A

V1: ophthalmic nerve
V2: Maxillary nerve
V3: mandibular nerve

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53
Q

CN5 trigeminal V1: ophthalmic nerve branches

A

1a: supraorbital nerve
1b: supratrochlear nerve
1c: infratrochlear nerve
1d: external nasal nerve

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54
Q

CN5, trigeminal V2: maxillary nerve branches

A

2a: zygomaticotemporal nerve
2b: zygomaticofacial nerve
2c: infraorbital nerve

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55
Q

CN5, trigeminal V3: mandibular nerve branches

A

3a: auriculotemporal nerve
3b: buccal nerve
3c: mental nerve

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56
Q

Epidural hemorrhage

A

Bleeding between the Dura matter and the skull, usually involves rupture of middle meningeal artery

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57
Q

Subdural hemorrhage

A

Bleeding between the arachnoid matter and the Dura matter, usually involves rupture of cerebral veins (because they transverse the meninges)

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58
Q

Subarachnoid hemorrhage

A

Occurs between the subarachnoid membrane and the pia matter, usually involves rupture of cerebral artery (deep)

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59
Q

Cranial nerves: sensory, motor, both

A

Some say money matters, but my brother says big brains matter more

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60
Q

Cranial nerves

A

Olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, vestibulocochlear, glossopharyngeal, vagus, spinal accessory, hypoglossal

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61
Q

Glial cells in the CNS

A

Ependymal cells, oligodendrocytes, astrocytes, microglia

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62
Q

Glial cells in the PNS

A

Satellite cells, Schwann cells

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63
Q

How do glial cells differ from neurons?

A

1.) do not form synapses
2.) only one type of process
3.) retain the ability to divide
4.) less excitable

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64
Q

Functions of glia

A

1.) modulate electrical signals
2.) repair damage or regenerate
3.) prevent uncontrolled regrowth

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65
Q

Astrocytes

A

• maintain chemical environments for neural signaling, including formation of the BBB
• secrete substances to facilitate new synapse formation
• retain the characteristics of stem cells for neural repair (can differentiate into neurons)

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66
Q

Microglia

A

• migrate to injury site following brain damage
• remove debris after injury (macrophage)
• secrete cytokines to modulate inflammation

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67
Q

Oligodendrocytes and Schwann cells

A

• form myelin
• regenerative stem cells in response to injury

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68
Q

Mechanisms of myelination

A

• inductive/attractive cue: binds myelinating cell to axon
• repulsive cue: prohibits binding of myelinating cell to axon
• retraction: terminate the process of myelination

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69
Q

Oligodendrocyte progenitor cells (OPC)

A

Originate in neuroepithelium of the spine and migrate to the brain. Their differentiation into oligodendrocytes involves re-organization of cytoskeleton proteins, allowing them to myelinate axons

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70
Q

Protein composition of myelin

A
  1. MBP– myelin basic protein
  2. PLP– proteolipid protein
  3. CNP– cyclic nucleotide phosphodiesterase
  4. MAG – myelin associated glycoprotein
  5. MOG – myelin oligodendrocyte glycoprotein
  6. OMgp– oligodendrocyte-myelin glycoprotein
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71
Q

MBP is essential for

A

Membrane compaction and cytoplasm extrusion

— CNP counteracts MBP compacting, critical for a metabolite diffusion and protein delivery

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72
Q

CMT— Charcot Marie tooth

A

A disease of the peripheral nerves that control the muscles, unlike the muscular dystrophies, which affect the muscles themselves. Usually slowly, progressive, causing loss of normal function and/or sensation in the feet/legs and hands/Arms.

— onion bulb, formations of various thickness are present around myelin sheaths in CMT

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73
Q

Neurocranium

A

Braincase: bones enclosing the brain. Forms via both endochondral and intramembranous ossification

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74
Q

Viscerocranium

A

Face: contains special sensory organs for site and smell

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75
Q

Where does the craniofacial cartilage and bones originate?

A

From the neural crest via the ectoderm

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76
Q

Where does the base of the skull derive from?

A

Sclerotome: via somites, via mesenchymal tissue, derived from paraxial mesoderm

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77
Q

Neurocranium development

A

Initiate it from ossification centers within the desomocranium mesenchyme

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78
Q

Cartilaginous neurocranium

A

Mesenchyme condenses to form condrification centers, ossification of the cartilages forms the skull base

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79
Q

Membranous neurocranium

A

Forms the flat bones of the calvaria (cranial skull), also from mesenchyme. Bones are separated by fibrous joints (cranial sutures)

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80
Q

Viscerocranium development

A

Cartilaginous viscerocranium: neural crest cells migrate into pharyngeal arches to form craniofacial bones. Hox genes are crucial for the patterning of the head and face.

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81
Q

What are pharyngeal arches

A

• six pairs, fifth disappears, and four and six fuse
• mesoderm lined externally with ectoderm, internally with endoderm
• contain cartilage, blood supply, and a nerve to supply the arch structures

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82
Q

Pharyngeal arch skeletal derivatives

A

Arch 1: maxilla, mandible, incus, malleus, zygomatic
Arch 2: stapes, upper hyoid
Arch 3: lower hyoid
Arch 4-6: laryngeal cartilages

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83
Q

What is formed via endochondral ossification?

A

Neurocranium: ethmoid, sphenoid, occipital base, Petrous temporal, bottom temporal

Viscerocranium: malleus, incus, stapes

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84
Q

What is formed via intramembranous ossification?

A

Neurocranium: parietal, frontal, squamous occipital, temporal squamous

Viscerocranium: pre-maxilla, maxilla, zygomatic, palatine, mandible, lacrimals, nasals, Vomer

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85
Q

Postnatal skull

A

• face is relatively small in neonate’s compared with calvaria
• sinuses are small or absent
• sutures are open to allow for brain enlargement (two years)

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86
Q

Metopic suture

A

Between two frontal bone halves. Is typically not present in adults, but occasionally persists.

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87
Q

Craniosynostosis

A

Premature closure of the cranial sutures, resulting in abnormal skull shape

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88
Q

Scaphocephaly

A

Craniosynostosis, fusion of sagittal, suture, results in long (A-P) skull

— most common type

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89
Q

Brachycephaly

A

Craniosynostosis, fusion of coronal, suture bilaterally, results in a shortened (A-P), wider (M-L) skull

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90
Q

Trigonocephaly

A

Craniosynostosis, fusion of metopic, suture, results in a median frontal Ridge (no frontal bone expansion)

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91
Q

Plagiocephaly

A

Craniosynostosis, fusion of one coronal and/or lambdoidal, suture, results in asymmetrical skull

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92
Q

Microcephaly

A

Abnormal development of the CNS, brain fails to grow, resulting in relatively small head

— Zika virus

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93
Q

Acrania

A

Complete or partial absence of the neurocranium

Meroencephaly: partial absence of the brain, incompatible with life. Results from failure of the cranial end of the neural tube to close in the fourth week.

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94
Q

Hydrocephalus

A

Significant enlargement of the head. Results from an imbalance between the production and absorption of cerebral spinal fluid.

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95
Q

Injuries to facial nerve: bell palsy

A

Dripping of the lips on the affected side, saliva dribbling, nasolabial, fold flattened, lower eyelid, falls away from the eyeball, food accumulates (Buccinator not working)

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96
Q

Danger zone

A

Triangle from bridge of the nose to corners of the lips that holds facial vein.

Facial vein—> internal jugular
Facial vein—> superior ophthalmic v.—> sphenoparietal sinus—> cavernous sinus

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97
Q

CT of the brain

A

Best test for screening the brain for acute hemorrhage, best for quickly looking for mass effect or herniation of the brain.

CT contrast: iodine base

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98
Q

Blood brain barrier defects

A

Various abnormalities, such as infection, inflammation, and tumors can disrupt the BBB, which is seen more clearly with contrast (will enter the brain, looks white)

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99
Q

Risks of IV contrast

A

1.) allergic reaction.
2.) contract induced nephropathy for CT contrast.

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100
Q

Risk factors for developing renal dysfunction

A

• diabetes
• nephrotoxic drugs
• reduced intravascular volume

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101
Q

When should contrast not be used in a CT?

A

Trauma. IV contrast and acute hemorrhage appear white and dense, making them indistinguishable from one another.

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102
Q

MRI disadvantages

A

• expensive
• claustrophobia
• metal causing artifacts
• contraindications: pacemakers, aneurysm clips, surgical devices

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103
Q

When is MRI used frequently?

A

• assess for acute ischemic changes or infarction
• assess for demyelinating disease, tumors, or seizure foci

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104
Q

Sylvian fissure

A

Separates frontal and parietal from temporal lobe

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105
Q

Gyri

A

Complex convolutions of the brain cortex (bumps)

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106
Q

Sulci

A

CSF filled grooves or clefts (indentations)

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107
Q

Intra-axial

A

Originating from the brain

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108
Q

Extra axial

A

Originating from surrounding tissue, such as meninges, vessels, or nerves

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109
Q

Arachnoid matter is only visible when

A

Abnormalities are occurring— typically not visible

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110
Q

In Which plane should an MRI be performed first?

A

Sagittal

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111
Q

Corpus callosum

A

Midline, commissural fibers
— rostrum, genu, body, and splenium

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112
Q

Basal ganglia: caudate nucleus, putamen, Globus pallidus

A

Subcortical nuclear masses located in the base of the forebrain. Relay centers for motor and sensory circuits. Metabolically active and susceptible to systemic disease, and those altering cerebral perfusion and oxygenation.

— small lesion= big problem

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113
Q

Stroke

A

• injury to the brain caused by blockage in the blood supply
• thrombotic, or embolic
• 87% ischemic and 13% hemorrhagic
• current treatment includes TPA within 3-4.5 hours

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114
Q

Ideologies of ischemic strokes

A

1.) atherosclerosis: especially cervical carotid arteries, most common in adults over 40
2.) cardioembolism: clot formed in heart, most common in a fib pts
3.) small vessel occlusion
4.) arterial dissection: most common in adults younger than 40, especially carotid or vertebral arteries
5.) vasculitis
6.) global hypoperfusion

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115
Q

Imaging preference for stroke

A

CT is typically the first imaging modality, needed to exclude an area of hemorrhage which would alter therapy options.

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116
Q

Acute versus chronic infarct of stroke

A

Acute: diffusion sequence is very sensitive, hard to see, gray and white matter less distinguishable between each other

Chronic: very distinguishable dark area

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117
Q

Intracranial hemorrhage

A

Head trauma: most common in younger

Ruptured vessels: elevated BP, aneurysms, AVM

Amyloid angiopathy: abnormality of vessel wall associated with aging

Embolic stroke with reperfusion

Coagulopathies/blood dyscrasias

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118
Q

Subdural hemorrhage

A

• potential space between Dura and arachnoid
• typical Crescentic shape

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119
Q

Epidural hemorrhage

A

• superficial to Dura between Dura and periosteum of skull
• biconvex, lentiform shape (football)
• associated with skull fx and high pressure arterial injury
• 75% associated with injury to middle meningeal artery

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120
Q

Subarachnoid hemorrhage

A

• most commonly related to ruptured aneurysm
• symptoms: sudden, severe headache, with loss or impairment in consciousness
• CT and potential LP done

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121
Q

Meningitis

A

• inflammation of Pia and arachnoid membranes
• infection may be caused by viruses, bacteria, fungi
• CSF analysis is best way to diagnose

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122
Q

Infection of parenchyma vs abscess

A

Cerebritis or encephalitis. Mass Effect, cloudy.

Abscess more localized ring, enhancing mass with surrounding edema (walled off)

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123
Q

Multiple sclerosis

A

Most common nontraumatic, disabling disease of young adults, more common in females

Theory: viral induced antigens cause autoimmune response, leading to edema and inflammation. Perivenular inflammatory lesion is hallmark of MS (progresses to demyelinating plaque)

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124
Q

Findings of mass effect

A
  1. Effacement of ventricles
  2. Effacement of sulci
  3. Effacement of basiler cisterns
  4. Shift in the midline structures
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125
Q

Symptoms of non-accidental trauma

A

Seizures, developmental delay, visual impairment, cerebral palsy, language or behavioral disorders

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126
Q

What makes babies susceptible to head injury?

A

• large head relative to body mass
• weak neck muscles
• large subarachnoid spaces
• thin skull offers less protection
• flat skull base more susceptible to rotational injury
• softer brain more susceptible to shearing injury

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127
Q

Intracranial findings of non-accidental trauma

A

Skull fracture, subdural hematoma, cerebral contusion, diffuse axonal injury— shear-type injury at gray-white interface,parenchymal lacerations, spinal injuries: including fx and ligamentous injuries, retroclival hematoma, retinal hemorrhage (seen in 85%— rare in accidental injury)

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128
Q

Important proteins in vesicle recycling (endocytosis)

A

Clathrin, Dynamin, SNARE proteins

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129
Q

Familial infantile myasthenia:

A

Reduces vesicle size and affects presynaptic terminal

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130
Q

Congenital myasthenic syndrome results in

A

Impaired vesicle recycling, it affects presynaptic terminal

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131
Q

What triggers vesicle fusion in the presynaptic terminal?

A

Latrotoxin

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132
Q

Botulinum and tetanus toxins affect what?

A

SNARE proteins involved in vesicle fusion

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133
Q

Cognitive disorders impair what?

A

Transsynaptic signaling

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134
Q

LEMS attacks what?

A

Presynaptic calcium channels

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135
Q

Excitatory neurotransmitters

A

Acetylcholine, glutamate, catecholamines, serotonin, histamine, ATP, neuropeptides, nitric oxide

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136
Q

Inhibitory neurotransmitters

A

GABA, glycine, neuropeptides, Endocannabinoids, nitric oxide

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137
Q

Ligand gated ion channels

A

• ionotropic receptors
• fast (ms)
• NT binds, channel opens, ions, flow across membrane through pore

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138
Q

G protein coupled receptors

A

• metabotropic receptors
• NT binds, G protein is activated, G protein subunits or intracellular messengers modulate ion channels, ion channel opens, ions flow across a membrane through pore

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139
Q

Acetylcholine pathways

A

Nicotinic acetylcholine receptors: permeate sodium, calcium, potassium. Ionotropic receptors. Muscle contraction.

Muscarinic acetylcholine receptors: reduce cAMP, increase calcium, and activate voltage gates K channels. Decreased cardiac activity/ CNS cognition and memory

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140
Q

Myasthenia gravis treatment

A

Neostigmine: inhibits acetylcholineesterase preventing the breakdown of acetylcholine

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141
Q

NMDARS— ionotropic glutamate receptor

A

Slow kinetics, calcium permeability, co-agonist glycine, magnesium blockade

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142
Q

AMPARS — ionotropic glutamate receptor

A

Fast gating, calcium impermeable in most cases

— resting, activated, desensitized

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143
Q

GABA receptors can also be targeted by:

A

Benzodiazepines, ketamine, inhalant anesthetics, ethanol, lipids

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144
Q

In the developing brain, GABA is what?

A

Excitatory. The intracellular chloride is greater than extra cellular chloride in the growing brain.

Channels that change as we age: KCC2, NKCC1

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145
Q

What blocks a glycine receptor?

A

Strychnine

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146
Q

Dopamine pathways:

A

• metabotropic
• D1, D5: increase cAMP
• D2, D3, D5: inhibit cAMP

Physiology: executive function, learning, reward, motivation, and neuroendocrine control

Pathology: Parkinson’s disease, ADHD, OCD, addiction

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147
Q

Serotonin pathways

A

• metabotropic (5-HT)

• ionotropic (5-HT3): used to prevent nausea and vomiting, nonselective cation channel

Physiology: circadian rhythm, motor behaviors, emotion, mental arousal

Pathology: depression, anxiety, schizophrenia

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148
Q

Opioid peptide pathway

A

Distributed throughout the brain. Colocalize with GABA and 5-HT.

Physiology/pathology: depressive, analgesic, resulting in aggression or submission, leading to tolerance and addiction after repeated administration

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149
Q

Endocannabinoid

A

Retrograde signaling to CB1 receptor: acts like G-coupled, and modulates other neurotransmitter release

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150
Q

Short term synaptic plasticity

A

Presynaptic: depression (depletion of readily releasable synaptic vesicles), and facilitation (accumulation of intra-terminal calcium concentration)

Postsynaptic: desensitization (knock out of receptors), and saturation (inability to work faster)

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151
Q

Long-term synaptic plasticity (long-term potentiation)

A

More receptors in response to an increased intracellular calcium level, nerve becomes more sensitive and responsive

OR

A decrease in receptors from low frequency, stimulation, nerve becomes less sensitive and responsive

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152
Q

Rostral versus caudal

A

Rostral: Up the neuraxis

Caudal: down the neuraxis

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153
Q

Arrangement of neurons in cerebral cortex

A

1: axons, few neurons
2-3: output to the other areas of cerebral cortex
4: input from thalamus
5: output to brainstem and spinal cord
6: output to thalamus

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154
Q

Frontal lobe:

A

Motor control, production of language, executive function, decision making

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155
Q

Parietal lobe:

A

Somatosensation: feeling, touch, pain, vibration, proprioception

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156
Q

Occipital lobe:

A

Vision

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157
Q

Temporal lobe:

A

Hearing, creation of memories, fear, comprehension of language

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158
Q

Insular lobe:

A

Emotional responses to sensory input— ex. the aversiveness of pain

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159
Q

Precentral gyrus

A

Motor control

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160
Q

Postcentral gyrus

A

Somatosensory control

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161
Q

Cortical Maps

A

Specific parts of the cerebral cortex sense (or control) specific body parts. Sensory is the left hemisphere and motor is the right hemisphere.

• head toward bottom of central sulcus on the lateral side
• trunk and hands are found superior to head on lateral side
• feet toward bottom of inter-hemispheric fissure

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162
Q

The calcarine fissure

A

Vision: this sulcus forms a spur off the parieto-occipital fissure. It’s separates the occipital lobe into the cuneus and the lingual gyrus

Primary visual cortex: found along bank of calcarine sulcus : lower half of visual field lies above the sulcus. Left side of the brain views the right visual field.

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163
Q

Superior temporal gyrus

A

Hearing: on the superior edge of the temporal lobe, right below the lateral fissure

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164
Q

Transverse temporal gyri

A

Primary auditory cortex: runs across the top of the superior temporal gyrus

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165
Q

How are frequencies mapped?

A

Tono topically across the transverse temporal gyri

100 Hz— anterior laterally
10000Hz— posterior medially

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166
Q

Primary motor cortex

A

Found in front of the central sulcus, performs simple movements around single joints

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167
Q

Premotor cortex

A

Anterior to primary motor cortex, performs coordination of multiple muscles to make complex movements

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168
Q

Supplemental motor cortex

A

Extends down the medial bank of inter-hemispheric fissure, performs the planning of movements

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169
Q

Frontal eye fields

A

Located somewhat superiorly in the premotor cortex, performs movement of the eyes by coordinating the contractions of the extraocular muscles

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170
Q

Wernicke’s area: left temporal lobe

A

Language comprehension

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171
Q

Broca’s area: left anterior inferior frontal lobe

A

Language production, grammar

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172
Q

right anterior inferior frontal lobe

A

Creation of language, “prosody”, differences in intonation and tempo that convey meaning

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173
Q

Right posterior temporoparietal cortex

A

Comprehension of prosody

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174
Q

Limbic system

A

Interconnected group of structures (both cortical and subcortical) involved with memory, emotion, motivation, etc.

Includes: hippocampus, parahippocampal gyrus, collateral fissure, Uncus, cingulate gyrus, prefrontal cortex, insula

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175
Q

Hippocampus

A

Learning and memory: declarative memory, such as names, places, events, etc.
— seahorse found by parahippocampal gyrus and collateral fissure

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176
Q

Association cortex

A

The rest of the cerebral cortex, higher level functions, and multiple inputs

Ex. Fusiform gyrus: recognition of faces (deficiency in this= prosopagnosia)

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177
Q

Central nervous system

A

Brain and spinal cord, protected by the cranium and vertebral column

— formed from the neural tube

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178
Q

Peripheral nervous system

A

Neurons outside of the CNS, cranial nerves, spinal nerves, associated ganglia. Connect the CNS and peripheral structures.

— formed from the neural crest

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179
Q

Autonomic nervous system

A

Neurons that innervate, smooth muscle, cardiac muscle, glandular epithelium. Has parts in both the CNS and PNS.

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180
Q

Marginal zone

A

Composed of the outer parts of the neural epithelial cells. Becomes the white matter of the spinal cord, as axons grow into it from the nerve cell bodies in the spinal cord, spinal ganglia, and brain.

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181
Q

Glioblasts

A

Differentiate from the Nuroepithelial cells and migrate from the ventricular zone into the intermediate and marginal zones. Can become astrocytes or oligodendrocytes.

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182
Q

Sulcus limitans

A

A groove that separates the dorsal part from the ventral part of the spinal cord

183
Q

Alar plates— dorsal, spinal cord

A

Forms, the dorsal gray columns, dorsal gray horns (afferent nuclei)

184
Q

Basal plate

A

Forms the ventral and lateral gray columns, axons of the ventral horn cells, grow out of the spinal cord, inform the ventral root of the spinal nerves

185
Q

Unipolar neurons in the spinal ganglia, are derived from:

A

Neural crest cells

186
Q

Spinal meninges are developed from:

A

Neural crest and mesenchyme cells that migrate to surround the neural tube

187
Q

Which roots are myelinated first?

A

Motor roots before sensory

188
Q

Spina bifida

A

Neural tube defect

Occulta < meningocele < myelomeningocele in severity

189
Q

Meroencephaly

A

Partial absence of the brain, incompatible with life, can be seen in ultrasound. Opposite of spina bifida, defective closure of rostral neuropore.

190
Q

Three primary brain vesicles

A

1.) forebrain (prosencephalon)
2.) midbrain (mesencephalon)
3.) hindbrain (rhombencephalon)

191
Q

Bends in the embryonic brain during development

A

Ventral Bend: midbrain flexure
— cervical flexure
— pontine flexure (opposite side)

192
Q

The pontine flexure separates

A

The metencephalon, and myelencephalon

193
Q

Metencephalon: hindbrain

A

Becomes the pons and cerebellum

194
Q

Myelencephalon: hindbrain

A

Becomes the medulla, caudal medulla resembles the spinal cord
• ventral area contains pyramids
• rostral medulla contains fourth ventricle

195
Q

Mesencephalon: midbrain

A

• contains cerebral aqueduct
• superior colliculi: visual reflexes
• inferior colliculi: auditory reflexes

196
Q

Midbrain development

A

Neuroblasts from basal plates, give rise to the tegmentum of the midbrain: red nuclei, nuclei of the third and fourth cranial nerves, reticular nuclei
• substantia nigra

197
Q

Optic vesicles

A

Forebrain, to lateral outgrowths appear on either side

198
Q

Telencephalic vesicles

A

Two diverticula arise dorsally and Rostrally (primordia of the cerebral hemispheres)

199
Q

Forebrain: diencephalon

A

Three swellings develop in the lateral walls of the third ventricle; epithalamus, thalamus, hypothalamus

Ventral surface of hypothalamus: mammillary bodies
— also included: pituitary, gland, anterior lobe: adenohypophysis, oral ectoderm. Posterior lobe: neurohypophysis, neuroectoderm

200
Q

Hypophyseal diverticulum

A

Part of the diencephalon, forebrain, elongates, and comes into contact with the infundibulum

201
Q

Infundibulum

A

Ventral outgrowth of the diencephalon, and gives rise to the median eminence and infundibular stem (pituitary— hypothalamus connection)

202
Q

Forebrain: telencephalon

A

Consists of two cerebral vesicles in a median sections—> creates the cerebral hemispheres, and third ventricle. Choroid plexus of the lateral ventricle also forms here, from the choroid fissure

203
Q

Corpus striatum

A

Forebrain, telencephalon: appears, as a prominent swelling in the floor of each cerebral hemisphere. —> becomes the lentiform nucleus, and caudate nucleus

204
Q

Cerebral commissures: forebrain

A

Groups of fibers connect corresponding areas of the cerebral hemispheres with each other

205
Q

Lamina terminalis

A

Forebrain cerebral commissure, rostral end of the forebrain from the roof plate of the diencephalon to the optic chiasm

206
Q

Anterior commissure

A

Forebrain cerebral commissure, connects olfactory bulbs

207
Q

Hippocampal commissure

A

Forebrain cerebral commissure, connects the hippocampal formations

208
Q

Corpus callosum

A

Forebrain cerebral commissure, connect neocortical areas

209
Q

CSF

A

Ventricles are lined with pia mater, Pia and ependymal roof forms the tela choroidea —> which differentiates into the choroid plexus and creates CSF

210
Q

Median aperture: foramen of Magendie

Lateral aperture: foramen of Luschka

A

Openings between the fourth ventricle and the subarachnoid space allowing for CSF flow

211
Q

Hydrocephalus

A

Significant enlargement of the head, resulting from an imbalance between the production and absorption of CSF— excessive CSF in the ventricular system of the brain

212
Q

Holoprosencephaly

A

Incomplete separation of the cerebral hemispheres— associated with facial abnormalities

213
Q

Alobar holoprosencephaly

A

Forebrain is small and lateral ventricles often merge to form one large ventricle

214
Q

Arnold Chiari malformation

A

Most common cerebellar birth defect— tonguelike projection of the medulla, inferior displacement of the vermis, through the foramen magnum, resulting in interference of the absorption of CSF.

• associations with spina bifida, meningomyelocele, hydrocephaly

215
Q

Encephalocele

A

Herniation of intercranial continents through a defect in the cranium (cranium bifidum)

Meningocele: hernia contains meninges
Meningoencephalocele: hernia contains part of the brain
Meningeohydroencephalocele: hernia contains meninges, part of the brain, and part of the ventricular system

216
Q

All sensory (somatic, and visceral) cells of the PNS are derived from:

A

Neural crest cells. The cell bodies of the sensory cells are located outside of the CNS.

217
Q

All peripheral sensory cells are initially bipolar, except:

A

The cells of the spiral ganglion of the cochlea, and the vestibular ganglion of CN VIII

218
Q

Motor nerve fibers

A

Arise from cells in the basal plate of the developing spinal cord. Emerge as a series of rootlets along the ventral lateral surface of the spinal cord, forming a ventral nerve root.

219
Q

Dorsal nerve root fibers

A

Formed by axons derived from neural crest cells that migrate to the dorsal lateral aspect of the spinal cord. Differentiate into cells of the spinal ganglion.

220
Q

Dorsal primary Rami

A

Innervates, the dorsal axial musculature, vertebrae, posterior intravertebral joints, and part of the skin on the back

221
Q

Ventral primary rami

A

Innervates the limbs, ventral lateral parts of the body wall, major nerve plexuses (cervical, brachial, lumbosacral)

222
Q

Greater part of the oculomotor (CNIII):

A

arises from the somatic efferent column of the brainstem and supplies most muscles of the eye

223
Q

Trochlear nerve (CN IV):

A

Somatic efferent cranial nerve, arises from the nerve cells in the somatic efferent column in the posterior part of the midbrain. Emerges from the brainstem DORSALLY and passes ventrally to supply the superior oblique muscle of the eye.

224
Q

Abducens nerve (CN VI):

A

Somatic efferent cranial, nerve: Arises from the nerve cells in the basal plate of the Metencephalon, innervates the lateral rectus muscle of the eye

225
Q

Hypoglossal nerve (CN XII):

A

Somatic efferent cranial nerve: Develops by the fusion of the ventral root fibers of 3-4 occipital nerves. Somatic motor fibers originate from the hypoglossal nucleus fibers, leave the ventral lateral wall of the medulla to form the hypoglossal nerve to innervate the tongue.

226
Q

First pharyngeal arch

A

Trigeminal nerve (V): ophthalmic, maxillary, mandibular branches. Trigeminal ganglion lives near the pons (cells from neural crest)

— maxilla, mandible, incus, malleus, zygomatic
— muscles of mastication, ventral mylohyoid, and to your belly of digastric, tensor tympani, tensor veil palantini

227
Q

Second pharyngeal arch

A

Facial nerve (VII): motor fibers (special visceral, efferent column in the caudal pons), visceral efferent components (peripheral autonomic ganglia), sensory fibers (geniculate ganglion)

228
Q

Third pharyngeal arch

A

Glossopharyngeal nerve (XI): motor fibers arise from special and visceral, efferent columns of the myelencephalon, nerve forms from rootlets out of medulla caudal to the developing ear, general efferent fibers are distributed to the Otic ganglion, sensory fibers, posterior part of the tongue

— lower hyoid
— Stylopharyngeus

229
Q

Fourth pharyngeal arch

A

Vagus nerve (X): fourth, and sixth pharyngeal arch, visceral efferent and afferent to the heart, foregut, and part of the midgut. Fourth arch becomes the superior laryngeal nerve, and the sixth arch becomes the recurrent laryngeal nerve

— laryngeal cartilage
— soft palate muscles, pharyngeal, and laryngeal muscles

230
Q

Olfactory nerve (I)

A

Receptor neurons differentiate from cells in the epithelial lining of the primordial nasal sac. Nerve fibers end in the olfactory bulb.

231
Q

Optic nerve (II):

A

Formed by more than 1 million nerve fibers, fibers grow into the brain from neuroblasts in the primordial retina

232
Q

Vestibulocochlear nerve (VIII): auditory

A

Comprised of the vestibular and cochlear nerves. Vestibular, nerve originates in semicircular ducts, and cochlear nerve proceeds from the cochlear duct

— VIII has bipolar instead of unipolar cell bodies

233
Q

Development of the autonomic nervous system

A

Divided into the sympathetic (thoracolumbar) and parasympathetic (craniosacral) parts

234
Q

Sympathetic nervous system:

A

Sympathetic nervous system: neural crest cells in the thoracic region, migrate along each side of the spinal cord to form paired ganglion (sympathetic chain gang). Axons of SNS located in the lateral horn— presynaptic: white, post synaptic: gray

235
Q

Parasympathetic nervous system:

A

• Presynaptic, parasympathetic, fibers arise from neurons in the nuclei of the brain stem, and in the sacral region of the spinal cord.
• brainstem, derived fibers, leave through the oculomotor, facial, glossopharyngeal, and vagus nerves
• postsynaptic neurons are located in the peripheral ganglia or plexuses near the target structure

236
Q

Facial nerve

A

“ two zebras bit my cookie”

— temporal, zygomatic, buccal, marginal mandibular, cervical, posterior auricular

237
Q

Motor areas of the brain

A

Primary motor cortex, premotor cortex, frontal eye field

238
Q

How to define motor cortex?

A
  1. Cytoarchitectural anatomy (layout of neurons.)
  2. Physiological response (movement) to stimulation
239
Q

Primary motor cortex cytoarchitecture

A

• Poorly developed granular layer 4 (stellate neurons)
• well developed pyramidal layer (pyramidal neurons, Betz cells)

240
Q

Frontal eye fields regulate gaze control by

A
  1. Stabilize an image on the fovea
  2. Shift point of fixation
241
Q

Fixation

A

Maintain gaze in a position

242
Q

Vestibular ocular reflex (VOR)

A

Stabilize images on the fovea

243
Q

Optokinetic response

A

Stabilize vision during slow or constant head movements

244
Q

Saccades

A

Move eyes rapidly, ballistic eye-movement, voluntary or automatic, bilateral control

245
Q

Smooth pursuit

A

Move eyes slowly to follow a moving target

246
Q

Cancellation of VOR

A

Shifts gaze

247
Q

Vergence

A

Shift fixation target from a far to near location

248
Q

Cranial nerve nuclei innervate the extraocular muscles

A
  1. Superior oblique, innervated by CN4, trochlear nerve
  2. Superior rectus, medial rectus, inferior oblique, inferior rectus, innervated by CN3, oculomotor nerve
  3. Lateral rectus, innervated by CN6, abducens nerve
249
Q

Horizontal gaze center

A

Paramedian Pontine reticular formation (PPRF)

250
Q

Vertical gaze center

A

Rostral, interstitial nucleus of the medial longitudinal fasciculus

251
Q

Frontal eye fields project to

A

• contralateral PPRF/vertical gaze center: directly, and indirectly via superior colliculus
• frontal eye fields select targets of visual interest and ignore others, and initiate saccades and smooth pursuit

252
Q

Regulation of gaze control

A

Left frontal eye fields—> right PPRF—> abduction of right eye and adduction of left eye (rightward saccade)

253
Q

Injury to frontal eye field

A

• loss of voluntary saccades to the contralateral side (fast component of nystagmus)
• deviation of eyes to the side of the lesion
• loss of ability to move gaze away from stimulus (superior colliculi important for orienting to a stimulus)

254
Q

Primary motor cortex: functional organization

A

• homunculus
• stimulation usually evokes simple movement of an individual body part
• movement is generated at low stimulation intensity
• distinguishes M1, projects large and direct pathway to brainstem and lower motor neurons

255
Q

Primary motor cortex: afferent input

A
  1. Periphery via dorsal column nuclei and thalamus — proprioceptive information
  2. Cerebellum and basal ganglia via thalamus
  3. Cortical areas— somatosensory cortex, premotor cortex, supplementary motor area/cingulate, posterior parietal cortex
256
Q

Primary motor cortex: functions

A

Neurons in the primary motor cortex fire 5-100 ms before the onset of a movement and encode the movements: force, direction, extent, velocity

257
Q

Neurons in primary motor cortex in code:

A

The amount of force needed to move a muscle against a load

258
Q

Premotor cortex: afferent inputs, and efferent projections

A

Afferent inputs: prefrontal cortex, supplementary motor area, posterior parietal cortex, cingulate motor area, cerebellum and basal ganglia via thalamus

efferent projections: area 4, supplementary motor area, posterior parietal cortex, prefrontal cortex, basal ganglia, brainstem, red nucleus, corticospinal

259
Q

Premotor cortex: function

A

• performs more complex task related processing and requires higher stimulation intensity
• selects appropriate motor plans for voluntary movements, where as the primary motor cortex executes these movements
• signals the preparation for movement, and various sensory aspects associated with a particular motor acts
• sensitive to the behavioral context of movement and signals to correct and incorrect actions

260
Q

Premotor cortex: consequences of lesions

A

Inability to:
• respond properly to stimuli
• plan appropriate movement based on circumstances
• learn new sensorimotor associations
• steer arm accurately

261
Q

Supplementary motor area: afferent inputs, and efferent projections

A

Afferent inputs: primary motor cortex, PFC, posterior parietal cortex, basal ganglia, and cerebellum via thalamus

262
Q

Supplementary motor area: functional organization

A

• homunculus
• evokes, contralateral, limb movement, including multiple joints
• evoke postural changes

263
Q

Supplementary motor area: function

A

• SMA selects movement based on remember to sequences of movements
• response to sequences of movements, and to mental rehearsal of sequences of movements
• transform kinematic (distant, and angle) to dynamic (force) information
• habit forming, highly proficient

264
Q

Supplementary motor area: consequences of lesions

A

• reduction in volitional movements
• loss of suppression of motor programs triggered by visual stimuli
• neglection of the affected limb

265
Q

Alien hand syndrome

A

Lesion in the supplementary motor area, leading to contralateral semi-purposeful movement that are outside of the patients volitional control

266
Q

Utilization behavior

A

Lesion in the supplementary motor area, leading to use of objects in an inappropriate setting (excessive response to external stimuli)

267
Q

Primary first order neuron

A

Received the information and synapses with a second order neuron. The first order neuron does not cross the midline.

268
Q

Second order neuron

A

Crosses the midline and projects to the thalamus

269
Q

Third order neuron

A

Projects from thalamus to cortex on the same side

270
Q

Dorsal root ganglion

A

Houses first order sensory neuron cell bodies. Typically unipolar neurons.

271
Q

Somatosensory pathway: dorsal column/medial lemniscus

A

Find touch, vibration, join position

Dorsal root —posterior column—> posterior column nuclei (caudal medulla) — medial lemniscus—> thalamus (VPL) — internal capsule—> somatosensory cortex

272
Q

Primary afferent neurons for touch and proprioception have cell bodies housed in the:

A

Medial portion of the dorsal root

273
Q

Somatotopic map

A

Around the T6 level and above
• lower body medially
• upper body laterally

274
Q

Organization of axons in the dorsal column

A

Fasciculus gracilis: sacral (medial), lumbar (lateral)

Fasciculus cuneatus: thoracic (medial), cervical (lateral)

275
Q

Caudal medulla and termination

A

Neurons traveling in the fasciculus gracillus from the lower body, terminate in the nucleus gracillus

Neurons traveling in the fasciculus cuneatus from the upper body terminate in the nucleus cuneatus

276
Q

Axons of second order neurons cross and form the

A

Medial lemniscus (ribbon)

277
Q

The medial lemniscus has a

A

Somatotopic organization— like a person standing on the pyramid (upper body projections are superior to the lower body projections)

278
Q

lesions of the medial lemniscus produce

A

Contralateral sensory deficits, because it is a crossed pathway

279
Q

From VPL to the somatosensory cortex, axons from third order, neurons pass:

A

Laterally through the internal capsule and project to the postcentral gyrus of the cortex on the same side. (primary somatosensory cortex (S1) in parietal lobe

280
Q

Somatosensory pathways: spinothalamic tract

A

Pain, temperature, crude touch

Dorsal root —> substantia gelatinosa— crossover, spinothalamic tract—> thalamus— internal capsule—> somatosensory cortex

281
Q

Chordotomy

A

Surgical cutting a ventral lateral funiculus to reduce pain in terminally ill patients.

282
Q

Syringomyelia

A

A hole develops (cyst) in the center of the cord, in the central canal, and expands out and rostral/caudally— cause can be CSF blockage, most common in C8-T1 region, and with Chiari malformation

— blocks the crossing, STT fibers, bilateral lots of pain and temperature sensation

283
Q

Axon from nociceptors enter the

A

Lateral dorsal root, and passed through Lissaur’s tract before synapsing on dorsal horn neurons

284
Q

First order nociceptive neurons release

A

Glutamate and substance P with intense noxious stimuli— lead to changes in second order neuron (up regulation of receptors, plasticity)

** can result in chronic pain

285
Q

Most STT axons terminate at the:

A

VPL nucleus and are organized somatotopically, with cervical projections positioned medial to the lumbar projections
** lesion of VPL will result in difficulty localizing pain

286
Q

As STT ascends, axons can synapse with:

A

• Ipsilaterally to the primary somatic sensory cortex in the parietal lobe
• periaqueductal (central) gray
• reticular neurons

287
Q

Synapse of STT axons to central gray

A

Gives input to brainstem nuclei that modulate STT neurons. Releases neural transmitters, enkephalin and serotonin, that impact incoming pain signals in the substantia gelatinosa.
— reduces/blocks the transmission of pain via the STT pathway —> VPL thalamus

288
Q

Synapse to reticular formation by STT axons:

A

Produces arousal (waking from sleep, increased attention), depolarization of cortical neurons, desynchronization of EEG
— involved with suffering response (projects to limbic critical areas involved with emotion and memory) Lesion of this area will block suffering, but not localization.

289
Q

Brown-Séquard syndrome

A

Hemiplegia: loss of sensation and motor function due to a lateral hemisection of the spinal cord (damage, usually from lack of blood flow)

290
Q

LeFort fractures

A

Fractures of the middle third of the face, typically occurs as a result of blunt force trauma.

LeFort I: floating palate, through maxilla, above alveolar

LeFort II: pyramidal fracture, maxilla, lacrimal, nasal bone involvement

LeFort III: detach midface from calvaria, zygomatic, orbital, pterygoid plates

291
Q

TMJ

A

Articulation of the condyloid process of the mandible with the mandibular fossa of the temporal bone. Ligaments attempts to hold the joint together, it is a modified hinge joint because it flexes, extends, and glides.

292
Q

Transmembrane proteins that make up tight junctions

A

Claudins, occludin, junction adhesion molecule. ZO-1 links the C terminal of these transmembrane proteins to cytoskeletal actin.

293
Q

Neurovascular unit

A

The cells of the brain vascular system that were collectively to maintain a constant neuronal environment, provided metabolic substrates, and exclude potentially toxic blood-borne agents

294
Q

Most important transporters in the BBB

A

ATP binding cassette (ABC) transporters— specifically ABCB1, ABCG2, ABCC1

295
Q

What is P-glycoprotein?

A

One of several efflux transporters (ABC transporter) — 12 transmembrane protein. Difficuly because it prevents anti-cancer, anti-epilepsy therapeutics through BBB

296
Q

Erlotinib

A

A tyrosine kinase inhibitor targeting cancers. Enters the brain only when efflux transporters are absent (ex. KO Mdr1a/b or Bcrp1)

297
Q

How are drugs delivered to the brain?

A

Receptor mediated transcytosis, a Trojan horse approach

298
Q

How do white blood cells get into the brain?

A

Diapedesis: rolling (weak adhesion), emigration (strong adhesion) — ICAM1,3
— leukocytes able to squeeze through after inflammatory signal by chemokines

299
Q

Disease examples involving blood brain barrier

A

1.) GLUT1 deficiency syndrome (no glucose in brain, no growth, seizures)

2.) MCT1 deficiency

3.) creatine transporter deficiency

300
Q

Creation of CSF

A

Additional differentiation of ependymal cells— choroid plexus.

CSF secretion : sodium, chloride, bicarb, that transport H2O by osmosis. 0.2 mL of CSF/minute/g

301
Q

Blood CSF barrier: important channels in the epithelial cells

A

1.) AQP1– water transport in/out
2.) NKCC1– water, Na, K, 2Cl in
3.) NKA— 2K out CSF, 3Na into CSF
4.) KCC1– K and Cl out

302
Q

Drugs to reduce CSF production

A
  1. Acetazolamide: carbonic anhydrase inhibitor.
  2. Ouabain: inhibitor of sodium potassium ATPase.
  3. Furosemide: inhibits Na/K/Cl channels
303
Q

Glymphatic system

A

Supports interstitial, fluid and solute clearance from the brain (lymphatic transport system— connects arteries to veins—> paravenous efflux out of brain)

— reduces beta amyloid and tau proteins in the brain (happens more during sleep)

304
Q

Other diseases of the blood brain barrier

A

• hydrocephalus
• Alzheimer’s
• traumatic brain injury, AQP4, minocycline
• amyotrophic lateral sclerosis
• frontal temporal dementia
• stroke
• epilepsy
• cavernous malformations

305
Q

Lecanemab

A

FDA approved Alzheimer’s drug; antibodies against Beta amyloid

306
Q

Development of the brain and spinal column

A

Prosencephalon—> telencephalon, diencephalon—> cerebrum(Tele), thalamus/hypothalamus(dien)

Mesencephalon—> mesencephalon—> midbrain

Rhombencephalon—> metencephalon, Myelencephalon—> Pons/cerebellum(meten), medulla(myelen)

307
Q

Spinal nerves

A

• 31, sensory= dorsal root (afferent), motor= ventral root (efferent)
• cervical, brachial, lumbar, sacral plexuses

308
Q

Cranial nerve components: sensory

A

Sensory:
1.) general sensory afferent (GSA)— mediates, pain, touch, temperature pressure, vibration, and proprioception

2.) general visceral afferent (GVA) — mediate sensory input from the viscera … CN 9,10

3.) special sensory afferent (SSA)— smell. vision, taste, hearing and balance… CN 1,2,7,8,9

309
Q

Cranial nerve components: motor

A

1.) general somatic efferent (GSE)— motor innervation to voluntary muscles

2.) special visceral efferent (SVE)— motor innervation to brachial/pharyngeal arches… CN 5,7,9,10,11

3.) general visceral efferent (GVE)— parasympathetic, efferent nerve fibers from autonomic nervous system to glands, etc. … CN 3,7,9,10

310
Q

Cranial nerve 1: olfactory

A

• sensory
• nuclei in the forebrain
• comes out of olfactory foramina in the cribriform plate
• responsible for smell

311
Q

Cranial nerve 2: optic

A

• sensory
• nuclei in the forebrain
• comes out of the optic foramen
• responsible for vision

312
Q

Cranial nerve 3: oculomotor

A

• motor
• nuclei in the midbrain
• comes out of superior orbital fissure
• responsible for superior/media/inferior rectus, inferior oblique, and PSNS to ciliary and constrictor pupillae muscles

313
Q

Cranial nerve 4: trochlear

A

• motor
• nuclei in the midbrain
• comes out of superior orbital fissure
• motor to superior oblique (eye)

314
Q

Cranial nerve 5: trigeminal

A

• both sensory and motor
• nuclei in the pons
• V1 out of superior orbital fissure, V2 out of rotundum, V3 out of ovale
• responsible for general sensory to face/scalp, and motor to muscles of mastication

315
Q

Cranial nerve 6: abducens

A

• motor
• nuclei in the pons
• comes out of the superior orbital fissure
• responsible for motor to lateral rectus (eye)

316
Q

Cranial nerve 7: facial

A

• both sensory and motor
• nuclei in the pons
• comes out of Stylomastoid Foramen
• responsible for motor to muscles of facial expression, general sensory to ear, taste anterior 2/3 of the tongue, PSNS to all glands except parotid

317
Q

Cranial nerve 8: vestibulocochlear

A

• sensory
• nuclei in the pons
• comes out of the IAC
• responsible for hearing and balance

318
Q

Cranial nerve 9: glossopharyngeal

A

• both sensory and motor
• nuclei in the medulla
• comes out of the jugular foramen
• responsible for general sensory oropharynx, larynx, tympanic cavity, Eustachian tube
• visceral sensory from carotid body
• special sensory from posterior 1/3 tongue
• motor to stylopharyngeus
• PSNS to parotid and carotid body

319
Q

Cranial nerve 10: Vagus

A

• both sensory and motor
• nuclei in the medulla
• comes out of the jugular foramen
• responsible for general sensory pharynx, larynx, external ear, tympanic membrane
• visceral sensory from lower pharynx, larynx, trachea
• motor to constrictors, larynx, levator veli Palatini, salpingopharyngeus, palatopharyngeus, palatoglossus
• PSNS to pharynx, larynx, abdominal viscera

320
Q

Cranial nerve 11: spinal accessory

A

• motor
• nuclei in the medulla
• comes out of the jugular foramen
• responsible for motor to SCM and trapezius

321
Q

Cranial nerve 12: hypoglossal

A

• motor
• nuclei in the medulla
• comes out of hypoglossal foramen
• responsible for motor to intrinsic and majority of extrinsic tongue muscles

322
Q

Key features of the midbrain

A

• cerebral aqueduct
• cerebral peduncles
• cranial nerve 3 present
• superior colliculi

323
Q

Key features of the rostral pons

A

• pon= bridge
• cerebral aqueduct
• Pontine nuclei with pontocerebellar fibers
• transverse pontine fibers
• 4th ventricle
• CN5

324
Q

Key features of the caudal pons

A

• large 4th ventricle
• MCP, Pontine nucleus
• facial colliculi in the fourth ventricle

325
Q

Key features of the rostral medulla

A

• olive
• pyramids
• 4th ventricle
• hypoglossal what are nuclei
• dorsal motor nuclei of vagus nerve
• vestibular nuclei

326
Q

Reticular formation

A

Neuronal bodies and axonal processes making up the “stuff” within the pons. It is a large, diffuse group of gray matter in the brain stem.
— general awareness of sensation and motion, center for respiration and heart rate
— receives nonspecific, somatic, and visceral sensory information
— sends descending projections down to spinal cord to have effect on motor aspects

327
Q

Input of sensory information

A

The process of receiving, converting, and transmitting information from the outside world

328
Q

Perception

A

The process by which the brain selects, organizes, and interprets sensations

329
Q

Somatic sensory (afferent)

A

General: touch, pain, pressure, vibration, temperature, and proprioception from the skin, body wall, and limbs

Special: hearing, equilibrium and vision

330
Q

Visceral sensory (afferent)

A

General: stretch, pain, temperature, chemical changes, and irritation in the viscera; nausea and hunger

Special: taste and smell

331
Q

Somatic motor (efferent)

A

Motor innervation to the skeletal muscles

332
Q

Visceral motor (efferent, autonomic)

A

Motor innervation to the smooth muscle, cardiac muscle, and glands

333
Q

Smell

A

• cranial nerve 1
• nasal epithelium—> olfactory, receptor, neurons stimulated by chemicals

334
Q

Vision

A

• cranial nerve 2
• retina —> photo receptor cells stimulated by visible light

335
Q

Hearing

A

• cranial nerve 8
• cochlea—> inner ear—> mechanoreceptive hair cells, stimulated by sound waves

336
Q

Touch

A

• cranial nerve 5, 7
• skin, tongue—> mechanoreceptive, neurons stimulated by mechanical forces

337
Q

Taste

A

• cranial nerves 7,9,10
• tongue, mouth wall, esophagus—> taste, receptor cells stimulated by chemicals

338
Q

Mechanoreceptors

A

• activated by changes in pressure
• common receptors include Pacinian corpuscles (subcutaneous tissue), meissner corpuscles (non-hairy skin), baroreceptors (carotid sinus), hair cells (organ of Corti, semicircular canals), photoreceptors, rods/cones

339
Q

Chemoreceptors

A

• activated by chemicals
• olfaction and taste

340
Q

Thermoreceptors

A

• located in the skin and include cold and warm receptors

341
Q

Nociceptors

A

Extreme pressure, temperature, or noxious stimuli. In the skin.

342
Q

Olfactory mucus comes from:

A

Bowman’s glands deep in the lamina propria (most common), and the adjacent respiratory mucosa from goblet cells

343
Q

How odorant chemical information turns into electrical action potential

A

With the binding of the receptor to an odorant, adenylate cyclase is activated by G protein-coupled receptors, and converts adenosine triphosphate into cyclic adenosine monophosphate. The cAMP then binds to a sodium/calcium ion channel to allow inflow of the ions causing cell depolarization, and action potential production.

344
Q

Olfactory bulb layers

A
  1. Olfactory nerve.
  2. Glomerular
  3. External plexiform.
  4. Mitral cell
  5. Internal plexiform
  6. Granule cell
345
Q

Olfactory pathway

A

First order neuron: olfactory epithelium to glomerulus

Second order neuron : formed of the cells of the olfactory bulb (mitral, and tufted cells). Pass essentially as the olfactory tract.

Third order neuron : piriform cortex (area, 28) contain primary olfactory cortex

346
Q

Old olfactory system

A

Medial olfactory stria—> septal nuclei—> hypothalamus/limbic system

Lateral or factory stria—> pre-piriform cortex/piriform cortex/entorhinal area/amygdala—> limbic system (hippocampus)

•• these are more associated with memory and emotion

347
Q

New olfactory system

A

Lateral olfactory stria—> orbitofrontal cortex

•• this system, more involved with behavior changes and senses of danger

348
Q

Anosmia

A

Absence of smell

349
Q

Hyposmiamicrosomia

A

Diminished olfactory sensitivity

350
Q

Dysosmia

A

Distorted sense of smell

351
Q

Phantosmia

A

Perception of an odorant when none is presented/olfactory hallucination

352
Q

Agnosia

A

Inability to classify, contrast, or identify odor sensations verbally, even though the ability to distinguish between odorants maybe normal

353
Q

Hyperosmia

A

Abnormally acute smell function (rare)

354
Q

Transport olfactory loss

A

Olfactory dysfunctions can be caused by conditions, that interfere with the access of the odorant to the old factory Neuroepithelium.

This includes: swollen nasal mucosa membrane, structural changes, mucus secretions.

Caused by: allergy, bacterial rhinitis and sinusitis, encephalocele, deviated nasal septum, neoplasms/polyps, surgery, old age, viral infection

355
Q

Sensory olfactory loss

A

Olfactory dysfunctions can be caused by conditions that damage the neuroepithelium.

This includes: drugs, inhalation of toxic chemicals, viral infections, neoplasms, radiation therapy

356
Q

Neural olfactory loss

A

Olfactory dysfunctions can also be caused by conditions to damage the central or factory pathways.

Such as: aids, Alzheimer’s, alcoholism, chemical, toxins, cigarette, smoke, diabetes, Huntington’s, neoplasm, Parkinson’s, trauma, B12, deficiency, zinc deficiency

357
Q

Microglial cells

A

Derived from mono side cells, are effectively tissue resident macrophages of the CNS. They participate in the innate immune response to a pathogen as a phagocyte, and can also activate T lymphocytes as an antigen presenting cell.

358
Q

What causes encephalitis?

A

Arboviruses, herpes simplex virus one or two, JC virus

359
Q

What causes subacute encephalitis?

A

Toxoplasma gondii, measles, prions

360
Q

What causes tetanus?

A

Clostridium tetani

361
Q

What causes African sleeping sickness?

A

Trypanosoma brucei

362
Q

What causes Creutzfeldt Jakob disease?

A

Prions

363
Q

What causes meningeoencephalitis?

A

Naegleria Fowleri, acanthamoeba

364
Q

What causes meningitis?

A

Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, listeria monocytogenes, cryptococcus neoformans, coccidioides immitis, etc

365
Q

What causes neonatal and infant meningitis?

A

Streptococcus agalactiae, E. coli, listeria monocytogenes, Cronobacter Sakazakii

366
Q

Meningitis

A

Information of the meninges. More serious infections caused by bacteria, initial infection, facilitated by URI viral infection.
— LP and cultures ordered
— associated with photophobia, HA, nuchal stiffening, fever, increased WBC in the CSF

367
Q

Polio virus, causing poliomyelitis

A

Acute enter a viral infection of the spinal cord that can cause neuromuscular paralysis. Virus infiltrates the motor neurons of the anterior horn of the spinal cord.

Virus: RNA, icosahedral, non-enveloped, SS(+) genome (class 4), picornavirus, enterovirus

368
Q

Rabies

A

• slow, progressive zoonotic disease that causes fatal encephalitis
• fever, HA, vomit, fatigue
• rabies specific acute symptoms: agitation, disorientation, seizures, twitching, hydrophobia
• common from raccoons, skunks, coyotes, foxes, and bats
• Negri bodies present in tissue

369
Q

How does the rabies virus cause encephalitis?

A

The virus present in saliva of the rabid animal, enters the body through a wound from a bite or contamination of mucous membranes. The virus multiplies at the site of inoculation, and then travels to the CNS via retrograde axonal transport.

370
Q

What does rabies virus look like?

A

Lyssavirus: RNA ss (-), class 5, enveloped, helical nucleocapsid, rhabdovirus

371
Q

Encephalitis symptoms

A

• altered level of consciousness
• focal deficits— aphasia, hemispatial neglect, movement disorders, hemiparesis
• seizures
• coma

372
Q

What is encephalitis caused by?

A

• HSV1,2, VZV
• auto immune disorders
• post infectious encephalitis caused by aberrant immune response to primary infection
• tuberculosis
• enterovirus
• JC virus (immuno compromised)

373
Q

MRI abnormalities of encephalitis

A

HSV: temporal> frontal> other

ADEM: supratentorial> infratentorial, white matter, cortical> subcortical, spinal cord involvement frequent

374
Q

Post infectious encephalitis

A

Most commonly caused by measles, mumps, rubella, varicella, zoster, influenza, and acute disseminated encephalomyelitis (ADEM) is most common result

375
Q

Complications of measles

A

Otitis media, croup, bronchiopneumonia, encephalitis, subacute sclerosing panencephalitis (SSPE)

376
Q

What genetic polymorphism predisposes individuals to neurological complications of measles?

A

Lower production of interferon gamma (IFN-gamma) and interleukin-2 (IL-2)

377
Q

Primary measles encephalitis (PME)

A

• virus, invades and replicates within brain cells typically at the same time as rash presentation
• directly injures, neurons and triggers lymphocytic infiltration
• symptoms include fever, headache, AMS, motor deficits, and seizures
• treatment is supportive
• 10 to 15% mortality rate

378
Q

Measles induced acute disseminated encephalomyelitis (APME)

A

• resultant demyelination after recent measles infection
• Myelin basic protein found in the CSF an absence of infectious virus (post infection)
• sensory defects, motor defects, ataxia, mental status changes
• MRI confirmation of disseminated white matter lesions in the brain and spinal cord
• treatment is corticosteroids to dampen the immune response

379
Q

Subacute sclerosing panencephalitis (SSPE)

A

• children who contract measles before the age of two are at the greatest risk
• SSPE remain symptom-free for 6-15 years Post acute infection and survive 1-3 years after symptoms develop
• slow infection— Cell to cell causing neuronal damage
• defective and protein assembly allows viruses to go undetected
• symptoms include behavioral problems from academic decline to eventual complete dysfunction. 100% mortality rate.

380
Q

What measles looks like

A

SsRNA (-), class 4, non-segmented, helical nucleocapsid, enveloped, paramyxovirus, morbillivirus

381
Q

What Herpes virus looks like

A

dsDNA (class 1), icosahedral nucleocapsid, herpes virus, Simplex virus

382
Q

Carotid sheath contents

A

Common carotid artery, medially

Internal jugular vein, laterally

Vagus nerve, posteriorly

383
Q

Carotid sinus

A

At the bifurcation of the common carotid artery. Reacts to changes in the arterial blood pressure

384
Q

Carotid body

A

Sitting between the internal and external carotid artery. It monitors the level of O2 in the blood

385
Q

Branches of the external carotid artery

A

1.) ascending pharyngeal (posterior)
2.) occipital (medial)
3.) posterior auricular (medial)
4.) superior thyroid (anterior)
5.) lingual (anterior)
6.) facial (anterior)

386
Q

Lyre sign

A

Tumor of carotid body, causing excessive splay of internal and external carotid

387
Q

Motor system

A
  • most important for localization
  • Corticobulbar + corticospinal
  • Cortical/subcortical
  • Anterior horn starts in the PNS
388
Q

Sensory systems

A
  • Dorsal Columns (high cross, medulla)
  • Spinothalamic (low cross, immediately)
389
Q

Cerebellar

A
  • ABOVE cervicomedullary junction, usually contralateral to affected side
  • BELOW cervicomedullary junction, tracts cross twice, lesion is ipsilateral to an affected side
390
Q

intersegmental findings

A

Depend on the involvement of the major motor (Corticospinal and corticobulbar tracts) and sensory (posterior column–medial lemniscus pathway) as they pass through the area of lesion

391
Q

Segmental findings

A

involve specific components of the CNS or periphery, locally restricted to area of lesion, and have the most locational value (examples: facial nerve, hypoglossal nerve, spinal cord segments, nerve root)

392
Q

Nerve root and function

A

C5: shoulder abduction
C6: Elbow flexion
C7: Wrist extension
C8: Finger flexors
T1: Finger abductors
L2: hip flexors
L3: knee extensors
L4: ankle dorsiflexors
L5: Long toe extensors
S1: ankle plantar flexors
S4-5: Deep anal pressure, voluntary anal contraction

393
Q

Upper motor neuron (UMN) syndrome

A
  • proximal to the anterior horn cell or proximal to cranial nerve nuclei
  • tone and weakness: Spastic paralysis
  • Muscle bulk: delayed atrophy
  • Abnl movement: Fasciculations not usually seen
  • Reflexes: Brisk and hyperactive
  • Plantar/babinski: upgoing toes
394
Q

Lower motor neuron (LMN) syndrome

A
  • anterior horn cells, motor nerve fibers, or NMJ
  • Tone and weakness: Flaccid paralysis
  • Muscle bulk: prominent weakness and atrophy occurs early
  • Abnl movements: Fasciculations present
  • Plantar/babinski: Downgoing toes (normal)
395
Q

Falx cerebri

A

Vertical: between cerebral hemispheres in longitudinal cerebral fissure, contains superior and inferior sagittal sinuses between its layers

396
Q

Falx cerebelli

A

Vertical: Between cerebellar hemispheres, extends from tentorium cerebelli superiorly to inner occipital protuberance in the posterior cranial fossa

397
Q

Tentorium cerebelli

A

Horizontal: separates the posterior cranial fossa from the middle cranial fossa, separates the temporal and occipital lobes from the cerebellum and infratentorial brainstem. contains the tentorial incisure through which the brainstem passes.

398
Q

Diaphragma sellae

A

Forms root of hypophyseal fossa, contains aperature through which the hypophyseal stalk passes

399
Q

Supratentorial lesion

A

loss of sensation and or weakness of face +body contralateral to the lesion

400
Q

Posterior fossa lesion

A

Loss of sensation and or weakness of face ipsilateral to the lesion and body contralateral to the lesion
- ipsilateral cranial nerve deficits
- cerebellar incoordination ipsilateral to the lesion

401
Q

Spinal lesions

A
  • Loss of pain + temperature contralateral to the lesion
  • Weakness ipsilateral to the lesion
  • loss of position sense and vibration ipsilateral to the lesion
402
Q

Peripheral lesions

A
  • loss of sensation to all modalities in the distribution of a single root or nerve, or “stocking/glove pattern” if diffuse
    -Muscle weakness confined to a single root or nerve
403
Q

Sensory pathway 3 major neurons

A
  1. primary sensory, cell bodies outside the CNS in sensory ganglia
  2. Secondary sensory: cell bodies located in cranial nerve nuclei in the brain stem and axons go to thalamus
  3. Tertiary sensory: cell bodies in the thalamus, project to the sensory cortex

Pathway: Periphery sensory ganglion–> primary neuron–> Cranial nerve nuclei in brainstem–> secondary neuron–> thalamus–> tertiary neuron–> cerebral cortex

404
Q

Motor pathways

A
  1. Upper motor neuron (UMN): cerebral cortex with axon through the corticobulbar tract to contact the lower motor neurons in the brainstem
  2. Lower motor neuron (LMN): cell bodies located in the brainstem of the cranial nerve nuclei up upper cervical cord. Axons leave to go to muscle.

Pathway: Cerebral cortex–> UMN–> CN nuclei (brainstem)–> LMN–> Muscle

405
Q

Sensory (general somatic) of trigeminal nerve (CN5)

A

Face and head

406
Q

Motor (branchial motor) of trigeminal nerve (CN5)

A

Muscles of mastication, anterior belly of digastric, mylohyoid, tensor veli palatini, tensor tympani

407
Q

Where is the Trigeminal ganglion located?

A

sits on the floor of the petrous apex of the temporal bone– Meckel’s cave: dural pouch that holds trigeminal ganglion and proximal trigeminal rootlets

408
Q

Cavernous sinus

A
  • Paired dural venous sinuses that are intracranial on either side of pituitary gland
  • CN 3, 4, V1, V2, 6
  • Petrous ICA
409
Q

Cavernous sinus thrombosis

A

-Rare: infection
-Headaches, orbital proptosis, cranial neuropathy
- increased ICP, 56% mortality rate

410
Q

Trigeminal nuclei

A
  • located at midbrain to the medulla and intro cervical spine
    1.) Main sensory nucleus: posterior pons, lateral to the motor nucleus (TOUCH AND POSITION)
    2.) Spinal nucleus: extends through entire medulla to upper cervical cord (PAIN AND TEMP)
    3.) Mesencephalic nucleus: midbrain extending inferiorly to pons (PROPIOCEPTION FROM MUSCLES OF MASTICATION)
    4.) Motor nucleus: pons medial to the sensory nucleus, (MOTOR TO MUSCLES OF MASTICATION)
411
Q

Pathway for trigeminal nerve sensory

A

touch/position–> V1, V2, V3–> trigeminal ganglion–> principal nucleus–decussates–> medial lemniscus–trigeminothalamic tract–> VPM Thalamus

412
Q

Oral cavity trigeminal pathway

A

Receives signal from oral cavity which ascends ipsilaterally via the posterior trigeminothalamic tract to the ventral posterior thalamic nucleus

413
Q

Ventrolateral aspect of trigeminal nucleus

A

decussates and travels via medial lemniscus to the contralateral anterior trigeminothalamic tract to VPM nucleus

414
Q

3rd order neurons and trigeminal pathway

A

Cell bodies reside in the medial aspect of VPM nucleus and travel via the posterior limb of the internal capsule to the primary somatosensory cortex

415
Q

Spinal nucleus of trigeminal complex

A
  • Continuous with the principal sensory nucleus and extends to the cervical spinal cord
  • Continuous with dorsal gray matter of spinal cord
  • Synapse with second order neurons in spinal nucleus and decussates and ascend via trigeminal lemniscus in the trigeminothalamic tract to the ventral posteriomedial (VPM) nucleus or medial dorsal nucleus of the thalamus
416
Q

Mesencephalic trigeminal nucleus

A
  • first order pseudounipolar cell bodies lie within the CNS (bypass trigeminal ganglia, receives input from V2 and V3
  • send signals from muscle spindles (mastication) and from mechanoreceptors in oral cavity
  • Send central processes from mesencephalic nucleus to the motor cortex
417
Q

Motor trigeminal nucleus

A

-innervates 1st pharyngeal arch (temporalis, masseter, medial and lateral pterygoids, tensor veli palatini, tensor tympani, anterior belly digastric, mylohyoid
-Received input from primary motor cortex via corticobulbar tract and sensory info from oral cavity both directly and via the pontine reticular formation

418
Q

Clinical testing of sensory of CN5 trigeminal

A
  • Discriminative touch: toothpick
  • Pain/temp: cool metal tuning fork
  • Light touch: Cotton swab
419
Q

Clinical testing of motor CN5 trigeminal

A
  • palpate the masseter and temporalis and ask to clench jaw
  • open mouth and look for jaw deviation (weak= deviates toward side of lesion)
420
Q

Jaw jerk reflex

A

Tap with tuning fork on chin with mouth slightly open– get a sudden slight closing of the jaw
- afferent limb tested: sensory neurons in mesencephalic nucleus to the trigeminal motor nucleus
- efferent limb tested: V3 motor to masseteric

421
Q

Trigeminal Neuralgia

A
  • Short burst like pain commonly described as “electrical shocks”
  • usually affects V2 and V3
  • Usually brought on by any stimuli of the region
  • Women 2x more likely
  • Pathophysiology: compression of the sensory nerve root, idiopathic or secondary to superior cerebellar artery compression or brain tumor (meningioma, schwannoma)
422
Q

Trigeminal Neuralgia

A
  • Short burst like pain commonly described as “electrical shocks”
  • usually affects V2 and V3
  • Usually brought on by any stimuli of the region
  • Women 2x more likely
  • Pathophysiology: compression of the sensory nerve root, idiopathic or secondary to superior cerebellar artery compression or brain tumor (meningioma, schwannoma)T
423
Q

Six segments of the Facial nerve

A
  1. intracranial (brainstem to porus acoustics, internal auditory canal)
  2. Meatal (porus acoustics to meatal foramen)
  3. Labyrinthine (meatal to geniculate)
  4. Tympanic ( geniculate to second genu)
  5. Mastoid (second genu to stylomastoid foramen)
  6. Extratemporal (SMF to the world)
424
Q

General visceral motor of the facial nerve CN7

A
  • parasympathetic fibers to lacrimal gland, SMG and sublingual
425
Q

Special sensory of the facial nerve CN7

A

Taste from anterior 2/3 tongue and soft palate

426
Q

General somatic sensory of the Facial nerve CN7

A

touch, pain, temperature from external ear, EAC, and lateral surface of tympanic membrane

427
Q

Branchial motor of the facial nerve CN7

A
  • Branchial/pharyngeal arch 2
  • Motor to facial expression muscles, posterior belly of digastric, stapedius
428
Q

Nuclei of the facial nerve CN7

A

1.) Facial: branchial motor fibers
2.) Superior salivatory: ventral pons, to lacrimal, sublingual, and mandibular glands
3.) Trigeminal: General sensory from ear to principal/spinal trigeminal nuclei
4.) Solitary tract: Caudal pons and dorsolateral medulla, special sensory (taste) anterior 2/3 tongue

429
Q

Central branchial motor of CN7 facial nerve

A
  • UMN ganglia–> posterior limb of IC of thalamus via corticobulbar tract
  • Upper facial muscles get BILATERAL stimulation
    -Lower facial muscles get CONTRALATERAL stimulation
430
Q

Facial nerve CN7 extracranial course

A

Stylomastoid foramen–> parotid parenchyma

Branches to:
- Temporal
- Zygomatic
- Buccal
- Marginal mandibular
- Cervical

431
Q

Internal auditory canal spacial set up

A

“7 up, coke down, 8 falls back”

  • Superior anterior: Facial nerve
  • Inferior anterior: Cochlear
  • Superior posterior: Superior Vestibular
    -Inferior posterior: inferior Vestibular

– Dividing Facial and vestibular is Bill’s bar, dividing superior from inferior is Falciform crest

432
Q

Lesion at geniculate or proximal for facial nerve CN7

A
  • Facial weakness
  • Hyperacusis
  • altered state
  • decreased lacrimation/salivation
433
Q

Lesion of mastoid segment for Facial nerve CN7

A
  • Facial weakness
  • Hyperacusis
  • Decreased salivation and taste

** LACRIMATION INTACT

434
Q

Lesion of Stylomastoid foramen

A
  • Facial weakness

**NO HYPERACUSIS, SALIVATION/TASTE/LACRIMATION INTACT

435
Q

Corneal blink reflex

A

input: corneal stimulation
afferent: V1
efferent: motor facial nerve
Effect: bilateral blink
- interneurons from spinal trigeminal nucleus gives bilateral innervation to the CN7 motor nucleus

436
Q

Clinical testing of the Facial nerve CN7

A

– Motor: smile, pucker, wrinkle nose, raise eyebrows
– Lacrimation: Schirmer’s test (great superficial petrosal nerve
– Taste: Different tastes on both sides of tongue
– Salivary flow: Chorda tympani, Cannulation of submandibular duct

437
Q

Bells Palsy

A
  • unilateral facial paralysis
  • 24-48hr onset facial weakness of all branches
438
Q

Herpes zoster oticus

A

-varicella reactivation at sensory afferents of facial nerve
- Elderly and immunocompromised
- symptoms: Intense otalgia and vesicular eruption

439
Q

Ramsay Hunt Syndrome

A
  • Progression of HZO to motor efferents of facial nerve and facial paralysis
  • second most common cause of facial paralysis
440
Q

Acute otitis media

A

Cause of facial paralysis, dehiscent facial nerve, mastoiditis

441
Q

Chronic otitis media

A

Cause of facial paralysis, usually associated with cholesteatoma. Surgery

442
Q

Malignant otitis externa

A

Cause of facial paralysis, DM, immunocompromised, symptoms of severe painful inflammation of EAC with purulent otorrhea, granulation tissue at bony cartilaginous junction
– Caused by pseudomonas bacteria

443
Q

Causes of Bilateral facial paralysis

A
  • Guillain Barre syndrome
  • Sarcoidosis
  • Infection (Lyme, HIV, syphilis, men/encephalitis)
  • Melkersson-Rosenthal syndrome
    -diabetes
  • Intrapontine/pre-pontine tumors
  • Bells palsy
444
Q

Internal auditory meatus carries:

A
  • facial nerve CN7
  • Vestibulocochlear nerve CN8
  • Labyrinthe artery
445
Q

Jugular foramen carries:

A
  • Glossopharyngeal nerve CN9
  • vagus nerve CN10
  • Accessory nerve CN11
  • Inferior petrosal sinus
  • Sigmoid sinus
446
Q

Carotid canal carries:

A
  • internal carotid artery
  • Postganglionic, sympathetic fibers
447
Q

Foramen rotundum carries:

A

Maxillary nerve (V2)

448
Q

Stylomastoid foramen carries

A

Facial nerve branch

449
Q

Foramen ovale carries

A

Mandibular nerve (V3)

450
Q

Foramen spinosum carries

A

Middle meningeal artery

451
Q

Superior orbital fissure carries:

A
  • ophthalmic nerve (V1)
  • Oculomotor nerve (CN3)
  • Trochlear nerve (CN4)
  • Abducens nerve (CN6)
452
Q

Optic canal/foramen carries

A
  • Optic nerve
  • Ophthalmic artery
453
Q

Sphenopalatine foramen carries:

A

Sphenopalatine artery

454
Q

Central lateral nucleus

A

Receives input from the reticular formation on the contralateral side of the body. The CLN then projects to the limbic cortex to provide an emotional, suffering response to pain from the contralateral side of the body.

Neuro/Behavior I (3 decks)

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