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Y2B4 - Central Nervous System 📙 > SDL 👨‍💻 > Flashcards

SDL 👨‍💻 Flashcards

1
Q

Site of Olfactory receptors

A
  • extreme superior region of nasal cavity (olfactory recess)
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2
Q

Number of Olfactory receptors

A
  • Ten million olfactory neurons.
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3
Q

Life span of Olfactory receptors

A
  • regenerate every 2 monthes
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4
Q

what regenerates Olfactory receptors?

A
  • basal cell
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5
Q

what neurons have the most exposed nerve endings of any neurons?

A

The primary olfactory neurons, and they are constantly being re-placed

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6
Q

what is charachterestic Olfactory receptors?

A
  • They are constantly being re-placed
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7
Q

Threshold of Olfactory receptors

A
  • The threshold for the detection of odors is very low,
  • So very few odorant molecules are required to trigger the response.
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8
Q

Specifity of Olfactory receptors

A
  • Low specificity in the olfactory epithelium
  • A given receptor may react to more than one type of odorant.
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9
Q

Characters of Methyl-mercaptan

A
  • Has a nauseating odor similar to that of rotten cabbage
  • Added to natural gas at a concentration of about 1 part per million
  • A person can detect the odor of about 1/25 billionth of a milligram of the substance
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10
Q

Significance of Methyl-mercaptan

A

Awarness of natural gas leakage

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11
Q

Mechanism of stimulation of olfaction

A
  • Odorant enter nasal cavity then dissolve in fluid of nose and bind to chemoreceptor of olfactory hair resulting in depolarization by unknown mechanism
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12
Q

what is the number of types of odors can be discriminated by olfactory receptor?

A

4000 types of odors, by unknown mechanism

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13
Q

what are the seven primary classes of odours?

A
  1. Camphoraceous
  2. Floral
  3. Ethereal
  4. PutridIt’s very unlikely
  5. Musky
  6. Pepperminty
  7. Pungent
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14
Q

what is the only major sensation that doesn’t pass by the thalamus? and where does it pass?

A
  • Olfaction
  • Passes directly to the frontal cortex
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15
Q

First order neuron of Neural pathway Olfaction

A

Olfactory receptor = Bipolar cell

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16
Q

what part of ethmoid bone does the olfactory nerve pass by during its course?

A

Cribriform plate

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17
Q

2nd order neuron of Neural pathway Olfaction

A

Olfactory tract (Mitral cell & Tufted cell)

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18
Q

the olfctory bulb is considered a part of …….

A

brain

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19
Q

What does the olfactory tract pass to?

A

Medial, lateral & Intermediate olfactory areas

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20
Q

Function of medial olfactory area

A

Visceral & Emotional response to odour —> limbic system & Hypothalamus

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21
Q

Function of lateral olfactory area

A

Conscious perception of smell

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22
Q

Function of intermediate olfactory area

A

Synapse with association neuron to modulate sensory information within olfactory bulb

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23
Q

Neural pathway olfaction

A
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24
Q

what is another name for taste?

A

Gustation

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25
Q

Site of Taste buds

A

Tongue papille except filiform papille, Palate, Lips, Throat (in children).

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26
Q

Types of Taste buds

A

According to their shape:

  • Fungiform
  • Circum-Vallate
  • Foliate
  • Filiform
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27
Q

Shape of Fungiform papillae

A

Mushroom-shaped

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28
Q

Distribution of Fungiform papillae

A
  • scattered irregularly over the entire superior surface of the tongue and appear as small red dots () filiform papille
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29
Q

Characters of Circum-Vallate papillae

A
  • The largest but least numerous of the papillae

-

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30
Q

Number and distribution of Circum-Vallate papillae

A
  • 8 to 12 of these papillae form a V-shaped row along the border between the anterior and posterior parts of the tongue.
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31
Q

Shape of Foliate papillae

A
  • Leaf-shaped
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32
Q

Site of Foliate papillae

A
  • on the lateral sides of the tongue and contain the most sensitive taste buds.
  • They are located mostly posteriorly in adults.
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33
Q

Number of Foliate papillae

A
  • most numerous in young children and decrease with age.
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34
Q

Characters of Filiform

A

Filament-shaped , Most numerous

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35
Q

What is the only type of papillae with no taste buds?

A

Filiform papillae

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36
Q

Number of taste buds

A

10,000 , each taste bud has 50 gustatory cell.

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37
Q

Shape of taste buds

A

oval

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38
Q

Life span of taste buds

A

10 days

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39
Q

what does each gustatory cell have?

A
  • Each gustatory cell has several microvilli called gustatory hair extending from gustatory pores.
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40
Q

what is a must for taste to be felt?

A
  • Tasten must be dissolved in saliva
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41
Q

Do taste receptors generate their own action potential?

A
  • Theses cell does not generate their own action potential
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42
Q

what stimulates AP in sensory neurons of taste?

A
  • Neurotransmitter is released from taste cell and stimulate action potential in sensory neuron associated with them.
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43
Q

what are types of tastes?

A
  • Salt (metal ion , side of tongue)
  • Sour (acid , side of tongue)
  • Sweet (sugars , some other carbohydrates , some proteins , tip of tongue)
  • Bitter (alkaloid or bases , most of them are poisonous, back of tongue)
  • Umami (delicious as glutamate , many protein and Amino acids , all over tongue)
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44
Q

Examples of salty tastes

A
  • Salt (metal ion)
  • side of tongue
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45
Q

Mechanism of salty tastes

A
  • stimulation of epithelial Na channel
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46
Q

Examples of Sour tastes

A
  • Sour (acid)
  • side of tongue
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47
Q

Mechanism of Sour tastes

A
  • Stimulation of H channel
  • Inhibition of ligand gated K channel
  • Stimulation of ligand channels for any positive ions.
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48
Q

Examples of sweet tastes

A
  • Sweet (sugars , some other carbohydrates , some proteins, lead, alcohol, aldehyde)
  • tip of tongue
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49
Q

Mechanism of sweet tastes

A

through G protein mechanism

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50
Q

Examples of bitter tastes

A
  • alkaloid or bases , most of them are poisonous
  • back of tongue
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51
Q

Mechanism of bitter tastes

A
  • through G protein mechanism
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52
Q

Exampels of Umami tatses

A
  • Umami (delicious as glutamate , many protein and Amino acids
  • All over tongue
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53
Q

Mechanism of Umami tatses

A

through G protein mechanism

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54
Q

How does the texture of food in the oral cavity affect the perception of taste?

A
  • The texture of food in the oral cavity also affects the perception of taste
  • Hot or cold food temperatures may interfere with the ability of the taste buds to function in tasting food
  • If a cold fluid is held in the mouth, the fluid becomes warmed by the body, so that taste becomes enhanced.
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55
Q

Which type of food is tasted better, Hot or Cold?

A

Hot

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56
Q

Adaptation for taste

A
  • Adaptation is very rapid for taste.
  • This adaptation occurs both at the level of the taste bud and within the CNS.
  • Adaptation may begin within 1 or 2 seconds after a taste sensation is perceived, and complete adaptation may occur within 5 minutes.
57
Q

Is taste affected by olfaction?

A

Yes

58
Q

How to demomstare the relation between olfaction and taste

A
  • by pinching one’s nose to close the nasal passages, while trying to taste something. With olfaction blocked, it’s difficult to distinguish between the taste of a piece of apple and a piece of potato.
59
Q

what are the number of tastes diffrentiated by humans?

A
  • Only five primary tastes have been identified, humans can perceive a fairly large number of different tastes by combining the five basic taste sensations.
60
Q

Specifity of taste receptors

A
  • The specificity of the receptor molecules is not perfect.
  • For example theartificial sweeteners have different chemical structures than the sugars they are designed to replace and are often many times more powerful than natural sugars in stimulating taste sensations.
61
Q

which type of tastes has the highest sensitivity?

A

bitter substances

62
Q

which type of tastes has the lowest sensitivity?

A

sweet and salty tastes

63
Q

Significance of high sensitivity for bitter foods

A

protective

64
Q

why do humans tend to crave sweet, salty, and umami tastes?

A
  • in response to the body’s need for sugars, carbohydrates, proteins, and minerals.
65
Q

what percieves taste form the anterior 2/3 of tongue?

A

Chorda tympani of facial nerve

66
Q

what percieves taste form the posterior 1/3 of tongue?

A

glossopharygneal nerve

67
Q

what percieves taste form the epigolttis?

A

vagus nerve

68
Q

1st order neuron of taste pathway

A

ipsilateral tractus solitarius in medulla

69
Q

2nd order neuron of taste pathway

A

medial leminiscus

70
Q

3rd order neuron in taste pathway

A

PVMNT of thalamus

71
Q

where does taste pathway end?

A

extreme inferior part of post-central gyrus

72
Q

Neural pathway for taste

A
73
Q

what are the symptoms of upper motor neuron lesion?

A
  • Paralysis
  • Spasticity
  • Reflex abnormalities
74
Q

Symptoms of paralysis of UMNL

Mnemonic: Multiple Paretic fatigue alternating synkinesia Re Fine atrophy

A
  • Affects multiple muscle groups (but not all)
  • Bilaterally innervated movements are only mildly paretic.
  • Voluntary movement of paretic limbs requires greater effort and causes greater muscular fatigue
  • Rapid alternating movements are slowed
  • There may be synkinesia, undifferentiated accessory movements, or spinal automatisms
  • Paralysis that is initially total usually improves with time, but recovery may be accompanied by other motor disturbances such as tremor, hemiataxia, hemi- chorea, and hemiballism.
  • Fine motor control is more severely impaired than strength.
  • Neurogenic muscular atrophy does not occur.
75
Q

What structures might be mildly paretic in UMNL?

A
  • Bilaterally innervated movements (e.g., of eyes, jaw, pharynx, neck)
76
Q

what do voluntary movements of paretic limb require in UMNL? and what does that cause?

A
  • Requires greater effort
  • Causes greater muscular fatigue.
77
Q

what happens to Rapid alternating movements in UMNL? and why?

A
  • slowed
  • due to hypertonia
78
Q

what is a characteristic feature for paralysis of UMNL?

A

synkinesia, undifferentiated accessory movements & spinal automatisms

79
Q

what is synkinesia?

A
  • involuntary movement of paretic limbs associated with other movements e.g. yawning
80
Q

what is another name for undifferentiated accessory movements?

A

mass movements

81
Q

what is spinal automatism?

A
  • involuntary movements triggered by somatosensory stimuli
82
Q

what happens to total paralysis over time in cases of UMNL?

A
  • usually improves with time, but recovery may be accompanied by other motor disturbances
83
Q

what happens after partial recovery from paralysis of UMNL?

A
  • Recovery may be accompanied by other motor disturbances such as tremor, hemiataxia, hemichorea, and hemiballism.
84
Q

what is more impaired in UMNL, Fine motor control or strength?

A

Fine motor control

85
Q

Does neurogenic muscle atrophy occur in UMNL?

A

No

86
Q

Symptoms of spasticity in UMNL

A
  • velocity-dependent
  • Usually, but not always, accompanied by hypertonia
  • Clasp-knife phenomenon
  • affects antigravity muscle
87
Q

What is Spasticity?

A
  • velocity-dependent increase of muscle tone in response to passive stretch.
88
Q

what is spasticity usually associated with?

A
  • Usually, but not always, accompanied by hypertonia.
89
Q

what is Clasp-knife phenomenon?

A
  • sudden slackening of muscle tone on rapid passive extension
  • Rare
90
Q

Does spasticity affect antigravity muscles?

A

affects antigravity muscle (arm flexors, leg extensors).

91
Q

what are reflex abnormalities associated with UMNL?

A
  • The intrinsic muscle reflexes are enhanced with clonus.
  • the extrinsic reflexes are diminished or absent.
  • Pathological reflexes such as the Babinski reflex can occur.
92
Q

what are another names for UMNL?

A

Central lesion = UMNL = pyramidal tract lesion

93
Q

what are types of cerebral lesions?

A
  • Monoparesis
  • Contralateral hemiparesis
  • Ipsilateral paresis
  • Quadriparesis
  • Paraparesis
94
Q

what causes Monoparesis?

A

Isolated lesions of 1ry motor cortex (area 4)

95
Q

what does Isolated lesions of 1ry motor cortex (area 4) cause?

A
  • cause flaccid weakness of the contralateral face, hand, or leg.
96
Q

what does Lesions affecting adjacent precentral or postcentral areas, or areas deep to cortex cause?

A
  • cause spasticity and possibly an associated sensory deficit.
97
Q

Difficulity in determination by examination alone whether monoparesis is of upper or lower motor neuron

A

The difference: Accessory movements of antagonistic muscles are present in UMNL

98
Q

what causes Contralateral hemiparesis?

A
  • Lesions of internal capsule
  • Unilateral lesions in rostral brain stem
  • Involvement of corticopontine fibers
  • A rare isolated lesion of medullary pyramid
99
Q

what do Lesions of internal capsule cause?

A

cause spastic hemiparesis

100
Q

What do unilateral lesions in rostral brain stem cause?

A
  • cause contralateral spastic hemiparesis
    and ipsilateral nuclear oculomotor nerve palsy (crossed paralysis)
101
Q

What does Involvement of corticopontine fibers cause?

A
  • causes (central) facialparesis,and impairment of corticobulbar fibers causes dysphonia and dysphagia.
102
Q

what does rare isolated lesion of medullary pyramid cause?

A
  • can cause contralateral flaccid hemiplegia without facial paralysis
103
Q

what does rare isolated lesion of medullary pyramid at mid-decussational level cause?

A
  • contralateral arm paresis and ipsilateral leg paresis (Hemiplegia alternans)
104
Q

what causes Ipsilateral paresis?

A
  • Lesions of lower medulla below pyramidal decussation
105
Q

what does a lesion in lower medulla below pyramidal decussation cause?

A
  • cause ipsilateral paralysis and spasticity (as lesions of lateral corticospinal tract).
106
Q

what causes Quadriparesis?

A
  • extensive destruction of Both the cerebral cortex and underlying white matter possibly extending into the diencephalon
  • Involvement of midbrain
  • Involvement of pons or medulla
107
Q

what causes decortication syndrome?

A

extensive destruction of Both the cerebral cortex and underlying white matter possibly extending into the diencephalon

108
Q

Symptoms of decortication syndrome

A
  • Flexion of upper limb and extension of lower limb
109
Q

what causes decerebration syndrome?

A
  • Involvement of midbrain
110
Q

Symptoms of decerebration syndrome

A

Extension of both upper and lower limbs

111
Q

what does Involvement of pons or medulla cause?

A
  • causes initial quadriplegia: in the later course
    of illness, spinal automatisms may be seen in response to noxious stimuli.
112
Q

what is Paraparesis?

A

Paralysis in both upper or lower limbs

113
Q

What causes Paraparesis?

A

bilateral, paramedian, pre-central cortical lesions (parasagittal cortical syndrome).

114
Q

what may occur with Paraparesis?

A

Bladder dysfunction and focal seizures

115
Q

what causes Peripheral paralysis (LMNL)?

A
  • lesions of the anterior horn
  • nerve root
  • peripheral nerve
  • motor end plate
116
Q

what should Peripheral Paralysis be distinguished from?

A
  • must be distinguished from weakness due to disease of the muscle itself (myopathy).
117
Q

what are signs of Peripheral Paralysis (LMNL)?

A
  • Paralysis
  • Reflex abnormalities
  • Muscle atrophy
  • Spontaneous movements
118
Q

what is paralysis of Peripheral Paralysis (LMNL) accompanied by?

A
  • diminution of muscle tone (flaccidity).
119
Q

what does teh extent of weakness in Peripheral Paralysis (LMNL) depend on?

A
  • The extent of weakness depends on the type, severity, and distribution of LMN or myopathic involvement.
120
Q

reflex abnormalities in Peripheral Paralysis (LMNL)

A

Intrinsic muscle reflexes:
- are diminished or absent

Extrinsic reflexes:
- are unaffected unless effector Ms is atrophic.

Pathological reflexes:
- are absent.

121
Q

Proportion between intrinsic muscle reflexes and degree of weakness in Peripheral Paralysis (LMNL)

A

Intrinsic muscle reflexes:

  • are diminished or absent to a degree that may be disproportionate to the degree of weakness.
  • in LMN-type paralysis, loss of reflexes is independent from the loss of strength (in myopathy, it parallels the weakness)
122
Q

Muscle atrophy in Peripheral Paralysis (LMNL)

A
  • Muscle atrophy due to an LMN lesion may be disproportionate to the degree of weakness (either greater or less).
  • Progressive atrophy of paralyzed muscles begins 3 weeks after a peripheral nerve injury.
123
Q

what are spontanious movements associated with Peripheral Paralysis (LMNL)?

A
  • Fasciculations
  • Myokymia
124
Q

what are fasiculations?

A
  • are involuntary, non rhythmic contractions of motor units in a relaxed muscle.
125
Q

Are fasiculation of Peripheral Paralysis (LMNL) exclusively caused by anterior horn lesions?

A

No

126
Q

what is myokymia?

A
  • rhythmic contraction of muscle fibers
127
Q

are spontaneous movements of Peripheral Paralysis (LMNL) visible?

A
  • if the affected muscle is superficial (e.g. the orbicularis oculi), waves of muscle contraction are visible under the skin.
128
Q

what are types of LMN lesions?

A
  • Anterior horn
  • Radicular syndrome
  • Peripheral nerve
  • Motor end plate (neuromuscular lesion)
  • Myopathy & MSK lesions
129
Q

site of lesion in case of Anterior horn

A
  • Loss of motor neurons in spinal cord
130
Q

Signs in case of Anterior horn

A
  • No sensory deficit.
  • The flaccid segmental weakness may be proximal or distal acc. to etiology
  • asymmetrically with severe muscle atrophy.
  • The intrinsic reflexes are lost at an early stage.
131
Q

Site of lesion in case of Radicular syndrome

A
  • A lesion of a single ventral nerve root and dorsal root (e.g, by herniated disk).
132
Q

Signs in case of Radicular syndrome

A
  • Involvement of dorsal root produces pain and paresthesia in associated dermatome, which triggered by straining (sneezing, coughing), movement or local percussion.
  • Muscles supplied by multiple nerve roots are only slightly weakened, but those supplied by a single root may be paralyzed and atrophic
  • Autonomic deficits are rare.
133
Q

Signs in case of Peripheral nerve

A
  • The deficit may be motor, sensory, or mixed, with autonomic dysfunction.
  • Paralysis may be caused by Reflex abnormalities.
134
Q

Signs in case of Motor end plate = neuromuscular lesion

A
  • No sensory deficit
  • Myasthenia gravis & Lambert eaton syndrome and botulism
135
Q

what characterizes fatigue of Myasthenia gravis?

A

Exercise-induced muscle fatigue

136
Q

Other characters of Myasthenia gravis

A
  • hyporelexia parallel to ms weakness
137
Q

what characterizes Lambert eaton syndrome and botulism?

A
  • lesion may be disproportionate to degree of weakness (greater or less)
  • hyporeflexia
  • autonomic dysfunction.
138
Q

Site of lesion in case of Myopathy & MSK lesions

A

Of tendons, ligaments, joints, and bones.

139
Q

Signs in case of Myopathy & MSK
lesions

A
  • No sensory deficit.
  • MSK lesions may restrict movement, particularly when they cause pain, sometimes to the extent that ms becomes atrophic from disuse.
  • Severe autonomic dysfunction.

Y2B4 - Central Nervous System 📙 (8 decks)

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