Chapter 19: Cranial Nerves Flashcards
Cranial nerves
most of cranial nerves are innervated/myelinated by Schwann cells
Location of cranial nerves
In the head: CN1, CN2
In the midbrain: CN3, CN4
Parked in the pons: CN 5, 6, 7, and 8
Down in the medulla part: CN 9, 10, 11, and 12
Functions of the cranial nerves
motor innervation:
-face, eyes, tongue, jaw, and neck
Somatosensory innervation:
-skin and muscles of face and the TMJ
Special sensory:
-visual, auditory, vestibular, gustatory, olfactory, and visceral
Parasympathetic control:
-eye, heart, lung airways, digestive system.
*some parasympathetic control especially through the vagus down through the thorax to the abdomen
Intro content
Corticobrainstem tract: UMN to cranial nerves.
-UMN that start in the cortex of the cerebrum and end on the other side of the bainstem.
Cranial nerves themselves are:
- Peripheral sensory
- LMN- crosses the midline so that the right side of our brain controls the left side of our body/face.
- any damage to cranial nerves themselves will always be same side damage because they are peripheral nerves.
CN I- Olfactory
- Olfactory tract to insular cortex, amygdala, and parahippocampal gyrus.
- Where: poked through the top of the bone of the nasal sinuses. Send projections through the roof of the nasal sinus (can be depolarized at that location).
- Insular cortex- receives a lot of olfactory senses
- Amygdala- based on smell we can decide if something is potentially harmful or good for us
- Parahippocampal gyrus- deals with emotions and memories
CN 1- has a strong connection to our primal brain.
CN I broken?
Loss of the sense of smell. Trauma to the head (sheer force-shaking of the head and shaking of the brain against the skull the cranial nerves can get sheered off) concussions can cause the same type of sheering. MVA are very common causes (back and forth movements of the skull). can be a precursor to Alzheimer’s and dementia (neurodegenerative diseases).
Complaints: for some reason the food doesn’t taste the same as it used to.
CN II- Optic
Bundle of axons of cells that live in the retina (excited by light and send action potentials back to the brain) section form the eyeball to the giant X (first segment of the vision pathway).
Problems: discussed in chapter 21 (problems in visual field and acuity)
CN III, IV, VI
extraocular muscles
Occulomotor (CN III)- pokes out of front of midbrain)
Troclear (CN IV)- pokes out and wraps around
Control eye movements:
-CN III- oculomotor- directly does or helps do everything else (straight up, straight down, straight adduction, up and in and eyebrow, everything else)
-CN IV- Troclear- Under normal circumstances- allows us to voluntarily look down and in as if to look at the tip of my nose
CN VI- Abducens- abducts in a straight plane (helps us look out)
- control eye movements
CN V- Trigeminal
So big compared to all the others. Innervates the face (has a high density of neurons and many small receptor fields) tons of sensory neurons from the face.
Both sensory and motor component to it:
-Motor- moves the muscles of the now (opens and closes the jaw), also involved in speaking through the same muscle movements
- Sensory- all modalities of sensation on the face (only the face and nothing else around it)
- contains axons for all of the modalities of sensation (discriminative touch axons, proprioception axons from the jaw, (muscles of mastication), discriminative pain, and divergent pain/dull aching pain)
- if damaged on right side of the face, the right side will be damaged,
- 3 neuron pathway (first, second, and third order neurons) discriminative parts will pass through the thalamus to the cortex)
CN V test
cotton ball to white part of the eye to test blink reflex- CN V innervates the surface of the eyeball. Inside CN V hands off messages to CN 7 that closes eye and tears up. 5 and 7 work together (5 senses it and 7 closes and water to wash away). Can indicate damage to one or both of cranial nerves inside. If she can voluntarily close eye then 5 is damaged not 7.
CN V dysfunction
- sensory loss on the same side as cranial damage
- Loss of blink reflex
- Jaw weakness
- Trigeminal Neuralgia- nerve pain- allodynia (stimulus that would not normally cause pain produces sensation of pain)
CN VII- facial
moves muscles of facial expression.
- Sensory from tongue, Pharynx, ear
- Taste anterior 2/3 (sweet, salty, sour)
- Muscles of facial expression
- Gland (salivary-buried under the tongue, nasal, and lacrimal-above the eye and nasal in the bone)
Upper half- open eyes wide and close them tight
Lower half- Smile big, blow balloon
CN VII dysfunction
when damaged it is a peripheral motor nerve so damage shows on same side of damage.
-Bell’s Palsy
Bell’s Palsy
a paralysis of muscles of facial expression that comes from some damage of CN VII- damaged the LMN going to the muscles of facial expression. Feels like whole side of face is sagging off. Damages CN not its central connection.
-cannot close eye, eye is open to the air and starts to dry out, lacrimal gland is broken and doesn’t tear at all. common to use patch or eye tape to keep eye closed and use artificial tears.
-A LMN disorder, paralysis or paresis of all facial muscles on side where CN VII is damaged.
differentiating facial weakness Bell’s Palsy vs CVA
Lower facial droop with upper face still working is the sign of a stroke. Hot to differentiate Bell’s Palsy from a CVA.
-Forehead gest bilateral innervation from the brain (key to help us distinguish stroke from bells palsy.
Bell’s Palsy- LMN damaged of CN VII on left side of the face (cant close eye or smile. all of one side of the face is broken).
CVA- follow over to the full side of the face the person wont be able to smile and they can squeeze their eyes shut tightly, lose lower face on one side but keeps upper face because of bilateral innervation of upper face (forehead)
