physiology lGW Flashcards

(120 cards)

1
Q

What is saltatory conduction?

A

Saltatory conduction is the propagation of action potentials along myelinated axons from one node of ranvier to the next node, increasing the conduction velocity of actio potential

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2
Q

How does inhibitory transmitters such as GABA reduce the probabilty that apostynaptic cell generate an action potential?

A

It triggers opening cl- channels in the postsynaptic neuron, which hyperpolarizes its membrane

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3
Q

What are metabotropic receptors?

A

Act as G coupled receptors
SLow effects
Change postsynaptc membrane metabolism
CAMP or calciu mobilization
Has a diffuse synaptic connection

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4
Q

Whata are examples of metabotropic receptors?

A

Monoamines, neuropeptides

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5
Q

What are ionotropic receptors?

A

Close or open ion channels
Fast effect
CHange postsynaptic membrane polarity
Has a focused synaptic connection

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6
Q

What is an example of ionotropic receptors?

A

Glutamate, GABA, Glycine

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7
Q

What is sensory transduction?

A

Conversion of sensory stimulus from one form to another

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8
Q

What are the different tye of mechanoreceptors and where are they located?

A
  1. Free nerve endings: epidermis, dermis
  2. Merkel’s disc: superficial epidermis
    3.Meissner’s corpuscle: superficial, papillary dermis of the palm of hands and sole of foot
  3. Pacinian corpuscle: Deep layers of palmar dermis, palmar, subcutaneous tissues and near periosteum of proximal phalanges
  4. Ruffini’s end organ: Deep, encircle hair follicles
    6.Krause’s endings: superficial: superficial layers of dermis
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9
Q

What is the somatosensory cortex? Name its parts

A

Lies in the postcentral gyrus
Occupying areas 1,2,3,5,7 and 40
Divided into 3 main parts:
1.Somatic sensory area I (SI)
2.Somatic sensory area II (SII)
3.Association sensory cortex

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10
Q

What is the effect of lesion on SI?

A

Inability to perceive epicretic sensation
Fine localization is lost but crude localization is present.
Pain sensation is poorly affected (slow pain and extreme temperature are protopathic sensation)

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11
Q

What is the site of somatic sensory area I?

A

Post central gyrus 1,2,3

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12
Q

what are the charecters of SI?

A

1.Crossed representation
2.Inverted representation of the body
3.Size is proportional to the amount of receptors present
4.Modality orientation

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13
Q

What type of sensation is recieved in the posterior part of SI?

A

Pressure and tactile sensation

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14
Q

What type of sensation is recieved in the anterior part of SI?

A

Proprioceptive sensation

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15
Q

What is the function of SI?

A

Center of perception of
1.Fine touch: tactile localization and discrimination
2.Localization of paina nd temperature
3.Stereognosis
4.Proprioception (static and dynamic)
5.Vibration sense, pressure, texture of material, weights
6.Discrimination of various grades of temperature

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16
Q

What is the site of SII?

A

Behind and below SII
Occupies area 40 above the lateral sulcus

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17
Q

Where does SII recieve afferent fibers from?

A

Thalamic nucleus
SI
Other sensory areas e.g.visual and auditory areas

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18
Q

What are the characters of SII?

A

The body part representation

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19
Q

Which area of the somatosensory cortex is stronger?

A

SI Is stronger than SII

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20
Q

What is represented in the anterior part of SII?

A

The head area

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21
Q

What is represented in the posterior part of SII?

A

THe leg area

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22
Q

What is the function of SII?

A

1.Potentiates the functions of SI
2.Begins to make meaning of the sensory signals (shape or texture of n object placed on a hand)

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23
Q

What does a lesion in SII lead to?

A

Deficit learning based on tactile discrimination

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24
Q

Where is the somatic association cortex?

A

Lies behind SI and above SII (areas 5 and 7)

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25
Where does the somatic association cortex recieve signals from ?
SI, SII, thalamus, visual and auditory areas
26
What is the function of the somatic association area?
1.Interpretation of information entering the somatic sensory areas for understanding and giving meaning to them 2.Center for stereognosis 3.Shares in planning of movements
27
What is the effect of a lesion in the somatic association area?
1.Astreognosis 2.Amorphosynthesis (-autopognosia) forgetting the other side 3.Neglect syndrome: movement occur without planning
28
When you are dealing with a neurological case what questions do you ask yourself?
Where is the lesion? What is the lesion?
29
What are the dorsal column syndromes?
Deficits in touch and proprioception 1.Tabes dorsalis (most common form of neurosyphilis) 2.Friedreich's ataxia 3.Brown sequard syndrome
30
What are spinothalamic syndromes?
Deficits in pain and temperature sense 1.Anterior spinal artery syndrome: atherosclerosis or spinal injury 2.Syringomyelia:Occlusion of crossing pathways by degenerative expansion of the spial centeral canal
31
What are the type of lesions found in syringomyelia?
1.Congenital 2.Overgrowth of abnormal glial tissue (gliosis) around the central canal of spinall cord which then falls leading to cavitation and damage of the crossing fibers of lateral and ventral spinothalamic tracts 3.Srinex= Cyst ( a rare fluid filled neurological cavity within spinal cord or brain stem)
32
Where is the lesion in syringomyelia found?
1.Spinal cord (lower cervcical and upper thoracic C4-T10) 2.May extend to affect lumbar segments 3.Brain stem (syringobulbia)
33
What are most common genre of people with syringomyelia?
Middle age and female
34
What is syringomyelia charcterized by?
Loss of pain, Temperature and crude touch on both sides of the body at the level of the affected segments (Jacket ditribution of sensory loss)
35
Which sensations are not affected in syringomylia?
Sensatios carried in dorsal column (dissociated sesnory loss)
36
What are the complications of syringomyelia?
Bilateral muscle paralysis at level of lesion (AHCs lesions) Unilateral or bilateral horner's syndrome (LHCs lesion) Syringobulbia (Damage of 9th, 10th, 12th cranial nerve) causing dysphagia & longue atrophy
37
Which dermatomes are affected by the jacket-like dissociated sensory loss?
C4-T2
38
Explain the sensory loss that occurs in syringomyelia.
Due to damage of the crossing fibers of the lateral and ventral spinothalamic tract by the gliosis or fibrosis around the central canal (loss of pain & temperatur) while the dorsal column tract is intact (tactile sensation & proprioception)
39
If you examine for light touch, in syrngomeylia, what would you find?
It would be partially affected as it is carried to a little extent by the dorsal column (which is intact) together with the ventral spinothalmic tract (which is affected)
40
What is the type of lesion found in Tabes Dorsalis?
1. Infalmmatory (neurosyphilis) 2.Inflammation of the dorsal roots with comression of the afferent fibers leading to demylination and degeneration of large myelinated fibers, so in early course of the disease, it involves the dorsal column sensations rather than the spinothalamic. later on, all sensations in the regions innervated by affected dorsal nerve root will be affected.
41
Where is the lesion of tabes dorsalis found?
1.Spinal cord (dorsal roots of lumbosacral segments & upper thoracic segments) 2, pretectal area in the midbrain
42
What is the symptom of Tabes dorsalis in the pretectal area in the midbrain?
Argyll robertson pupil
43
What is Argyll Robertson's pupil?
The physical exam findings of bilateraly small pupils that do not constrict when exposed to bright light but do constrict when focused on nearby onjects
44
In which gender is Tabs dorsalis more common?
Males
45
What are the early manifestations of Tabis dorsalis?
Inflammation --> Irritation of pain fibers in the central part of the dorsal root causing attacks of severe pain felt in the lower limbs Degeneration---> Loss of dorsal colum sensations leading to sensory ataxia (positive romberg's sign) Stamping gait
46
What are the late manifestations of Tabes dorsalis?
1.Loss of all sensations in the regions innervated by affected dorsal nerve root= deafferentation slow pain remains for long period (resists compression) 2.Loss of all reflexes (both superficial, deep and visceral) which have its centers in the affected segment due to irritation of the afferents fibers of these reflexes 3.Micturition disturbance: in form of retetion with overflow 4.Loss of pain sensation: (very late) due to affection of the pain fiber 5.May be accompanied with (Argyll robertson pupil) where the pupil is irregular, shows miosis in response to near objects (intact acocommodatio) but no miosis in response to light (lost pupillary light reflex)
47
Explain the loss of position and vibration sensation Tabes dorsalis
The lost position and vibration sensations are due to compression on the afferent fibers (AB fibers) that carry the sensations at the dorsal rooot lesion, leading to failure of sensory impulse transmission to the cortex
48
Explain the absent deep reflexes in tabes dorsalis
The absent deep reflexes are dut to compression on the afferent fibers of reflexes (muscle spindle reflex) at the dorsal root
49
Explain the positive Romberg's sign in Tabes dorsalis
The positive romberg's sign is due to proprioceptive sensations from lower limbs leading to inability to maintain balance while closing eye
50
What are the other effects of a dorsal column lesion in tabes dorsalis?
Loss of fine touch Loss of stereognosis Loss of superficial reflexs (flexor withdrawl) Loss of visceral reflxes
51
Why do patients complain of pain in Tabes dorsalis?
Due to irritation of pain conducting fibers at the dorsal root by the inflammatory process, leading to transmission of impulses through the fibers to the brain and perception of pain
52
What is brown-sequard syndrome?
Damaged one side of the spinal cord
53
What is the clinical picture of brown-sequard syndrome when it is above the level of lesion?
Cutaneous hyperthesia (increased sensitivity to sensations due to irritation of dorsal roots)
54
What is the clinical picture of Brown-sequard syndrome at the level of the lesion?
Loss of all sensations in corresponding dermatomes on the same side Motor affection=Flaccid paralysis (LMNL) and loss of all reflexes mediated via the affected segments
55
What is the clinical picture of Brown-sequard syndrome below the level of lesion?
Loss of pain and temperature on the opposite side of the lesion= Cotralateral analgesia and athermia Crude touch is decreased on both sides but not lost Loss of fine touch, proprioceptie sensations, vibratio, pressure on the same side due to interruption of fibers of the dorsal column tract
56
Where in brown sequard syndrome does UMNL occurs?
Same side
57
Where in brown sequard syndrome does Horner's syndrome occur?
Cervical lesion
58
What are the symptoms of brown sequard on the same side as lesion?
UMN weakness Loss of position & vibration
59
What are the symptoms of brown sequard syndrome on the same side of the lesion?
Loss of pain and temperature
60
What are the disorders produced by diesease of the basal ganglia?
Either hyperkinesia (excess involuntary spontaneous movements) or hypokinesia (lack of spontaneous movement, sloing of voluntary movement) No weakness Ballisus (jumping about) Dystonia (extreme contractions forcing unusual movements) Athetosis (Continul uncontrolled writhing) Chorea (COntinuing series of rapid, jerky movements that are fragments of purposeful movements ) No apraxia (Movements can be conceptualized)
61
what are diseases in the basal ganglia with hyperkinetic symptoms?
Ballism: Damage to the subthalamic nucleus-leads to disinhibition of movement via the indirect pathway Huntington's disease: Degeneration of the cuadate/putamen (striatum) causes choreiform movements. Striatal spiny neurons that inhibit the indirect pathway are most affected initially
62
What are tics?
Repeated, stereotyped fragments of movement
63
What are basal ganglia diseases with hypokinetic syndromes?
Parkinson's disease: Degeneration of dopamine producing neurons i the substania nigra pars compasta. Low dopamine input to the striatum cannot energize movements through the direct and the indirect pathways.
64
What are other symptoms of parkinsons?
Bradykinesia, resting tremor, rigidity- incuding cog-wheel rigidity
65
Explain the cerebellar control of movement.
1.Cerebellar control is ipsilateral- damage to the right side impairs movements onn the same side 2.The flocculo-nodular lobe controls balance and eye movements 3.The vermis and pars intermedia adjust ongoing movement of the whole ody 4.The cerebellar hemispheres help coordinate the planning of limbe movements- they project in particular in PM cortex.
66
Which part of the cerebellar is incharge of controlling balance and eye movements?
The flocculo-nodular lobe
67
Which part of the cerebellar is in charge of adjusting ongoing movement of the whole body ?
The vermis and pars intermedia
68
Which part of the cerebellar is in charge of helping coordinate the planning of limb movements?
Cerebellar hemisphere it projects in particula to PM cortex
69
describe the characteristic signs ofDUMNLs.
Spasticity Hyperactive reflexes No signs of muscle denervation Positive babinski sign Positive Bing sign
70
What are the 3 main types of stroke?
Thrombosis Embolism Hemorrhage
71
What are examples of lMN syndromes?
Poliomyelitis Tabes dorsalis Myasthenia gravis Injury in dorsal/ventral root Muscular atrophy
72
What is apraxia?
Inability to conceptualize and plan movement
73
What is the gait associated with UMNLs?
Scissoring gait/ walking with increased antogonist muscle reflexes
74
Describe upper motor neuron symptoms due to brainstem lesions.
UMN deficits on the contralateral side of the body often, LMN deficits of cranial nerve nuclei
75
List different forms of motor disturbances
Weakness Spasticity Rigidty Ataxia Hypokinesia or hyperkinesia Apraxia
76
What are the UMN symptoms due to spinal cord transections?
Looss of voluntary movement Anesthesia Temporry loss of reflexes (spinal shock) followed by hyper-reflexia Cervical transections produce quadriplegia Transections below cervical enlargement produce paraplegia
77
What is Ballism?
Degeneration of the subthalamic nucleus, leads to disinhibition of movement via the indirect pathway
78
What is hypotonus?
Loss of muscle tone-reduced spindle discharge
79
What is ataxia?
Loss of co-ordinaton
80
What is dysmetria?
Deficiencies in movement distance, velocity and rhythm of muscle contractions.
81
What is asyngeria?
Loss of co-ordination between different muscle groups
82
What is the affect of cerebellar lesions on cerebellar control?
Ataxia Hypotonus Dysmetria Asynergia Postural abnotmalities Ataxia of trunk and legs lead to ataxia of gait Ataxia of arms-loss of smooth movements with intention tremor Force and rhythm deficits revealed as dysdiadochokinesia
83
When is dopamine excitatory and when is it inhibitoy?
Inhibtory = indirect Excitatory = direct
84
What is the most characteristic initial physcial symptoms of huntington's disease?
Jerky, random and uncontrollable movements called chorea (Chorea can be initially exhibited as general restlessness, small unintentionally initiated or uncompleted motions, lack of coordination, or slow saccadic eye movements)
85
what is the lateral descending system?
Lateral corticospinal and rubrospinal
86
Where does the lateral descending system terminate?
Terminate on lateral alpha motor neurons in one segment only and terminate on interneurons too
87
What does the lateral desending system supply?
Distal limb muscles
88
What is the lateral descending system responsible for?
Responsible for fine movements
89
What is the medial descending system?
Ventral corticospinal, reticulospinal, vestibulospinal and tectospinal
90
Where does medial descending system terminate?
On medial alpha motor neurons in many segments
91
What does the medial descending system supply ?
Axial & proximal limb muscles
92
What is medial descending system responsible for?
Gross movements, balance, posture, stabilization
93
Which tract controls posture of the head and neck?
Medial vestibulospinal and tectospinal tracts
94
what do lesions in the lateral descending system lead to?
Loss of fine wrist and finger movement Preserved gross movement
95
What do lesions only in LCST lead to?
Inability to fractinate finger movements Preserved wrist movements
96
What do lesions in the medial descending system lead to?
Difficulty in sitting, standing and walking Paralysis of body axis and proximal parts of limbs
97
Where do all the corticospinal systems originate from?
The cortex
98
What are all the corticospinal systems?
1.Cortico-spinal tracts 2.Cortico-bulbar tracts 3.Cortico-nuclear tract
99
Where does the cortico-spinal tract terminate at?
AHCs odf spinal cord
100
What is the origin of the cortico-spinal tracts?
Primary motor cortex (30%) Premotor cortex (30%) SOmatosensory areas (40%)
101
What are the types of cortico-spinal tracts?
Lateral corticospinal tract Vetral cortico-spinal tract Uncrossed cortico-spinal tract
102
what is the pathway of the cortico-spinal tracts?
Cortex --> anterior 2/3 of posterior limb and genu of internal capsule --> Brain stem --> upper medulla ---> forming pyramid in lower medulla
103
What is the function of the lateral cortico-spinal system?
Initiate fine skilled movements of the distal parts of the opposite side of the body
104
What is the function of the ventral corticospinal tract?
Iitiate gross movements of the proximal parts of the opposite side of the body
105
What is the function of the uncrossed corticospinal tract?
Bilateral supply of abdominal and thoracic muscle
106
What are other corticospinal system functions?
1. Help in controlling muscl tone and postural background 2.Contribute the correct excitabillities for the normal plantar reflex, which is altered by CST damage leading to babiniski's sign
107
what is the origin of the cortico-bulbar tracts?
Sam as corticospinal tract
108
What is the pathway of cortico-bulbar tract?
Cortex --> anterior 2/3 of posterior lim and genu of interal capsule brainstem--> cranial nerve nuclei V, VII, IX, X, XI, XII, supplying the head and neck
109
What i sthe function of the cortico-bulbar tracts?
INitiate voluntary movement of head, face and tongu muscles Regulation of stretch reflex and mucle tone
110
What is the origin of the cortico-nuclear tract?
FRontal eye field area 8
111
What is the pathway of the corico-nuclear tract?
Cortex --> anterior 2/3 of posterior limb and genu of internal capsule -> parapontine reticular nucleus in braintem --> cranial nevre nuclei III, IV, VI, supplying extraocular muscles of both sides
112
What is the function of the cortic-nuclear tract?
Voluntary conjugate deviation of both eyes to the opposite side
113
Which body parts of the corticospinal system do not recieve contralateral innervation?
Trunk, neck, respiratory and abdominal muscles which receive bilateral innervation (contra and ipsi-lateral)
114
Which cranial nuclei do not revieve bilateral fibers in the corticospinal system?
Lower part of facial nerve nucleus and the part of hypoglossal nerve nucleus supplying genoglossus muscle which receive contralateral fibers only
115
What are the extrapyramidal tracts?
1.Retculospinal tract 2.Rubrospinal tract 3.Vestibulospinal tract 4.Tectospinal tract
116
what is the origin or the rubrospinal tract?
Red nucleus
117
What are the functions of the rubrospinal tracts?
Accessory route for initiation of fine movements - of stretch reflex + flexors & - of extensors involved in comparator function of cerebellum
118
What are the fibers in the rubrospinal tracts?
Cortex --> red nucleus--> crossing ---> lateral a in spinal cord
119
Where do reticulospinal medullary R.F recieve impulses from?
Red nucleus Basal ganglia Paleocerebellum
120
What are the fibers in reticulospinal tract of medullary R.F?
Lateral reticulosp. descends bilaterally