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Brain and Behavior > Week 2 (Test 1) > Flashcards

Week 2 (Test 1) Flashcards

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1
Q

What is pseudocyesis?

A

The false belief that you are pregnant

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2
Q

Atypical signs and symptoms that did not conform to established diseases

A

hysteria

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3
Q

What symptoms are necessary to make a diagnosis of Somatic Symptom Disorder?

A

A. Somatic sx: 1 or more, distressing, & disrupting of daily life B. Excessive thoughts, feelings, behaviors with >1 – Disproportionate & persistent thoughts of seriousness – Persistent high related anxiety – Excessive time & energy devoted to sxs or healthcare C. Chronicity > 6 months

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4
Q

What symptoms are necessary to make a diagnosis of Illness Anxiety Disorder?

A

A. Somatic sx are absent or mild B. Preoccupation with having or acquiring a serious illness C. >6 months

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5
Q

What do patients have in Conversion Disorder?

A

Nonintentionally produced symptoms or deficits affecting voluntary motor or sensory function —Commons presentation include pseudoseizures, blindness, deafness, sensory loss, paralysis or gait issues

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6
Q

How would you best manage Conversion Disorder?

A

–Direct confrontation is not recommended –Conservative approach of reassurance and relaxation is often effective ===“Suggestion” of recovery w/o intervention (Prognosis surprisingly good with >1/2 completely resolved by time of discharge) –Identifying underlying conflict and finding resolution can “cure” the symptoms

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7
Q

Physical or psychological symptoms are intentionally produced to assume sick role –Conscious/voluntary symptom production

A

Factitious disorder

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8
Q

Often in Factitious Disorder cases, the patients will inject themselves with insulin to become hypoglycemic. What can you do to help determine whether this symptom is legitimate?

A

check for increased serum insulin/C-peptide ratio during a hypoglycemic episode

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9
Q

How would you best manage Somatic Symptom Disorder?

A

–Frequent visits (15 min/month) –Short physical exam, nothing invasive –Aim: Prevent new symptoms Decrease admissions and ER visits –Discuss emotions/fears, use open ended questions

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10
Q

Intentional production of false or grossly exaggerated physical or psychological symptoms – motivated by external incentives

A

malingering

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11
Q

List the ectoderm germ layer derivatives.

A

CNS, PNS, sensory epithelium of nose, eye and ear, epidermis including hair and nails, pituitary gland, sweat glands, mammary glands and enamel of teeth, some eye mm neural crest cell derivatives

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12
Q

List the mesoderm germ layer derivatives.

A

muscle, cartilage and bone/connective tissues, subcutaneous tissue of skin, spleen and cortex of suprarenal glands vascular system (heart and vessels), urogenital system (kidneys, gonads, ducts) dura mater and connective tissue envestments of peripheral nerves

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13
Q

List the endoderm germ layer derivatives.

A

epithelial lining of the GI tract, respiratory tract and urinary bladder; the parenchyma of the tonsils, thyroid, parathyroid, thymus, liver and pancreas

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14
Q

the separation of the neural tube from the surface ectoderm

A

dysjunction

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15
Q

What marks the end of primary neurulation?

A

the completion of ectoderm fusion

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16
Q

When does the anterior neuropore (cranial end) close?

A

day 25

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17
Q

When does the posterior neuropore (caudal end) close?

A

day 27

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18
Q

Failure of the anterior neuropore to close will result in what?

A

anencephaly

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19
Q

Failure of the posterior neuropore to close will result in what?

A

spina bifida occulta

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20
Q

defect vertebral arches, covered by skin, patch of hair?, does not involve neural tissue, no clinical signs, ~10% population has this anomaly.

A

spina bifida occulta

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21
Q

neural tissue is included in the fluid-filled sac protruding through the defect. neurological symptoms present

A

myelomeningocele

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22
Q

a fluid-filled sac of meninges protrudes through the defect. neurological symptoms present

A

meningocele

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23
Q

total failure of neurulation; No dysjunction- incompatible with life, hemorragic fibrotic, degenerated mass

A

craniorachischisis totalis

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24
Q

What are the defects related to secondary neuralation?

A

diastematomyelia and tethered spinal cord

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25
Q

persistence of neurenteric canal causes split spinal cord

A

diastematomyelia

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26
Q

fixed caudal end (filum terminale) of spinal cord

A

tethered spinal cord

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27
Q

What is the most common environmental cause of neural tube defects?

A

mom has a folic acid deficiency

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28
Q

What secretes Sonic hedgehog (Shh) protein and what does this protein do?

A

secreted by the notochord and it induces overlying ectoderm to differentiate into neuroectoderm

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29
Q

What are the 3 primary vesicles of the rostral part of the neural tube?

A

prosencephalon, mesencephalon, rhombencephalon

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30
Q

hindbrain

A

rhombencephalon

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31
Q

forebrain

A

prosencephalon

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32
Q

midbrain

A

mesencephalon

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33
Q

What does the prosencephalon differentiate into?

A

Diencephalon and Telencephalon

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34
Q

What does the mesencephalon differentiate into?

A

midbrain

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35
Q

What does the rhombencephalon differentiate into?

A

metencephalon and and myelencephalon

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36
Q

becomes the thalamus/hypothalamus

A

diencephalon

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37
Q

becomes the pons and cerebellum

A

metencephalon

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38
Q

becomes the medulla

A

myelencephalon

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39
Q

becomes the cerebral hemispheres

A

telencephalon

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40
Q

Failure to Form the Two Cerebral Hemispheres (fails to cleave and remains fused as single midline entity)

A

holoprosencephaly

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41
Q

What do you see in holoprosencephaly cases?

A

malformation of the brain and face; facial defects (cleft lips, single nostril, single eye)

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42
Q

cleft brain

A

schizencephaly

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43
Q

smooth brain (few gyri)

A

Lissencephaly

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44
Q

broad gyri, too few gyri

A

Pachygyri

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45
Q

small gyri

A

polygyri

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46
Q

At what vertebral level will you see conus medullaris?

A

L1

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47
Q

Which part of the spinal cord did this section come from?

A

sacral; ‘ugly butterfly’, lots of gray matter and little white matter

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48
Q

Which part of the spinal cord did this cross section come from?

A

lumbar; ‘perfect butterfly’

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49
Q

Which part of the spinal cord is this cross section from?

A

thoracic; skinny butterfly and you can see Clark’s columns really well; the Thin white part of the gray matter (making it a skinny butterfly) is the substantia gelatinosa

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50
Q

Which part of the spinal cord did this cross section come from?

A

cervical; typically oval shaped and the white matter is very large

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51
Q

Which part of the spinal cord did this cross section come from?

A

cervical (C1 level); bunny ears

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52
Q

occurring on the same side of the body

A

ipsilateral

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53
Q

relating to or denoting the side of the body opposite to that on which a particular structure or condition occurs

A

contralateral

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54
Q

At what level does the spinal cord end?

A

L1-2

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55
Q

specializations of the pia matter that connect the dura mater to the spinal cord

A

denticulate ligaments

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56
Q

At what level does the dural sac end?

A

S2

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57
Q

During week 10 within the developing spinal cord, the alar plate forms _____ and provides _________.

A

forms dorsally and provides sensory function

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58
Q

During week 10 within the developing spinal cord, the basal plate forms ______ and provides _______.

A

forms ventrally and provides motor function

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59
Q

is a tough, pia derived extension from the conus medullaris that attaches to the coccyx

A

filum terminale

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60
Q

a clinical sign in which forced flexion of the neck elicits a reflex flexion of the hips.

A

Brudzinski’s sign

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61
Q

Can’t straighten the hamstring to 90 degrees without pain

A

Kernig’s sign

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62
Q

Which two physical signs are seen in meningitis patients?

A

<!--StartFragment-->

Brudzinski’s sign and Kerning’s sign<!--EndFragment-->

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63
Q

What are the symptoms you see in patients with meningitis?

A
  • -Sudden onset of fever, nausea, vomiting, headache, decreased ability to concentrate, and myalgias in an otherwise healthy patient
  • -also commonly see petechiae rash
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64
Q

What causes Disseminated intravascular coagulation (DIC) ?

A
  • -Cause is activation of extrinsic and intrinsic clotting cascade by macrophage production of procoagulant tissue factor.
  • -Widespread ischemic changes and bleeding due to using up of clotting factors
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65
Q

Describe the structure of Neisseria meningitidis

A

–Gram-negative

  • -Kidney bean-shaped diplococci
  • -Cell wall - typical gram negative cell wall; thicker peptidoglycan layer [makes them susceptible to beta lactams and glycopeptides]
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66
Q

What is the major cause of meningitis pathology?

A

<!--StartFragment-->

Lipooligosaccharide (LOS)<!--EndFragment-->

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67
Q

How does <!--StartFragment-->Lipooligosaccharide (LOS) bring about the symptoms of meningitis ?<!--EndFragment-->

A
  • Activates macrophages through Toll pathway
  • Production of proinflammatory cytokines, especially TNF-a; may result in septic shock, increased vascular permeability
  • Induces macrophage production of procoagulant tissue factor which may lead to clotting and subsequent bleeding.
  • Petechial hemorrhages result from TNF-a and bleeding.
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68
Q

What is the gold standard for diagnosing meningitis?

A

Culture of CSF on blood and chocolate agars
–problem is, this takes 24 hours so you need to do something with the patient before then

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69
Q

life cycle in cat gut

A

Toxoplasma gondii

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70
Q

In what patients are we really concerned with toxoplasmosis?

A

immunocompromised patients; disease is more severe and may be fatal

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71
Q

How would you diagnose toxoplasmosis from serum samples?

A

–Determination of 4-fold increase in titer essential to diagnosis of acute infection

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72
Q
  • Free-living amebo-flagellate in soil and water
  • Found in 50% of fresh water bodies; seems to prefer warm water
  • Opportunistic infection
  • Acquired by human by getting water in nose and penetration of cribiform plate by amoeba
A

Naegleria fowleri

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73
Q

Function: fine touch, proprioception, two-point discrimination

A

Dorsal column system

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74
Q

Function: sharp pain, temperature, crude touch

A

spinothalamic tracts

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75
Q

Function: movement and position mechanisms

A

Dorsal spinocerebellar tract

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76
Q

Function: movement and position mechanisms

A

ventral spinocerebellar tract

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77
Q

Function: fine motor function (controls distal musculatrue) modulation of sensory functions

–descending pathway

A

Lateral corticospinal (pyramidal) tract

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78
Q

Function: gross and postural motor function (proximal and axial musculature)

–descending pathway

A

Anterior Corticospinal tract

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79
Q

Spinal cord is a derivative of the _____

A

nerual tube

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80
Q

Where do we see CSF in (or rather around) the spinal cord?

A

We see CSF between arachnoid and pia, i.e., in the subarachnoid space.

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81
Q

dermatome for upper arm (lateral surface)

A

C5

82
Q

Dermatome for middle finger

A

C7

83
Q

Dermatome for thumb and lateral forearm

A

C6

84
Q

Dermatome of little finger

A

C8

85
Q

Dermatome of nipple

A

T4

86
Q

Dermatome of umbilicus

A

T10

87
Q

Dermatome of calf

A

L4,L5

88
Q

Dermatome of big toe

A

L5

89
Q

Dermatome of heel

A

S1

90
Q

Dermatome of back of thigh

A

S2

91
Q

Where does the spinal cord get its blood supply?

A

The anterior spinal artery irrigates the anterior 2/3 of the cord.

92
Q

In a spinal cord specimen, the anterior spinal artery is commonly hidden in a fissure called ________

A

ventral median fissure

93
Q

Where does the cell body of a pre-ganglionic sympathetic neuron reside?

A

intermediolateral cell column (stretches from T1-L2)

94
Q

In the dorsal column medial lemniscus pathway, if the sensation comes below T6, it enters the ____ part of the dorsal column, and the info travels in a fiber band collectively called ______.

A

medial

Gracile Fasciculus

95
Q

In the dorsal column medial leminscus pathway, if sensation comes above T6, it enters the ____ part of the dorsal column, and the info travels in a fiber band collectively called the ______.

A

lateral; Cuneate Fasciulus

96
Q

The “pain/temp” pathway

A

spinothalamic tract

97
Q

a drastic measure of pain relief; remember, the cut should be about ____ segments above the sensory fiber entry zone.

A

cordotomy

2-3 segments

98
Q

upper motor neuronal cell bodies reside in the ____

A

brain

99
Q

lower motor neuronal cell bodies reside in the ____

A

spinal cord

100
Q

What is the treatment for toxoplasmosis?

A

The treatment of toxoplasmosis is pyrimethamine (most effective) and sulfadiazine.

101
Q

What happens in Myasthenia Gravis?

A

<!--StartFragment-->

•Autoantibodies against acetylcholine receptors on the

post-synaptic membrane.

  • Immunological destruction of neuromuscular junction
  • Rapidly fading strength (‘myasthenia’)due to depletion of synaptic acetylcholine

<!--EndFragment-->

102
Q

What is this and what causes it?

A

Ragged red fibers. Ragged red fibers occur as a result of compensatory proliferation of mitochondria in mitochondrial disorders

103
Q

Polymyositis is associated with sarcolemmal expression of ________.

A

<!--StartFragment-->

polymyositis is associated with sarcolemmal expression of major histocompatibility antigen 1 (MHC-I)<!--EndFragment-->

104
Q

Dermatomyositis is associated with ______.

A

<!--StartFragment-->

dermatomyositis is associated with **vascular expression of complement component C5b9, also known as membrane attack complex (MAC). **

<!--EndFragment-->

105
Q

What is the pathology, pathogensis, and clinical presentation of polymyositis?

A

Pathology: intrafascicular inflammation

Pathogenesis: cytotoxic t cells

Clinical expression: pain

106
Q

What is the pathology, pathogenesis, and clinical presentation of dermatomyositis?

A

Pathology: extrafascicular inflammation; perifascicular atrophy

Pathogenesis: humoral

Clinical presentation: pain and rash

107
Q

<!--StartFragment-->

What is the pathology, pathogenesis, and clinical presentation of Inclusion Body Myositis?

<!--EndFragment-->

A

<!--StartFragment-->

Pathology: inclusions; rimmed vacuoles

Pathogenesis: degenerative

Clinical presentation: steroid resistance

<!--EndFragment-->

108
Q

what is this a picture of?

A

Dermatomyositis

The inflammation is predominantly in the perimysium, the connective tissue around (rather than within, which is endomysium) the fascicle. Also note that the fibers at the very periphery of the fascicle are smaller; hence, perifascicular atrophy.

109
Q

What is this a picture of?

A

Polymyositis

110
Q

What is this a picture of?

A

Inclusion Body Myositis

In spite of its name, this is not a viral disease and the inclusion refers to the eosinophilic material within the vacuole (as seen in this picture).

111
Q

What is this a picture of?

A

Duchenne MD: endomysial fibrosis with fiber ‘rounding,’ variation in fiber size, and myofiber regeneration (small blue fibers)

112
Q

What is this a picture of?

A

Central core myopathy: note central pale areas

113
Q

What is this a picture of?

A

rod body, or nemaline myopathy

Material similar to Z-bands accumulates into rod-shaped structures (nemaline rods).

114
Q

What is this an image of?

A

centronuclear myopathies

There is one central nucleus uniformly in essentially every fiber. Some appear like they don’t have a central nucleus, because the section did not pass through the nucleus.

115
Q

What causes Devic Disease
(neuromyelitis optica)?

A

•Autoantibodies to aquaporin-4 receptors (a water channel protein)
–causes Synchronous blindness and paraplegia

116
Q
  • Autoimmune myelin destruction
  • Mainly CD 4+ and some CD 8+ T-cells, and macrophages
A

multiple sclerosis

117
Q

•line ventricles can differentiate into choroid plexus cells (make CSF)

A

ependymal cell

118
Q

axonal swelling

A

spheroids

119
Q

single nerve, usually traumatic or entrapment (carpal tunnel)

A

mononeuropathy

120
Q

–random damage to individual nerves (wrist drop, radial neuropathy)

A

polyneuritis multiplex

121
Q

–symmetric, length dependent (worse in distal long nerves). “Stocking glove” pattern

A

polyneuropathy

122
Q

Describe Guillain- Barre Syndrome.

A

•Rapid demyelination of motor axons that can lead to weakness / respiratory failure
–Weakness starts distally (feet/hands) moves proximally
•Caused by infection or vaccine

123
Q

How do you treat Guillain- Barre Syndrome?

A

plasmapharesis

124
Q

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is similar to GBS, but less severe. What is the major difference between the two?

A

CIDP Follows a chronic, relapsing and remitting course

125
Q

What gene is mutated in duchennes muscular dystrophy?

A

Dystrophin gene (Xp21) [x linked]

126
Q

sustained muscle contraction

A

myotonia

127
Q

What causes Myotonic Dystrophy?

A

•Autosomal Dominant mutation in DMPK leading to increased CTG repeats (>30, usually 1000’s)
–Undergoes anticipation like Huntington Dz

128
Q
  • Myelin is not formed properly or is degraded faster than it is made
  • Usually due to a genetic defect associated with myelin production
A

dysmyelinating disease

129
Q
  • Normal myelin is lost
  • Typically (auto)immune mediated
A

demyelination

130
Q
  • Usually seen in the central pons
  • Often associated with rapid correction of hyponatremia (low sodium)
A

Central Pontine Myelinolysis

131
Q

What causes Progressive multifocal leukoencephalopathy (PML)?

A

polyoma virus (JC virus), which infects and kills oligodendrocytes

132
Q

•Posterior fossa abnormality
•Part of cerebellum missing
Presents with hydrocephalus

A

Dandy-Walker Malformation

133
Q

What are the 3 causes of hydrocephalus?

A

–3 causes (all dealing with CSF)
•Impaired flow
•Impaired reabsorption
•Increased production (rare, tumors)

134
Q

Describe Type I muscle fibers.

A

<!--StartFragment-->

Slow twitch fibers (I)- fatigue resistant

Smaller soma & smaller axon

*Many mitochrondria (oxidative metabolism)

*Extensive capillary blood supply

*Myoglobin for O2 storage

<!--EndFragment-->

135
Q

Describe Type IIa muscle fibers

A

<!--StartFragment-->

Intermediate fibers (IIA)- fast twitch, fatigue resistant

Intermediate in properties

<!--EndFragment-->

136
Q

Describe Type IIb muscle fibers.

A

<!--StartFragment-->

Fast twitch fibers (IIB)- fatigue rapidly

Larger soma & larger axon

*Fewer mitochondria

*Less extensive blood supply

*Glycogen store & glycolytic enzymes

Extensive sarcoplasmic reticulum (Ca++)

<!--EndFragment-->

137
Q

What determines muscle fiber type?

A

the particular innervation of the muscle

138
Q

In regards to reflexes what do you see with upper motor neuron lesions?

A

hyperactive reflexes

139
Q

In regards to reflexes what do you see in regards to lower motor neuron lesions?

A

hypoactive reflexes

140
Q

a muscle twitch; a small, local, involuntary muscle contraction and relaxation which may be visible under the skin

A

fasciculation

141
Q

In regards to muscle tone, what do you see in upper motor neuron syndromes?

A

Increased muscle tone - Spasticity

142
Q

In regards to muscle tone, what do you see in lower motor neuron syndromes?

A

Decreased muscle tone – Flaccidity

143
Q

What’s the dermatome level for the little toe?

A

S1

144
Q

What’s the dermatome level for the perineum?

A

S3-S5

145
Q

What do you suspect when you see cape like distribution of pain and temperature loss?

A

<!--StartFragment-->

Syringomyelia<!--EndFragment-->

146
Q

What distinguishes B12 deficiency from copper deficiency?

A

The types of anemia they cause. B12 deficiency causes megaloblastic anemia while copper deficiency causes microcytic anemia

147
Q

What are the presynaptic neuromuscular junction disorders?

A
  • Lambert Eaton myasthenic syndrome
  • Botulism
148
Q

<!--StartFragment-->

What causes Lambert Eaton Myasthenic Syndrome (LEMS)?<!--EndFragment-->

A

•Voltage gated calcium channel antibodies impede release of acetylcholine

149
Q

<!--StartFragment-->

Lambert Eaton Myasthenic Syndrome (LEMS) is Associated with a cancer in 40-60% of patients (paraneoplastic). Which cancer is the most common?
<!--EndFragment-->

A

small cell lung cancer

150
Q
  • Most common of the adult dystrophies
  • Autosomal dominant
A

myotonic dystrophy

151
Q

How do you treat Polymyositis?

A

§Treatment with immunosuppression

  • Prednisone
  • Methotrexate
  • Azathioprine
152
Q

What are the ectoderm derivatives in the head and neck?

A

<!--StartFragment-->

  • neural tube (CNS-motor neurons, preganglionic ANS)
  • neural crest (PNS-postganglionic ANS)
    • epithelial component of the skin (glands, invaginations, other structures)
    stomodeum (lining of the future oral cavity)nasal pit, external auditory meatus-thickens to form placodes (olfactory, lens and otic)

<!--EndFragment-->

153
Q

what are the endoderm derivatives in the head and neck?

A

<!--StartFragment-->

-epithelial lining (pharynx, larynx, trachea, esophagus, pharyngotympanic tube,

middle ear)

  • glands develop as evaginations of endodermal tube - “pharyngeal pouches”

(thymus, parathyroid, tonsil, thyroid, mucosal)

<!--EndFragment-->

154
Q

What are the mesodermal derivatives in the head and neck?

A

<!--StartFragment-->

  • notochord (nucleus pulposus)
  • somites that form bones, muscles, connective tissue

<!--EndFragment-->

155
Q

What are the Pharyngeal (Branchial) Arches composed of?

A

migrating neural crest cells in the head

156
Q

Which cranial nerve grows into the 1st pharyngeal arch?

A

Trigeminal nerve (V)

157
Q

Which cranial nerve grows into the 2nd pharyngeal arch?

A

facial nerve (VII)

158
Q

Which cranial nerve grows into the 3rd pharyngeal arch?

A

glossopharyngeal nerve (IX)

159
Q

Which cranial nerve grows into the 4th pharyngeal arch?

A

vagus nerve (X)

160
Q

Which cranial nerve grows into the 6th glossopharyngeal arch?

A

vagus nerve (X)

161
Q

<!--StartFragment-->

What is the muscle derivative of the 1st pharyngeal arch?

<!--EndFragment-->

A

muscles of mastication

162
Q

<!--StartFragment-->

What is the muscle derivative of the 2nd pharyngeal arch?

<!--EndFragment-->

A

muscles of facial expression

163
Q

<!--StartFragment-->

What is the muscle derivative of the 3rd pharyngeal arch?

<!--EndFragment-->

A

stylopharyngeus muscle

164
Q

<!--StartFragment-->

What is the muscle derivative of the 4th pharyngeal arch?

<!--EndFragment-->

A

laryngeal muscle

165
Q

<!--StartFragment-->

What is the muscle derivative of the 6th pharyngeal arch?

<!--EndFragment-->

A

Pharyngeal muscles

166
Q

<!--StartFragment-->

What are the derivatives of the 1st pharyngeal arch cartilage?

<!--EndFragment-->

A

<!--StartFragment-->

Malleus, Incus, (sphenomandibular lig.), rest of Meckel’s cartilage disappears

“M arch”

<!--EndFragment-->

167
Q

<!--StartFragment-->

What are the derivatives of the 2nd pharyngeal arch cartilage?

<!--EndFragment-->

A

<!--StartFragment-->

Stapes, Styloid process, Superior half of body of hyoid, (Stylohyoid lig.)<!--EndFragment-->
“S arch)

168
Q

<!--StartFragment-->

What are the derivatives of the 3rd pharyngeal arch cartilage?

<!--EndFragment-->

A

inferior half of body and greater horn of hyoid

169
Q

<!--StartFragment-->

What are the derivatives of the 4th pharyngeal arch cartilage?

<!--EndFragment-->

A

thyroid and epiglottic cartilages of larynx

170
Q

<!--StartFragment-->

What are the derivatives of the 6th pharyngeal arch cartilage?

<!--EndFragment-->

A

Laryngeal cartilages (cricoid, arytenoid, corniculate)

171
Q

Which nerves are tested in the biceps reflex?

A

C5, C6

172
Q

Which nerves are tested in the brachioradialis reflex?

A

C5, C6, C7

173
Q

Which nerves are tested in the patellar reflex?

A

L2, L3, L4

174
Q

Which nerves are tested in the achilles reflex?

A

S1, S2

175
Q

Which nerves are tested in the pupillary light reflex?

A

CN II, CN III

176
Q

Which nerves are tested in the jaw jerk reflex?

A

CN V

177
Q

Which nerves are tested in the corneal (blink) reflex?

A

CN V, CN VII

178
Q

which nerves are tested in the gag reflex?

A

CN IX, CN X

179
Q

CAPE-LIKE BILATERAL loss of pain and temperature sensation of the shoulders and upper extremities due to damage of the ANTERIOR WHITE COMMISSURE

A

Syringomyelia

180
Q

Where is the lumbosacral enlargement?

A

Around L1-S3

181
Q

Where is the cervical enlargement?

A

Around C3-T1

182
Q

Where is the intermediolateral cell column?

A

T1-L2

183
Q

In what part of the spinal cord are sympathetics located?

A

lateral/intermediate horn

184
Q

What can you see in lesions of the dorsal column medial lemniscus tract?

A

multiple sclerosis, Tabes Dorsalis (from syphilis), and vitamin B 12 deficiency

185
Q

What can you see with lesions of the spinothalamic tract?

A

Syringomyelia and Brown-Sequard syndrome

186
Q

What can you see with lesions of the corticospinal tract?

A

ALS and vitamin B 12 deficiency

187
Q

What are the functions of free nerve endings?

A

Free nerve endings function as thermoreceptor. Some of them also function as norciceptors that detect noxious stimuli.

188
Q

senses vibration of the skin

A

Pacinian corpuscle

189
Q

senses stretching of the skin

A

ruffini ending

190
Q

this occurs at the sensory receptor level; the receptor decreases its firing frequency

A

adaptation

191
Q

receptors that completely adapt to a stimulus, i.e., stop firing after some time

A

phasic receptor

192
Q

receptors that continue to fire as long as the stimulus is present

A

tonic receptor

193
Q

this occurs at the CNS level. The brain pays less attention to a constant stimulus

A

habituation

194
Q

The area of the body from which a stimulation influences the discharge rate of that neuron.

A

receptor field

195
Q

Pain is transmitted by which two fiber types?

A

A-delta and C

196
Q

What is involved in the triple vascular response of T Lewis?

A

redness (local vasodilation), flare (vasodilation in a wider area caused by axon reflex), weal (edema)

197
Q

Extrafusal fibers are activated by _____.

A

Extrafusal muscle fibers are activated by α-motor neuron

198
Q

Intrafusal muscle fibers are activated by _____.

A

gamma motor neurons

199
Q
  • Arranged in “parallel” with the regular muscle fibers, i.e., extrafusal fibers
  • It detects “stretch” when the muscle is stretched
A

muscle spindle

200
Q
  • Arranged in “series” with the muscle mass
  • It detects “tension” either when the muscle contracts by itself or is stretched passively
A

golgi tendon organ

201
Q

•What is the mechanism of action for local anesthetics?

A

Application of local anesthetics, such as lidocaine, can block Na+ channel on C fibers quickly, thus the transmission of action potentials signaling pain.

202
Q

•What is hyperalgesia?

A

an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.

Brain and Behavior (11 decks)

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