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Winter 2024 Neuroanatomy > Unit 4 > Flashcards

Unit 4 Flashcards

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1
Q

CN I

A

Olfactory
-Location: Arises from the cerebrum
-Type: Special Sensory
-Function: Afferent for olfaction
-Test: Smell with one nostril then the other
- Lesion Symptom: If there is a lesion the symptoms would include lack of smell and taste

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2
Q

CN II

A

Optic
-Location: The nerve begins in the retina–> leaving the eye at the optic disc and form the optic nerve
-Type: special sensory
-Function: Vision/ afferent for pupillary and accommodation reflexes
-Test:
1. snellen chart for visual acuity
2. visual fields assessment
3. accommodation
4. Pupillary Light Reflex
- Lesion Symptom: Depending on where the lesion occurs:
1. Monocular visual field loss only one eye is completely gone- same eye because the fibers haven’t crossed yet(2)
2. Nasal Hemianopsia = arises from a lesion of lateral fibers of the optic nerve- usually calcification of the internal carotid artery is a common preceding event (4)
3. Complete lesion of one optic tract which results in a contralateral homonymous hemianospia- patients may or may not be aware of the field cuts of losses (5)

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3
Q

CN III

A

Oculomotor
-Location: Midbrain
-Type:
Somatic motor–> oculomotor nucleus to skeletal muscle of the eye (5)

Visceral motor–> parasympathetic via EWN –> eye intrinsic for accommodation (ciliary muscle) and pupil constriction (sphincter pupillae muscle)

-Function: Constricts pupil

Lens accommodation ( ciliary muscle)

Moves eye up and down , medial. raises upper eyelid (levator palpebrae superioris)

Vestibuloocular reflex

-Test:
H-pattern
Check for ptosis
Accommodation
Pupillary light reflex
VOR gaze= stabilization during head movement (CN 3,6,8)
- Lesion Symptom: Could cause diplopia, upper eyelid ptosis, issues with pupil constriction, ipsilateral eye movement

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4
Q

CN IV

A

Trochlear
-Location: Trochlear nucleus from the midbrain
-Type: Motor/Somatic/efferent
-Function: Moves eye medially, inferior via the superior oblique
-Test: H test
- Lesion Symptom:
Diplopia
Downward lateral gaze

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5
Q

CN V

A

Trigeminal
-Location: 4 Nuclei in the brainstem

Trigeminal ganglion are located near the temple–> middle cranial fossa
-Type:
Motor is to the muscles of mastication: Temporalis/pterygoid/masseter
Sensory: 3 branches
V1 Ophthalmic
V2 Maxillary
V3 Mandibular

-Function:
Innervates muscles of mastication

Sensory to the face from the 3 branches MOM

-Test:
Cotton Ball test to test each branch
Jaw Jerk Reflex

  • Lesion Symptom:
    Trigeminal Neuralgia= when a patient tells you there is shooting/electric shock like pain in the distribution of the sensory potion of the cranial nerve 5 b/c of compression and has a shared path with superior cerebellar artery

Issues with chewing, speaking, sensory of the face

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6
Q

CN VI

A

Abducent
-Location: Located at the pons
-Type: Motor/Somatic Efferent
-Function:
Lateral rectus – down and out movement of the eye- inferior/abduction

-Test:
H-test

  • Lesion Symptom:
    If a lesion is present it could present with drooping of the eye and the eye turned up and medial
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7
Q

CN VII

A

Facial
-Location: Located at the brainstem–> extends to the abducens nerve and anteriorly to vestibulocochlear nerve
-Type:
Sensory
Motor
Parasympathetic
Mixed Nerve

-Function:
Ability to lift the forehead, squeeze eyes shut, smile, close your lips

Taste ANTERIOR 2/3 of tongue

Efferent/motor to lacrimal, nasal, salivary glands

Transmits touch, pressure, pain

-Test:
Corneal Reflex Loop

  • Lesion Symptom:
  • Cannot detect sweet vs. salty
  • Drooping smile
  • Can’t raise eyebrows
  • Cannot puff cheeks
  • Bells palsy – LMN disorder
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8
Q

CN VIII

A

Vestibulocochlear
-Location:
Located at the brainstem between the pons and medulla
-Type: Sensory
-Function: Hearing
-Test:
Tinnitus
Hearing loss
Observe gait for unsteadiness
Whisper or crunch paper in one ear then the other (gross exam)

  • Lesion Symptom:
    Lacking balance/ postural control
    Loss of hearing
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9
Q

CN IX

A

Glossopharyngeal
-Location:
Located at the medulla oblongata
-Type:
Sensory (trigeminal )
Motor (ambiguous
ANS (solitary)
Parasympathetic (salivary)

-Function:
Taste POSTERIOR 1/3rd of tongue,
Innervation to the palate pharynx, ear, gag and swallow
Pharyngeal muscles
BP/carotids
Motir to parotid gland sweat

-Test:
Trying to test the gag reflex to see if it is present

  • Lesion Symptom:
  • Absent gag reflex
  • Laryngeal paralysis
  • Difficulty swallowing
  • Absent taste/ sensation tongue
  • Impaired esophageal motility
  • Dysregulated HR
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10
Q

CN X

A

Vagus
-Location: Located in the Medulla runs all the way to the colon
-Type:
Sensory
Motor
Parasympathetic Efferent

-Function:
Gag swallow Reflex

Carries information from the throat, meningies, interna organs, neck, chest, abdomen, sensory from baroreceptors, pharynx/larynx all the way down to the colon and has 4 nuclei in the medulla

-Test:
Test Gag Reflex

  • Lesion Symptom:
  • Loss of gag and swallow
  • Hoarseness of voice
  • Loss of carotid sinus
  • GI problems
  • aphasia(garbled speech)
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11
Q

CN XI

A

Accessory
-Location:
Located from the spinal accessory nucleus located in the spinal cord beginning at the junction of the medulla to C6
-Type: Motor
-Function:
Innervates SCM and Trap muscles : motor
-Test:
MMT of shoulder/SCM to observe atrophy, movement, and assessing postural deficits if present
- Lesion Symptom:
Inability to raise shoulders/turning head

Weakness/atrophy

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12
Q

CN XII

A

Hypoglossal
- Location:
Located lower medulla branching to the tongue

-Type: motor

  • Function: Tongue movement: hypoglossal nerve innervates the tongue (genioglossus muscle)

-Test: - Have patient try and protrude their tongue to be able to observe movement and if there is deviation

  • Lesion:
    Tongue tilts to the side of the lesion

Ipsilateral tongue atrophy

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13
Q

Lesion of the right dorsal
column at L1 produces what
impairment?

A

Damage to the right dorsal column at L1 causes the
absence of light touch, vibration, and position
sensation in the right leg. Only fasciculus gracilis
exists below T6

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14
Q

Lesion of the left fasciculus gracilis
at T8 produces what impairment?

A

Damage to the left fasciculus gracilis at T8 causes
the absence of light touch, vibration, and position
sensation in the left leg and lower left trunk. Only
the fasciculus gracilis exists below T6

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15
Q

Lesion at T8 left fasciculus gracilis:
Lesion of the fasciculus gracilis
on the left: Neuroanatomical
Explanation

A

Because the tract has not
yet decussated, impairment
is ipsilateral to the lesion.
Lesion of first-order neurons
interrupts ascending
information so light touch,
vibration, and position
sensation is impaired in the
left leg and lower left trunk.
Receptors and reflex
connections below the
lesion level remain intact

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16
Q

Lesion of the right fasciculus
cuneatus at C3 produces what
impairment?

A

Damage to the right fasciculus cuneatus at C3
causes the absence of light touch, vibration, and
position sensation in the right arm and upper trunk

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17
Q

Lesion of the right lateral
corticospinal tract at L1
produces what impairment?

A

Damage to the right lateral corticospinal tract at L1
causes upper motor neurons signs (weakness or
paralysis, hyperreflexia, and hypertonia) in the right leg

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18
Q

Lesion of the right lateral
spinothalamic tract at L1
produces what impairment?

A

Damage to the right lateral spinothalamic tract at L1
causes the absence of pain and temperature
sensation in the left leg

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19
Q

Lesion of the anterior gray and
white commissures (central
cord syndrome) at C5-C6
produces what impairment?

A

Damage to the anterior gray and white commissures at
C5-C6 causes the absence of pain and temperature
sensation in the C5 and C6 dermatomes in both upper
extremities

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20
Q

Complete transection of the right
half the spinal cord (Hemicord or
Brown-Sequard syndrome) at L1
produces what impairments?

A

Damage to the right dorsal columns at L1 causes the
absence of light touch, vibration, and position sense in
the right leg. Damage to the lateral corticospinal tract
causes upper motor neuron signs in the right leg
(Monoplegia), and damage to the lateral spinothalamic
tract causes the absence of pain and temperature
sensation in the left leg

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21
Q

Complete transection of the
spinal cord (Transverse cord
lesion) at L1 would produce
what impairments?

A

Damage to the dorsal columns, bilaterally, causes the
absence of light touch, vibration, and position sense in
the both legs. Damage to the lateral corticospinal tracts,
bilaterally, cause upper motor neuron signs in the both
legs (Paraplegia), and damage to the lateral
spinothalamic tracts, bilaterally, cause the absence of
pain and temperature sensation in the both legs.

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22
Q

Complete transection of the
dorsal columns, bilaterally,
(posterior cord syndrome) in
the cervical region would
produce what impairments?

A

Damage to the dorsal columns (fasciculus gracilis
and cuneatus), bilaterally, causes the absence of
light touch, vibration, and position sense, bilaterally,
from the neck down (below the lesion level)

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23
Q

Complete transection of the lateral
corticospinal and lateral spinothalamic
tracts with sparing of the dorsal
columns, bilaterally, (anterior cord
syndrome) in the cervical region would
produce what impairments?

A

Damage to the lateral corticospinal tracts cause upper motor
neuron signs, bilaterally, below the lesion level. Damage to
lower motor neurons in the ventral horns cause lower motor
neuron signs, bilaterally, at the lesion level. Damage to the
lateral spinothalamic tracts cause absence of pain and
temperature sensation, bilaterally, below the lesion level.
Sparing of the dorsal columns leaves light touch, vibration,
and position sense intact throughout.

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24
Q

Lateral Spinothalamic Tract
- Function
- Clinical Presentation
- Decussation

Study These Flashcards
A
  • Ascending
  • Sensory
  • Immediately decussates in the spinal cord and then splits into anterior/lateral spinothalamic tracts–> terminates in the sensory cortex
  • For temperature/pain/light touch/pressure sensation
  • Clinical presentation:
    Lack of active sensation
    Lacking the ability to withdraw when touching sharp or hot objects
    Loss of pain perception and temperature
25
Anterior Spinothalamic Tract - Decussation -function -clinical presentation
- Ascending - Sensory - Decussates in the spinal cord then splits into the anterior/lateral spinothalamic tract --> terminates in the sensory cortex - Function: CRUDE TOUCH AND PRESSURE - Clinical Presentation: Loss of active sensation Loss of ability to withdraw when a sharp or dangerous object Loss of crude touch and pressure perception
26
Posterior Spinocerebellar
- Ascending - Sensory - Ipsilateral DOESN'T DECUSSATE--> terminates at cerebellar cortex - Function: Carries unconscious proprioceptive information Proprioceptive input from GTO muscle spindles and joint capsules of LE and trunk - Clinical Presentation: Ataxia, incoordination of arms, tremor, wide reeling base of gait, poor balance Loss of proprioception from lower limb
27
Anterior Spinocerebellar
- Ascending - Sensory - Decussates twice first int the spinal cord second in the pons --> terminates in the cerebellar cortex - IPSILATERAL - Carries proprioceptive information from the LE - Posture related movements - Proprioceptive feedback from muscles - Proprioceptive input from GTO, muscle spindles and joint capsules - Clinical Presentation: Ataxia, incoordination of arms, tremor, gait abnormalities, dysmetria
28
Lateral Corticospinal Tract
- Descending -Motor - Decussates in Lower medulla -Fine limb control -VOLUNTARY MOVEMENT OF CONTRALATERAL UE AND LE - Clinical Presentation: UMN syndrome Weakness or paralysis, hyperreactive reflexes, decreased motor control, abnormal muscle tone Function can return, but some abnormalities may persist *babinski sign*
29
Anterior Corticospinal Tract
- Descending -Motor - DOESN'T DECUSSATE - Movement of muscles of the trunk, neck, and shoulders -Clinical Presentation: UMN syndrome Weakness or paralysis, hyperreactive reflexes, decreased motor control, abnormal muscle tone
30
Corticobulbar Tract
- Descending -Motor - Carries efferent motor information from the primary motor cortex of the muscles of the face, head, and neck by synapsing with the motor cranial nerves in the brainstem - Innervates muscles of the head, face, neck and muscles with swallowing, phonation and facial expression - Clinical Presentation: Palsies of CN 7 (facial nerve) and CN 12 (muscles of the tongue and the ability of the pt to speak fluidly) Garbled speech, muscular weakness in the face, difficulty with tongue movement
31
Lateral Vestibulospinal Tract
- Descending -Motor - DOESN'T DECUSSATE - Posture balance, postural extensors of limbs to prepare for movement - Clinical Presentation Ataxia , especially with eyes closed Hypermetria Postural instability
32
Medial Vestibulospinal Tract
- Descending - motor - DOESN'T DECUSSATE - Vestibulo-ocular Reflex: visual fixation to stabilize the image on the retina - Function - anti-gravity muscles (head/neck extensors) - Clinical Presentation: Ataxia, nystagmus, overshooting (hypermetria), postural instability Typically pt falls to the same side as the lesion
33
If there is a Lesion in the reticulospinal tract how would it present and affect?
- Movement of the lower limbs - Steppage pattern generator - Ability to maintain muscle tone/axial tone - Ability to fire extensors and flexors
34
Lateral Reticulospinal Tract
- Descending - Motor - from upper medulla and goes to efferent motor to move the trunk limbs - function: Anticipatory postural adjustments to prepare for movement that would otherwise be destabilizing inhibits voluntary movement, decrease muscle tone - Clinical Presentation Spasticity Decreased postural control and reduced selectivity of postural control
35
Medial/Pontine Reticulospinal Tract
- Descending -Motor - Pontine= pounces - Voluntary muscle contraction increases muscle tone. Trunk, proximal extensors, prevents falls - Clinical Presentation: Decreased postural control and reduced selectivity of postural control Impaired locomotion and reaching LMN or UMN lesion signs depending on where injury is
36
Rubrospinal Tract
- Descending - Motor - Decussates in the midbrain descend through medulla to the LMN UE fine motor control - Function: Fine motor control, excitatory to UE flexors, inhibitory to extensors - Maintain muscle tone of the flexors of the body and to modulate their movements that are directed to the pyramidal system -Clinical presentation Decreased impact of fine tuning and fractionation of movement Decreased Reflexive flexion LMN or UMN signs depending where lesion is EX: dropping phone in toilet due to lack of fine motor coordination
37
1. Glial 2. Ependymal 3. Oligodendrocytes 4. Schwann Cells 5. Astrocytes 6. Microglia 7. Blood Brain Barrier
1. Glial= glue of the nervous system they transmit information 2. Ependymal= produce and regulate CSF fluid found in the ventricles of the brain 3. Oligodendrocytes= CNS; myelinate axons 4. Schwann Cells= PNS; myelinate axons 5. Astrocytes= Help clean up the CNS/Clean up neurotransmitters of the synaptic cleft 6. Microglia= clean up crew of dying cells 7. Blood Brain Barrier= A dynamic selective permeability layer that circulates blood and separates from the extra cellular fluid. These are formed by tight junctions
38
Saltatory Conduction
Process by which an AP appears to jump from node to node along an axon (supposedly faster)
39
Types of Neurons
1. Unipolar 2. Multipolar= interneurons ; common in CNS 3. Bipolar= in eyes, ears, and gut 4. Pseudounipolar= sensory; afferent
40
Temporal Summation Vs. Spatial Summation
Temporal summation is Multiple local potentials within milliseconds VS Spatial summation is multiple local potentials from different areas
41
Chemical Synapse VS Electrical Synapse
Chemical synapse= neurotransmitters ACH, norepin., epinephrine ect; Neurotransmitters need to bind to postsynaptic membrane so ion channels can open and allow ions to flow in VS Electrical synapse= sodium/potassium; action potentials causes gated ion channels to open across membrane due to potential energy turning into kinetic energy DIRECT EXCHANGE
42
Different Ion Channels 1. Resting 2. Voltage Gated 3. Ligand Gated 4. mechano-signal gated
1. Resting= leakage, always open, maintains gradient 2. Voltage gated= voltage change; Na+ ion channels- open + close instantaneously mostly involved in propagation of an action potential 3. Ligand Gated= opens when specific chemical binds to its neurotransmitters - any post synaptic receiver cell such as a dendrite 4. Mechano-signal gated= opens with stretch/pressure
43
Explain Action Potential
1. Stimulus from sensory cell/neuron causes target cell to depolarize past threshold (threshold is - 55 mV) 2. Threshold reached and Na+ channels open= membrane depolarizes 3. Peak action potential/absolute refractory period: K+ channels open & Na+ channels close (peak is +30 mV) 4. Influx of K+ ions causes repolarization to occur 5. Membrane is hyperpolarized due to K+ channels staying open longer than needed to ensure return to resting potential = relative refractory 6. K+ channels close + membrane potential goes back to resting state
44
Nicotinic VS Muscarinic Receptors of ACH
Nicotinic= skeltal muscle, somatic NS Muscarinic= smooth muscle, parasympathetic, G-protein coupled receptor, slow acting, longer lasting effects
45
Neurotransmitters: 1. GABA 2. Glycine 3. Glutamate 4. Dopamine
1. GABA= Inhibitory neurotransmitter of CNS 2. Glycine = inhibitory (post-synaptic membrane at brainstem and spinal cord) 3. Glutamate= excitatory, elicits neuronal changes, fast depolarization 4. Dopamine= neural activity, motor activity, reward seeking, thinking +planning in frontal lobe
46
Somatic NS
- Motor innervation of all skeletal muscle - Nicotinic receptor are always excitatory - ACH released= muscle contraction - In brain nicotinic= neuronal development, memory + learning - Fast acting + produce local depolarization Conditions related to Nicotinic Receptors 1. Myasthenia gravis= destroys receptors at the NMJ leading to muscle weakness + paralysis 2. Alzheimer's disease= loss of nicotinic receptors- expressing neurons in the brain
47
Embryology
Forebrain: 1. Telencephalon= cerebrum including cerebral cortex, white matter + basal nuclei 2. Diencephalon= thalamus, hypothalamus and epithalamus Midbrain: 1. Mesencephalon= part of the brainstem Hindbrain : 1. Metencephalon= pons and cerebrum 2. Myelencephalon= medulla oblongata
48
Apraxia
Inability to perform a movement- even if you understand the task
49
Aphasia
Disorder of language expression/comprehension
50
Agnosia
Inability to recognize objects, with specific sense even though discriminative sense is intact
51
Astereognosis
Inability to identify an object by touch
52
Ataxia
Abnormal voluntary movement : normal in strength but jerky
53
Dysphagia
Difficulty swallowing
54
Dysarthria
Difficulty speaking
55
Diplopia
double vision
56
Dysmetria
Difficulty controlling distance/speed of movement
57
Basal Ganglia Parts, function, movement
Parts = striatum, Globus pallidus, putamen, substantia nigra, subthalamic nucleus Function= motor control, learning, executive function Striatum= processes signals from cortex and prompts neurons in ganglia to indicate actions GP= controls conscious + proprioceptive movement Putamen= learning, language , motor control Substantia Nigra= controls movement, dysfunction--> Parkinson's Subthalamic nucleus= Movement regulation
58
CSF
Cerebral Spinal Fluid - It is made in the choroid plexus in the lateral and 3rd ventricles - CSF protects the CNS/buoyant/shock absorption/cushion/ provides ions, proteins, and nourishment Flow of the CSF 1. lateral ventricles 2. interventricular foramen 3. 3rd ventricle 4. cerebral aqueduct 5. 4th ventricle 5. subarachnoid space and central canal
59
Watershed Zon

Winter 2024 Neuroanatomy (2 decks)

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