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NS - Citow By Dorka > Anatomy, embriology: general > Flashcards

Anatomy, embriology: general Flashcards

1
Q

WM tracts
cingulum

A

Cingulate gyrus to the entorhinal
cortex
Affect, visceromotor control;
response selection in skeletomotor
control; visuospatial processing
and memory access

X: Left-sided lesions cause verbal amnesia, whereas right-sided lesions alter visuospatial (location) memory; bilateral damage causes global amnesia.

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2
Q

Fornix

A

Hippocampus and the septal area to
hypothalamus
Part of the Papez circuit; critical in
formation of memory; damage or
disease resulting in anterograde
amnesia

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3
Q

Superior longitudinal
fasciculus

A

Frontotemporal and frontoparietal
regions
Integration of auditory and speech
nuclei

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4
Q

SLF + FA

A

Originally, the AF was first described as a component of the SLF, and their names were used as a synonym of each other. Recently, researchers have separated these bundles as the SLF and the AF that connect the frontal cortex to the occipital and parietal cortex, respectively (Dick & Tremblay, 2012; Gierhan, 2013; Petrides & Pandya, 2009). Damage to this tract can cause speech impairments such as anarthria and dysarthria

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5
Q

Inferior longitudinal
fasciculus

A

Ipsilateral temporal and occipital
lobes
The role of the ILF is therefore central in all activities involving processing complex visual information, from objects, faces, and word perception to emotion recognition and semantics (ffytche et al., 2010). Some of the behavioral and cognitive deficits described in patients with anterior temporal lobe damage are due to disconnection of the ILF fibers that prevent visual inputs to reach the limbic, paralimbic, and temporopolar cortex.

X: object recognition, visual agnosias, prosopagnosia

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6
Q

Cholinerg projection brain

A
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7
Q

Dopamine projection brain

A
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8
Q

GABA pathway brain

A
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9
Q

Noradrenergic projection of the brain

A
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10
Q

Serotonin pathway brain

A
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11
Q

Limbic system Papez circuit

A
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12
Q

Neuralation

A
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13
Q

Basal plate give rise to…

A
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14
Q
A
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15
Q

Periferial nerves

A
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16
Q

Axonal injury

A
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17
Q

Neurapraxia (“Nerve Dysfunctional”)

A

Neurapraxia Overview:
Nerve injury causing temporary interruption of action potential conduction without permanent damage.
Preservation of axon with no axonal degeneration.
Mild and reversible pathological changes.
Full and rapid recovery expected, typically within days to a few months.

Variability in Nerve Susceptibility:
Motor nerves are most susceptible to injury.
Pain and autonomic nerves are least susceptible.
Proprioception, light touch, and temperature modalities show intermediate susceptibility to injury.

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18
Q

Axonotmesis (“Axon Cut”)

A
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19
Q

Neurotmesis (“Nerve Cut”)

A

In neurotmesis, there is complete loss of axonal continuity. The cut ends of the nerve either remain separated, or they may reconnect through a bridge of scar tissue consisting of fibroblasts, Schwann cells, and regenerating axons. In any event, recovery is negligible. Hope for any functional recovery requires surgery

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20
Q

Axonotmesis regeneration

A

In axonotmesis, degeneration occurs distal to the injury
site, while the proximal segment exhibits few histologic or
pathologic changes. Distal segment degeneration is called
Wallerian degeneration, or anterograde degeneration, the
principal histologic change of which is a breakdown of both
axons and myelin, leaving only ghost-like endoneurial
sleeves. Schwann cells, and later macrophages, consume
the axonal and myelin debris. The complete process
unfolds over a period of weeks, ultimately reducing nerve
fibers to a mass of Schwann cells and endoneurial sheaths.
When the endoneurium is disrupted (Sunderland
type III) Wallerian degeneration proceeds (as described
above), with this difference: intrafascicular injury impairs
axonal regeneration. That is, damage to the endoneurium
causes shrinkage, fibrosis, and ultimately obliteration
of the endoneurial tubes, limiting axonal regeneration.
What is more, Wallerian degeneration is now accompanied by an additional pathologic process: degeneration of
the proximal segment in a retrograde direction.

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21
Q

Axonal and cell body degeneration

A

Degenerative changes in the cell body may include migration of the nucleus to the periphery of the cell and the
breakdown and dispersal of Nissl granules in a process
named chromatolysis. This process depresses cell body
protein synthesis. Regeneration of the cell body reverses
this process, reinstating protein synthesis, which in turn
facilitates axonal regeneration.

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22
Q

Lesion of cervical plexus

A
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23
Q

Plexus brachialis

A
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24
Q

Polio

A
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25
Q

Guillan Barré

A
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26
Q

Spinal nerve

A
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27
Q

GM in spine

A
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28
Q

Rexed Laminae

A
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29
Q
A
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30
Q

Hippocampal fibers

A
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31
Q

WM tracts and striatum

A
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32
Q

Thalamic fibers

A
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33
Q

Thalamus vascular supply

A
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34
Q

Cerebellar neurons and inputs

A

Types of cerebellar neurons and their inputs: mossy fiber pro-
jections from pontine n., vestibular n., red n., deep cerebellar n., spinal cord, reticular formation; climbing fiber projections from inferior olive.

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35
Q

Anterior mesenchephalis syndromes

A
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36
Q

Mid pons lesion

A
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37
Q

Lower pons lesions

A
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38
Q

Superior medulla

A
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39
Q

Inferior medullar lesion

A
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40
Q

Spinal trigeminal tract; medial lemniscus

A
41
Q

Central herniation

A
42
Q

Long tracts of spinal cord

A
43
Q

reticulospinal tract

A

Course

Medial Reticulospinal Tract (Pontine): Descends ipsilaterally in the anterior funiculus [1] Responsible for controlling axial and extensor motor neurons e.g enable extension of the legs to maintain postural support ; Stimulation of the midbrain locomotor centre can result patterned movements (e.g. stepping)[3]

Lateral Reticulospinal tracts (Medullary): Descends bilaterally in the lateral funiculus [1] Responsible for flexor motor neurons [2]; Inhibits the medial reticulospinal tract and therefore extensor motor neurones enabling modulation of the stretch reflex [4]
Both the lateral and medial tracts act via interneurons shared with the corticospinal tract on proximal limb and axial muscle motor neurons.[1]

44
Q

reticulospinal tract lesion

A

Pathology

Spastic paraplegia
Lesions to the cortico-reticulospinal system can result in decreased postural control and reduced selectivity of postural control.[3] If the excitatory fibres in the reticular formation have a leison this can result in hypotonia by the loss of descending excitatatory impulses to the spinal cord. Conversly in the inhibitory fibres are disrupted in the reticular formation this could result in hypertonia (spasticity) As the lateral reticulospinal’s is involved in inhibition, if this pathway is disrupted it can result in spasticity [4]. In addition due to the lack of descending inhibition, the medial reticulospinal tract would then maintain spasticity in the musculature.[4]

45
Q

vestibulospinal tr

A

Upright Posture Maintenance: Performed by both the medial and the lateral vestibulospinal tracts. The medial tract supplies the muscles of the head and neck whereas the lateral tract supplies the muscles located in other parts of the body. When the head of the person moves, signals are sent by these vestibular tracts to specific antigravity muscles. These muscles contract and maintain the upright posture of the body.

Vestibulospinal Reflexes: A vestibulospinal reflex is the one that uses organs of the vestibular system and the skeletal muscles in order to maintain balance and posture[1]

46
Q

vestibulo ocular reflex

A

Medial Vestibulospinal Tract

Vestibulo-ocular reflex lateroflexion of neck
Head and Eye Coordination: Performs the synchronization of the movement of the eyes with the movement of the head so that eyes do not lag behind when the head moves to one side. This function is very important for maintaining the balance of the body.

Head righting reflexes. These are responsible for keeping the head and gaze horizontal

Eye righting reflex (Vestibulo-ocular reflex) This origniates in the ascending medial longitudinal fasciulus and extends to the extraocular muscles of the eyes. The horizonal position of the eyes when the head is an upright postural set is caused by cancelling of the tonic acitiy of the deiteroocular pathways.[2] It is therefore able to keep the eyes still while the head moves, allowing images to focus on the retina [4]

47
Q

Spinal grey matter somatotopy

A
48
Q

vascular watershed zones of SC

A
49
Q

Facial nerve components

A

bered 1 through 5) cause different neuro
-
logical symptoms because of the involved nerve components: 1
, facial weakness + impaired hearing + vestibular dysfunction; 2
, facial weakness + impaired taste sensa-
tion + decrease lacrimal & salivary secre-
tion; 3
, facial weakness + impaired taste sensation + decreased salivary secretion + hyperacusis; 4
, facial weakness + impaired taste sensation + decreased salivary secre-
tion; 5
, facial weakness. Greater petrosal nerve carries parasympathetics to the lac-
rimal and nasal glands. Stapedius nerve acts to dampen the tympanic membrane oscillation. Chorda tympani carries taste sensation from the anterior tongue

50
Q

accessorius

A
51
Q

Bladder disfunctions

A
52
Q

retinal representation

A
53
Q

CN III-VI

A
54
Q

oculomotor nucleus

A
55
Q

nystagmus types and patterns

A
56
Q

less common nystagmus types

A
57
Q

nystagmus types III

A
58
Q
A
59
Q

Bony jugular foramen

A
60
Q

Jugular foramen contents

A
61
Q

detailed jugular foramen

A
62
Q

acustic meatus

A
63
Q

Facial visceral motor

A
64
Q

IX visceral

A
65
Q

CNX visceral

A
66
Q

visceral CN nuclei

A
67
Q

CN nuclei organisation

A

Ten of the 12 cranial nerves have their nuclei in the brain-stem. (Cranial nerves I and II are the exceptions.) Like the spinal gray nuclei, the cranial nerve nuclei are grouped into longitudinal columns. These columns are both ana-
tomically and functionally distinct: medial columns con-
tain exclusively motor nuclei, and lateral columns contain exclusively sensory nuclei. This organization is explained by developmental events, as follows.
The alar and basal plates of the developing neural tube give rise to sensory afferents and motor efferents, respectively. Early in development, these plates are posi-
tioned in a dorsal/ventral orientation, an orientation that is maintained in the mature spinal cord. In the develop-
ing brainstem, however, this organization is changed: the lateral spread of the fourth ventricle causes the dorsal alar plate to rotate laterally in relation to the ventral ba-
sal plate. As a result, the lateral columns of the mature brainstem contain strictly sensory cranial nerve nuclei; the medial columns contain strictly motor cranial nerve nuclei

68
Q

Medial column motor nuclei

A

his column, which is not continuous longitudinally, is immediately adjacent to the midline, just below the floor of the ventricular system. It contains nuclei composed of neurons that innervate the striated muscles of the head and neck derived from embryonic myotomes (i.e., the extraocular muscles and the muscles of the tongue). In rostrocaudal order, the nuclei contained in this column include the following four structures

69
Q

Paramedian motor nuclei in BS

A

This column is located lateral and ventral to column 1. It contains nuclei composed of neurons that innervate the striated muscles of the head and neck derived from the **branchial arches **(i.e., the muscles of mastication, the muscles of facial expression, the muscles of the pharynx and larynx, and the sternocleidomastoid and trapezius muscles). I

70
Q

Immediately paramedian nuclei (Column 3)

A

This column is located immediately lateral to column 1. It contains nuclei of preganglionic parasympathetic neurons that innervate the smooth muscles and glands of the head and neck, as well as the thoracic and parts of the abdominal viscera. (Preganglionic parasympathetics originating in sacral segments of the spinal cord supply the rest of the abdominal and pelvic viscera.)

71
Q

BS Lateral Columns Contain Three Sensory Nuclei

A

The lateral columns are composed of sensory nuclei. Unlike most motor nuclei, whose axons are carried in a single corresponding cranial nerve, each sensory nu-cleus receives input from several different cranial nerves

72
Q

Long tract: ST

A

The lateral and anterior spinothalamic tracts are re-sponsible for pain, temperature, and light touch sensa-
tion. They are located in the lateral aspect of the teg-
mentum throughout the brainstem, adjacent to the descending sympathetic tract. They occur in essentially the same position they occupy in the spinal cord. The spi-
nothalamic tract consists of second-order neurons that originate in the dorsal gray horn
of the spinal cord, cross the midline in the anterior white commissure
, and project to the ventral posterolateral (VPL) nucleus of the thalamus
. Third-order neurons in the VPL thalamus send axons to the postcentral gyrus
. Because of the close proximity of the spinothalamic tract to the descending sympathetic fibers, both systems are typically impaired as a result of damage to the lateral tegmentum, where they represent important landmarks. An ipsilateral Horner syndrome (descending sympathetic lesion) is thus often associated with a contralateral hemisensory loss (spinothalamic le-
sion), which may be caused by a lesion in the lateral me-
dulla or pons

73
Q

Long tract: ML

A

The medial lemniscus, which is the rostral continu-ation of the dorsal columns of the spinal cord, medi-
ates position sense and discriminative touch. It consists of second-order neurons that originate in the nucleus cuneatus
and nucleus gracilis
. These nuclei receive input from the spinal cord via the cuneate and gracile fasciculi (dorsal columns), which carry impulses from the upper and lower extremities, respectively. After synapse in the ipsilateral cuneate and gracile nuclei, these axons act as the internal arcuate fibers and ascend to the contralateral VPL thalamus. From here they ascend to the sensory cor-
tex. The medial lemniscus is situated in the medulla close to the midline between the posteriorly situated medial longitudinal fasciculus (MLF) and the anteriorly situated corticospinal and corticopontine tracts. In its rostral as-
cent, the medial lemniscus moves laterally but remains an important landmark of the medial aspect of the me-
dulla and pons

74
Q

Long tract: CS

A

The corticospinal tract transmits motor-related im-pulses from the cerebral cortex to laminae IV through IX (few fibers synapse directly with IX motor neurons in laminae IX) of the spinal gray matter. The fibers of this tract traverse the corona radiata
and the posterior limb of the internal capsule
and continue in the middle of the midbrain crura cerebri, flanked by more numerous cor-
ticopontine fibers on each side. At the level of the pons, the corticospinal tract is broken up into small bundles by transverse pontocerebellar fibers, which cross the mid-
line to reach the contralateral cerebellar hemisphere via the middle cerebellar peduncle. At lower pontine levels, the corticospinal fibers come together again and form the medullary pyramids
. As they reach the caudal medulla
, approximately 85% of corticospinal fibers cross the mid-
line in the decussation of the pyramids to form the lateral corticospinal tract
(the other 15% of fibers continue in the uncrossed anterior corticospinal tract
, which later de-
cussates in the anterior commissure at cervical and up-
per thoracic levels). Separate from direct corticopontine fibers, numerous collateral branches of the corticospinal fibers innervate the pontine nuclei, including those of the reticular formation. Like the medial lemniscus, the cor-
ticospinal tract courses close to the midline throughout the pons and medulla, providing an important medial brainstem landmark

75
Q

Long tract: CB

A

The corticobulbar tract comprises fibers projecting from the cerebral cortex to the lower brainstem. Among the neurons that receive these projections are several motor cranial nerve nuclei, including the trigeminal, fa-cial, and hypoglossal nuclei. Except for part of the facial motor nucleus, the cortical input to these nuclei is more or less symmetrically bilateral. The muscles that receive their supply from these nuclei include the laryngeal, pha-
ryngeal, palatal, upper facial, extraocular, and muscles of mastication. Because of their bilateral innervation, uni-
lateral lesions interrupting the corticobulbar supply of these muscles cause only mild signs of paresis, whereas bilateral lesions are usually significant (pseudobulbar palsy). The clinically familiar contralateral paralysis of lower facial muscles (sparing the forehead) is evidence of predominantly crossed corticobulbar innervation of part of the facial motor nucleus. In addition to this direct corticobulbar pathway, corticoreticular fibers innervate neurons of the reticular formation, which serve to relay impulses indirectly from the cortex to the motor cranial nerve nuclei. As a landmark of the medial brainstem, the corticobulbar tract is associated with the medial lemnis-
cus and the corticospinal tract

76
Q

Afferent cerebellar path

A
77
Q

Efferent cerebellar pathw

A
78
Q

CN3

A
79
Q

CN3 palsy

A
80
Q

CN4

A
81
Q

CNVI

A
82
Q

Horizontal gaze

A
83
Q

supranucleas gaze palsy

A
84
Q

nuclear gaze palsy

A
85
Q

INO

A
86
Q

CN7

A
87
Q

CN9

A
88
Q

Foster Kennedy sy

A
89
Q

Gradenigo sy (itis)

A
90
Q

Tolosa Hunt sy

A
91
Q

Ramsay Hunt sy

A
92
Q

Vernet sy

A
93
Q

cortical leyer cells

A
94
Q

Brd 4

A
95
Q

Brd 6

A
96
Q

Brd 6 pre motor

A
97
Q

Brd 9-11 prefrontal

A
98
Q

Brd 3-1-2 SS

A
99
Q

Second SS

A

NS - Citow By Dorka (11 decks)

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