Term
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Definition
| Fight or Flight System -Neurons start at Thoracolumbar region These fibers do NOT go straight to the organ. There is a chain of 2 neurons (pre and post-shown in the diagram) The ganglia are right along the spine (most) or along the abdominal aorta. NO cranial nerves have a sympathetic supply to them- so NO sympathetic supply in the brainstem! Sympathetic supply to the head comes up the neck. You can get lesions in the throat or neck (top of lung) that cut off the sym. supply to the head. |
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Term
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Definition
Rest and Digest system
-There are 4 Cranial Nerves that have
Parasympathetic supply:
1)Vagal
2)Oculomotor
3)Facial
4)Glossopharyngeal
-Again, like the sympathetic there is a chain with a ganglia. These ganglion are usually close to or just next to the organ where the post-ganglion is neuron is about to start.
-Most come out at cranial nerves and a few come out at the sacral region (low organs). |
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Term
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Definition
Smallest of the Cranial Nerves
Very simple nerve-goes to one muscle
Supplies the superior oblique muscle
Nucleus starts in the midbrain
The only nerve that crosses after it leaves the brain stem (ex.- out of right side of brain stem and supplies left eye)
Points or pulls the eyeball downward |
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Term
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Definition
Damage to this nerve is rare
Related to Parinaud’s Syndrome-causes impingement on this nerve (due to pineal gland lesion)
Patient with damage will have trouble looking downward
Difficulty moving eyeball down and laterally so eyeball drifts up and medial (other muscles unopposed). |
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Term
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Definition
Supplies the Lateral Rectus muscle
Moves eye to the outside (abducts)
Nucleus is found in lower pons |
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Term
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Definition
Eye turns inward = medial or internal strabismus-(deviation of the eyeball) Can get bilateral strabismus which is crossed eyes.
This happens because medial rectus is unopposed |
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Term
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Definition
Nucleus is in lower medulla
Has cranial AND spinal nerve roots
Most of this nerve is displaced loop of the cervical plexus
Supplies trapezius and SCM (by itself- contralateral rotation, ipsilateral side bending. Bilaterally activation= flexion of neck. If head fixed with bilateral activation= lifts the chest.) muscles from spine.
Supplies muscles of larynx during swallowing from cranial nerve root and pharynx. So helps mediate swallowing |
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Term
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Definition
Cranial nerve root: dysphagia= difficulty swallowing
Spinal nerve root: difficulty rotating head contralaterally, flexing head laterally and forward, extending head, shrugging shoulders (elevation), and difficulty flexing arm above 90 degrees
Other things Ben mentioned:
Traps:
Atrophy- patient will have “L” shape shoulder on affected side
SCM:
Spasm= Tortocollis- which is ipsilateral side flexion and contralateral rotation |
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Term
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Definition
The most inferior of the cranial nerves
Supplies the tongue muscles (both sides)
Nucleus is found in medulla |
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Term
| Hypoglossal Nerve- Damage |
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Definition
trouble swallowing (dysphagia), talking and speech= dysarthria- cannot produce required movements for sound and production
-Long term damage will lead to muscle atrophy on the side of the tongue affected by lesion (ipsilateral atrophy) and sometimes paralysis. You will see ridges on that side of the patient’s tongue.
-To test: stick tongue straight out and tongue will deviate to the side of the lesion (ipsilateral deviation) |
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Term
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Definition
Nucleus is in midbrain
Supplies 4 eye muscles (all of the eye muscles except for 2):
1) Superior Rectus
2) Inferior Rectus
3) Medial Rectus
4) Inferior Oblique
Also supplies levator palpebrae superioris muscle which lifts the eyelid |
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Term
| Oculomotor Nerve & Damage |
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Definition
Oculomotor Palsy-
Weber's
Benedikt's |
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Term
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Definition
Eye turns outward (laterally) because abducens N. controls a more powerful lateral muscle
fixed and widely dilated pupil- myadriasis (this is bad because it may mean a cerebral herneation which presses on the brainstem which controls our vegetative functions); patient might report trouble reading.
ptosis (drooping eyelid)- because of that levator palpebrae superioris muscle; nystagmus |
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Term
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Definition
| contralaterally hemiplegia WITH oculomotor palsy |
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Term
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Definition
| contralateral body and face sensation loss WITH oculomotor palsy |
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Term
| Parasympathetic Supply of the Oculomotor Nerve |
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Definition
This muscle has parasympathetic supply.
These fibers start in the Edinger-Westphal Nucleus (equivalent of the ventral or dorsal gray horn for other nerves) The Edinger-Wesphal nucleus is the start of the pre-ganglionic neurons in the parasympathetic fibers of this nerve.
The named ganglion between the pre and post ganglionic neurons is the ciliary ganglion (just behind the eyeball). This is where the post-ganglionic neurons take over then go to the sphincter muscle of the eyeball to CONSTRICT it.
Also goes to ciliary muscle- supplied by post-ganglionic neurons of this oculomotor nerve.
This muscle changes the shape of the lens for focus.
Parasympathetic antagonist- Belladonna or atropine- kills or stops this nerve (sort of) so that the sympathetic supply beats it. Sympathetic supply then goes to the radial muscle to DILATE pupil. So these drugs cause DILATION of the pupil. |
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Term
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Definition
| (equivalent of the ventral or dorsal gray horn for other nerves) The Edinger-Wesphal nucleus is the start of the pre-ganglionic neurons in the parasympathetic fibers of this nerve |
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Term
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Definition
The named ganglion between the pre and post ganglionic neurons is the
(just behind the eyeball). This is where the post-ganglionic neurons take over then go to the sphincter muscle of the eyeball to CONSTRICT it. |
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Term
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Definition
Has parasympathetic supply
supplied by post-ganglionic neurons of this oculomotor nerve
This muscle changes the shape of the lens for focus |
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Term
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Definition
Parasympathetic antagonist-
kills or stops this nerve (sort of) so that the sympathetic supply beats it. Sympathetic supply then goes to the radial muscle to DILATE pupil. So these drugs cause DILATION of the pupil. |
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Term
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Definition
Motor and Sensory nucleus is in pons
3 Divisions for Sensory portion of this nerve:
Opthalamic
Maxillary
Mandibular
Pain and temp. from these travels contralateral. Touch and pressure travel bilateral.
Also has motor supply to:
Temporalis-closes mouth
Masseter-closes mouth
Lateral Pterygoid- opens mouth
Medial Pterygoid- closes mouth
TIP: All other muscles of the face are supplied by the facial nerve (facial expression)! |
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Term
| Sensory portion- Trigeminal |
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Definition
3 Divisions for Sensory portion of this nerve:
Opthalamic
Maxillary
Mandibular |
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Term
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Definition
Temporalis-closes mouth
Masseter-closes mouth
Lateral Pterygoid- opens mouth
Medial Pterygoid- closes mouth
TIP: All other muscles of the face are supplied by the facial nerve (facial expression)! |
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Term
| Trigeminal Nerve- Tracts & Lesions |
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Definition
Tract for the UMN’s for this nerve are found in the corticobulbar tract = cortex to bulb (brainstem)--contains the neurons that go to these motor nerves in the cranial nerves. These are UPPER motor neurons.
UMN lesion to this nerve- spasticity, hyper-reflexia
To test: Bang on patient’s chin downward- jaw will quickly go up just a little (normal). If there is an UMN lesion the chin will come back up fast and hard. |
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Term
| Trigeminal Nerve Pathways |
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Definition
Pain and temperature from 3 sensory divisions- comes down the descending nucleus (tract) we get a contralteral projection through the VPM to the somatosensorycortex=therefore pain and temp. from right side of face go to the left side of brain.
Touch and Pressure coming from these 3 divisions- goes through the semilunar ganglion ends in the main sensory nucleus Then bilateral projection to VPM then projects to somatosensory cortex= thus touch and pressure goes to both hemispheres of the brain |
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Term
| Trigeminal Nerve pathways- pain and temperature |
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Definition
| Pain and temperature from 3 sensory divisions- comes down the descending nucleus (tract) we get a contralteral projection through the VPM to the somatosensorycortex=therefore pain and temp. from right side of face go to the left side of brain. |
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Term
| Trigeminal nerve pathway-touch and pressure |
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Definition
| Touch and Pressure coming from these 3 divisions- goes through the semilunar ganglion ends in the main sensory nucleus Then bilateral projection to VPM then projects to somatosensory cortex= thus touch and pressure goes to both hemispheres of the brain |
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Term
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Definition
Most common thing seen:
-Trigeminal Neuralgia (a.k.a. Tic Douloureux): electrical shooting pain down sensory nerve branch of trigeminal nerve
Usually occurs in people over 40
Cause is unknown
Quite common
Light touch to cheek and shooting pain down the nerve usually for a second or so
Can come when eating cold foods or during dental issues.
Usually unilateral
Sometimes associated with MS
Often lose Cornea Reflex- the membrane over eye is innervated by trigeminal nerve and when eye is touched we normally blink to wipe it out. This can be lost and they might have to artificially lubricate the eye.
Not much a therapist can do for Trigeminal Neuralgia.
Usually give these patients anti-convulsants and analgesics |
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Term
| Trigeminal Neuralgia (a.k.a)? |
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Definition
| Tic Douloureux-electrical shooting pain down sensory nerve branch of trigeminal nerve |
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Term
| Trigeminal nerve damage- lose cornea reflex- |
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Definition
| Reflex- the membrane over eye is innervated by trigeminal nerve and when eye is touched we normally blink to wipe it out. This can be lost and they might have to artificially lubricate the eye |
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Term
| Trigeminal nerve damage- Sensory damage |
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Definition
Ipsilat. loss of sensation in the head, face and inner oral cavity
To test sensory you can just touch the patient’s face or head to see what happens. |
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Term
| Trigeminal nerve damage-Motor damage |
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Definition
| Weak chewing, jaw deviates to affected side, asymmetry of jaw movements, asymmetry of mouth opening. Chewing and speaking problems. |
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Term
| trigeminal-To test damage to motor supply of nerve |
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Definition
| Open jaw against resistance and jaw will deviate to the side of the lesion. |
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Term
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Definition
Nucleus is mostly in pons (some in medulla).
Supplies MOST facial muscles. Innervates ALL muscles of facial expression. Also innervates the stapes of the inner ear.
Parasypathetic fibers in this nerve go to:
Saliva glands- produce saliva
Three main salivary glands- 1)Parotid gland (NOT innervated by Facial N.) 2)submandibular (innervated by facial N.) 3)sublingual (innervated by facial N.)
Lacrimal glands- produce tears
Nasal glands- produce mucous
The superior salivatory nucleus produce the facial nerve saliva.
Special sense housed within this nerve= taste on anterior 2/3rds of tongue (taste buds on this portion of tongue are innervated by this nerve). |
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Term
| Parasypathetic fibers -of facial nerve |
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Definition
Saliva glands- produce saliva
Three main salivary glands- 1)Parotid gland (NOT innervated by Facial N.) 2)submandibular (innervated by facial N.) 3)sublingual (innervated by facial N.)
Lacrimal glands- produce tears
Nasal glands- produce mucous |
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Term
| facial-Special sense housed within this nerve |
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Definition
| taste on anterior 2/3rds of tongue (taste buds on this portion of tongue are innervated by this nerve) |
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Term
| The superior salivatory nucleus produce |
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Definition
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Term
| Facial Nerve- Skeletal Muscle Supply |
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Definition
Facial Nerve supplies the skeletal muscles in the face except for the 4 innervated by trigeminal N.
5 major branches of the motor supply to regions of the face:
Temporal
Zygomatic
Buccal
Mandibular
Cervical
Good way to remember those: Twelve Zebras Became My Clients |
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Term
| If damage to facial nerve you would see |
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Definition
| hypercusis- sound are WAY too loud! |
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Term
| Other smaller branches that supply muscles of face/head: |
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Definition
Little branch goes to Digastric-from mandible to hyoid bone: this elevates hyoid or depresses mandible.
Stylohyoid- from styloid process on temporal bone to hyoid. Elevates the hyoid. Helps in swallowing and movement of the throat area.
Another tiny branch goes to the stapedius- muscle of the inner ear that attaches to the stapes bone (a.k.a. stirrup) The stapedius muscle acts as a damper to the vibration ofthat bone when sound is loud. It dampens the vibration |
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Term
| Taste: How you get consciousness of taste: |
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Definition
| Comes up and goes through cell body=geniculate ganglion pons at nucleus solitarius where second order neuron takes over crosses other side of brain stem to thalamus (VPM) where it synapses and 3rd order takes over leaves and goes to lateral sulcus (gustatory area) on posterior central gyrus |
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Term
| How We Salivate When We Taste Something (Facial & Glossopharyngeal!) |
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Definition
How we salivate when we taste something (*REMEMBER- salivation with taste can be from Facial Nerve OR Glossopharyngeal Nerve!!):
-Brain stem reflex- taste something neuron goes to nucleus solitarius where there is reflex interneuron (in brainstem) that interneuron goes to superior salivatory nucleus then parasympathetic fibers go to saliva glands.
--When person has a sympathetic (fight or flight) response it causes thick saliva and dry mouth (opposite of parasympathetic fibers). |
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Term
| Damage to Facial Nerve-sensory |
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Definition
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Term
| damage to the facial nerve-motor |
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Definition
| Asymmetry of facial expression; cannot elevate eyebrows and forehead; smiling & frowning impaired, ear hypersensitivity |
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Term
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Definition
Usally unilateral (if you see bilateral problems in the clinic you would typically suspect myasthenia gravis)
Usually idiopathic
20 to 30 years old
Usually disappears in a few months
May be related to herpes simplex virus
Seen in patients who have Lyme Disease
Most facial muscles become weak
Weird facial expressions (can’t wink, whistle, twitch nose)
Drooping of ipsilateral face
Sagging eyebrow
Cannot close eye completely because of Orbicularis Oculi Muslce
Cannot produce tears (patch over eye, eye drops, or eye sewn shut)
Mouth drawn down and not shut tightly because of Orbicularis Oris Muslce= drooling
Ear hypersensitive to sound (a LMN lesion) |
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Term
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Definition
Electrical stimulation, massge, modalities to the muscles
Try to keep muscle tone
Not too much you can do |
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Term
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Definition
What tract are our upper motors neurons found in for the Facial Nerve?= corticobulbar tract
Facial Nerve going from brain stem to facial muscles = LMN
The lower part of the face is supplied contralaterally. (left brain supplies right chin). Bilateral supply to the upper face. Left and right brain both supply both sides of forehead.
If you get a lesion above the nucleus (UMN lesion) in the left motor cortex you would see:
left side of face=FINE
Right side of face= lose right lower face.
Right forehead is spared because it has connections from right motor cortex as well.
Left facial nerve lesion AFTER the nucleus (LMN lesion) you would see:
Right side of face= FINE (left nerve does not go to right face) |
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Term
| Crocodile Tears Syndrome: |
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Definition
| If you short circuit the facial nerve proximal to the geniculate ganglion what happens? Taste sensations comes up the nerve and then short circuits across to the nerve going to the lacrimal glands (that is the only place where parasympathetic fibers going to lacrimal glands is close to the sensory fibers coming in for taste. You taste something and you cry. |
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Term
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Definition
Bite from deer tick causes infection
You get a ring-worm rash and severe flu, then it goes away
Months later start getting weird symptoms:
Arthritis
Severe joint pain
Muscle weakness
Fatigue
If you catch it quickly it can be treated with oral antibiotics and you are fine. If you don’t realize you will start to develop serious symptoms |
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Term
| Glossopharyngeal Nerve IX |
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Definition
Supplies taste buds on the posterior third of the tongue.
Parasympathetic fibers going to the parotid gland (the other saliva gland). Control of this gland is produced by the inferior salivatory nucleus.
The superior salivatory nucleus produce the facial nerve saliva.
Innervates the Stylopharangeus muscle—helps with swallowing
*Remember that this nerve can also trigger the brain stem reflex that causes us to salivate when we eat something. |
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Term
| Glossopharyngeal nerve- innervates----- |
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Definition
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Term
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Definition
There are sensory neurons that come in from the carotid sinus- oxygen, carbon dioxide, and BP sensation receptors are here. The glossopharyngeal nerve senses these things. Little reflex sends BP changes to the Vagal nerve- which then lowers your BP.
Sensationcarotid sinusnucleus solitarius where there is interneuronnucleus of Vagal N
Sensations in the throat are sent via the glossopharyngeal nerve back into the brain stem
Gag and swallowing reflexes. If Glosso. N. is dead you won’t feel things going down your throat. When you do gag it is actually the Vagal N. that controls the motor part of that. |
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Term
| REFLEX-gag and swallowing |
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Definition
| When under general anesthetic the reflex of the epiglottis covering the lungs is paralyzed. Patients have to stop eating 10-12 hours before being under anesthesia because they don’t want you to throw up because your wind pipe is not covered by that epiglottis. This reflex is mediated by the Glossopharyngeal nerve. |
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Term
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Definition
Massive nerve
Wanders around the whole upper abdominal regions.
There are 3 portions to this nerve:
Motor fibers- go to some muscles in throat (help swallowing) and larynx (speaking- sometimes voice will change)
Sensory fibers- afferents of the autonomic nervous system. Sensations in all the organs that the Vagal Nerve goes to. These don’t usually reach consciousness.
Parasympathetic Supply- to all those organs that Vagal supplies. |
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Term
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Definition
Swallowing problems- dysphagia
Voice change
Dyphonia
Slurred speech
Motor portion of gag reflex impaired |
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Term
| If you increase Vagal Nerve stimulation (parasympathetic activity): |
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Definition
Saliva will increase
Heart rate will decrease
BP will decrease
Breathing will decrease
Smooth muscle of bronchial tree will constrict those airways.
Mucous increases
Peristalsis increases |
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Term
Vasovagal Syncopy
reflex, attack, neural mediated hypotension): |
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Definition
Fainting
WHY? -The Vagal Nerve cause vasodilation, and a drop in blood pressure (hypotension), heart rate decreases and it causes you to faint.
WHY do we faint? To make your brain level with your heart so blood can rush back to brain.
Vagal Nerve is mediated by the anterior hypothalamus which increases parasympathetic activity. |
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Term
Vasovagal Syncopy
There are 2 ways to influence the anterior hypothalamus: |
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Definition
Cerebral Cortex- Emotions, pain, etc.
Baroreceptors- found in aortic arch and carotid sinus
both go to
Anterior Hypothalamus
=increases parasympathetic activity
goes to Vasomotor Center
= in medulla
goes to Vagal Nerve
= causes vasodilation, BP decreasem Heart rate decrease= Loss of consciousness! |
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Term
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Definition
Need to be aware of:
The iris (that we change the shape of)
The pupil (the hole in the middle)
The retina
The lens (that focuses the light on the retina and then inverts it. Lens is controlled by the ciliary muscles, and the sensory ligaments) |
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Term
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Definition
| is in the back of he eyeball |
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Term
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Definition
| The lens will also flip images left and right! (not JUST up and down) |
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Term
| visual fields- sensations are perceived CONTRALATERALLY. |
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Definition
In other words, your LEFT arm will be perceived by the RIGHT side of you brain (or you right cortex- somatosensory cortex), and vice versa.
The same thing happens with our visual fields. |
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Term
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Definition
| is what is sent to the right hemisphere of the brain. Example- if you were to stare straight ahead everything on the left hand side of your “world” is your left visual field, and likewise—everything on the right hand side of your “world” is the right visual field. |
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Term
| Everything from the R visual field |
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Definition
| will go to L visual cortex and vice versa. |
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Term
| Pathways From Visual Field To Visual Cortex |
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Definition
| Light comes in through the pupil is bent by the lens is projected onto the retina then goes back through our optic nerve hits the rods and cones comes down to bipolar neurons(first order) then that signal is sent to our ganglionic neurons (which are the neurons that make up the optic nerve)(second order) optic nerve leaves the back of the retina |
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Term
| see picture of how visual fields work slide 5 of lecture 3 ppt |
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Definition
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Term
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Definition
| is made up of the Left Eye Nasal Visual field and the Right Eye Temporal Visual field. |
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Term
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Definition
| FIELD is made up of the Right Eye Nasal Visual field and the Left eye Temporal Visual field. |
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Term
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Definition
| ALWAYS refer to what the eye CANNOT see. Always refers to VISUAL fields. NOT retinal fields! So not what part of the eye is damaged (like the retina) but what the eye can’t see in the world (the visual field). |
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Term
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Definition
Once you’ve gone through optic chiasm then those neurons form into the optic tract (carries information from the left eye AND the right eye)
The Left Optic Tract carries ALL the right visual field information (which is made up of both right and left eye information—see diagram) going to the left visual cortex *remember the left visual field information goes to right brain and vice versa.
The optic tract ends or synapses at the lateral geniculate body (which is a nuclei in the thalamus).
The next neuron takes over at the geniculate body and projects the information out on the visual cortex (known as optic radiations OR geniculocalcarine fibers)—this is our 3rd order neuron. |
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Term
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Definition
If you were to look on the back of someone’s visual cortex you would see a little man upside down (if they were looking at a little man), because the image is inverted (like we talked about).
The visual cortex is found on the back of our occipital lobe. (The reason why we see stars when we hit the back of our heads)
We have a longitudinal fissure which separates the left visual cortex from the right visual cortex.
There is also a horizontal cut across the visual field (another fissure dividing top and bottom). This is known as our calcarine fissure.
The calcarine fissure is between the lingual gyrus (on the bottom –beneath the calcarine fissure) and the cuneate gyrus (which is above).
Example- if you are staying straight ahead at someone’s bellybutton what will you see on your lingual gyrus (what part of the person?= the top of the person
The bottom of the person will be seen on the cuneate gyrus. (because the person is inverted on the back of the visual cortex) |
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Term
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Definition
From the lateral geniculate body there are fibers going to the lower visual cortex or the lingual gyrus and they make a loop that come down to the temporal lobe= Meyer’s Loop.
Your fibers from the top of the visual field and the bottom of the visual field don’t run along side each other. They go different ways to get back to the visual cortex. This is important because you can lesion one part without hurting the other! |
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Term
| On either side of the optic chiasm are internal carotids |
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Definition
| carotids=frequent site of aneurysm- swelling out of blood vessel wall |
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Term
| Right internal carotid artery aneurysm |
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Definition
lose right eye’s nasal visual field
= right nasal hemianopsia= right eye half blindness- patient might not always notice this until they close their left eye |
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Term
| Lesion in the LEFT temporal lobe |
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Definition
| can’t see right upper visual field |
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Term
| Complete slice through right optic nerve before the optic chiasm= |
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Definition
| =right eye completely blind= right eye anopsia (aka anopia)- completely blind (right anopsia, or left anopsia |
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Term
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Definition
Left superior quadrantanopsia
Cause: lesion in the right temporal lobe
(lose top left corners of both eyes)
Bitemporal anopsia-Cause:lesion at the chiasm(point of crossing) rightside of right eye and left side of left eye blacked out)
Left homonymous hemianopsia-Casue:lesion in right optic tract AFTER it leaves the chiasm OR lesion in the right visual cortex--- (left side of right eye, left side of left eye) |
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Term
| Lateral internal corotid aneurysm |
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Definition
left nasal hemianopsia
nasal(inner) of left eye |
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Term
| Tumor that affects the pituitary gland (or at the chiasm?)= |
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Definition
?)= tunnel vision= bitemporal hemianopsia
(right eye right side)(left eye left side) |
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Term
| Right visual cortex lesion |
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Definition
lesion—so wipes out everything on the left visual field. SAME as lesion in the optic tract AFTER it leaves the chiasm. Both=left homonymous hemianopsia
(right eye left side)(left eye leftside) |
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Term
| lesion on left cuneate gyrus |
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Definition
| right inferior quadrant anopsia |
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Term
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Definition
Upper visual fields are transported through Meyer’s Loop
The right loop sees the left upper world, and the left loop sees the right upper world.
Meyer’s Loop goes through the temporal lobe then loops back and it carrying information from the upper visual world. |
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Term
| The right loop(meyers loop) |
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Definition
| sees the left upper world, and the left loop sees the right upper world. |
|
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Term
| the left loop (meyers loop) |
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Definition
| goes through the temporal lobe then loops back and it carrying information from the upper visual world |
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Term
| Not all of our optic tract goes to our optic cortex-1% of fibers go to- |
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Definition
| About 1% of the fibers coming out of the back of the eyeball going toward the lateral geniculate body stray off and go to our pretectal area= where our superior colliculi are located (visual reflexes- those very fast reactions to light |
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Term
| If you shine light into your right eye |
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Definition
| = Right eye constrict= direct pupillary reflex. Left eye will constrict a little= consensual pupillary reflex |
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Term
| How do we get the consensual pupillary reflex? |
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Definition
| Light through optic nerve through optic tract hits the superior colliculi little interneuron Edinger Westphal Nucleus where oculomotor Nerve takes over to ciliary ganglion pre ganglionic neuron post ganglionic neuron sphincter muscle |
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Term
| What nerve shuts the pupil down? |
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Definition
|
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Term
| Atropine is squirted into someone’s eye to kill |
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Definition
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Term
| Right visual cortex stroke would you still have pupillary reflex?= |
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Definition
YES!
If not working could be due to problems with the oculomotor nerve OR cerebral herniation, pressure on the brainstem |
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Term
| If you cut right optic nerve and shine a light in right eye will right eye constrict?= |
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Definition
|
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Term
| If you cut right optic nerve and shine light in left eye would right pupil constrict?= |
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Definition
| ?= Yes, a little bit (because of that concensual reflex) |
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Term
| Flash in front of eye and scare person= |
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Definition
| blink quickly (caused by the superior colliculi acting on the orbicularis oculi muscle via the facial nerve) |
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Term
| If your arms come up when you are scared to protection it is the |
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Definition
| tectospinal tract & superior colliculi- very rapid reflex |
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Term
| Superior colliculi and tectospinal tract are thought to be the origin of blind sight= |
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Definition
left visual field is gone but person is able to pick up a cup on a table to the left of them.
*These are all protective, quick reflexes |
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Term
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Definition
| tool doctor uses to look at retina to check for problems because you can see the optic nerve (optic neuritis) |
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Term
| Syphilis patients and diabetics- |
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Definition
| You can see optic neuritis in these patients by using the ophthalmoscope |
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Term
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Definition
| swelling in back of eye by optic nerve pushing forward (can be caused by cerebral herniation) |
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Term
| Don’t give people with brain injury morphine for pain because |
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Definition
| this drug will cause very narrow pin-point pupils that are unreactive to light (why police shine light in people’s eyes to see if they are doing drugs) and also cause more edema (swelling) in the brain. |
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Term
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Definition
| bring finger closer to face and see that eyeballs converge (medial rectus- oculomotor nerve), pupils constrict (because you want to narrow focus to see better), and the lens thickens (caused by ciliary muscle), |
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Term
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Definition
| pupil does NOT constrict with light but DOES constrict with near point reaction (see in patients with diabetes and syphilis) |
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Term
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Definition
| is the name given to the many fibers coming out of the back of each eye going to the optic chiasm. Once the fibers go through the optic chiasm they become the Optic Tract. |
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Term
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Definition
| Optic nerve optic chiasm optic tract synapses in lateral geniculate body form optic radiations(which are 3rd order) which get projected to the primary visual cortex |
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Term
| Upper visual field is on the bottom of the eye. It comes around Meyer’s Loop then through the temporal lobe and ends up on the lingual gyrus. |
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Definition
| So when you look at a person their head ends up on your lingual gyrus and their legs on your cuneate gyrus. |
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Term
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Definition
| you will hit the upper visual fields |
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Term
| Lesion in lingual or cuneate gyrus could lead to |
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Definition
| quadrant anopsia. Particularly seen in one side, although both sides can be lost. |
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Term
| “Vestibulo”cochlear Nerve |
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Definition
No motor supply to this nerve.
The vesibular aparatus is made up of semicircular canals (detect angular acceleration of the head) and otolith organs (utricle and saccule).
There are 3 semicircular canals on each side of the head arranged in three planes in space. Anterior, posterior and lateral (or horizontal).
Utricle & Saccule detect linear motion or translation (left, right, up, down, front, & back motions) |
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Term
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Definition
Each has a bony outer portion, and a membranous inner portion.
The most important stuff is the black stuff in the middle called endolymph- fluid, liquid--which can move.
If you move your head quickly to the right, and drag canals through the liquid, the liquid will stay behind (stay still).
At the end of each semicircular canal there is an ampulla- a big swelling that contains a big blob of jelly known as the cupula (floats in the endolymph)- projects into the ampulla and it is here that we find our hair cells- our dendrites of our neurons that project into this blob of jelly.
The blob of jelly is floating just as the endolymph (so it floats perfectly, and does not detect gravity).
The semicircular canals are arranged in 3 planes in space. Anterior, posterior, and the lateral (or horizontal). The horizontal plane angles upward 30 degrees. This is important for testing. |
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Term
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Definition
most important stuff is the black stuff in the middle
fluid, liquid--which can move
If you move your head quickly to the right, and drag canals through the liquid, the liquid will stay behind (stay still). |
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Term
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Definition
At the end of each semicircular canal
a big swelling that contains a big blob of jelly known as the cupula |
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Term
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Definition
| floats in the endolymph)- projects into the ampulla and it is here that we find our hair cells- |
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Term
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Definition
our dendrites of our neurons that project into this blob of jelly.
The blob of jelly is floating just as the endolymph (so it floats perfectly, and does not detect gravity). |
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Term
| The semicircular canals are arranged in 3 planes in space. |
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Definition
| Anterior, posterior, and the lateral (or horizontal). The horizontal plane angles upward 30 degrees. This is important for testing. |
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Term
| The posterior canal of one ear lines up with |
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Definition
| with the anterior canal of the other ear (parallel). |
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Term
| The left posterior canal aims at the |
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Definition
| right eye and lines up with the right anterior canal. |
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Term
| The right posterior canal aims at the |
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Definition
left eye and is lined up with the left anterior canal
These detect any angular movement of the head by the cupula. |
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Term
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Definition
Any movement of the cupula will move the hair cells and cause the vestibular nerve to fire.
Kinocilium and sterocilia are the parts of the hair cell that are sticking up into the jelly.
In one hair cell that is one big kinocilium and a bunch of stereocilia that are arranged in different sizes |
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Term
| When hair cells are at rest |
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Definition
| there is a constant firing rate(they are firing all the time)-even though they arent moving.-this is how we get balanced input from out ears letting us know we are stable. |
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Term
| when you move your head and the direction of flow pushes the stereocilia towards to kinocilium then you get--- |
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Definition
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Term
| Alternatively when you knock the kinocilium towards the stereocilia you get--- |
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Definition
inhibition
this is less activity than the resting state |
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Term
| What would happen if you had unilateral vestibular hypofunction?-- |
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Definition
With age some of these hair cells die—and you can get unilateral (one sided) death of some of the hair cells.
So one ear is sending more of that background stimulation at rest than the other. Normally this would mean that the person is moving, so the person is going to have a sensation that they are moving when they aren’t. This happens with a lot of older patients with bad balance. |
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Term
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Definition
means you are moving your head
*If you turn your head—in one ear the hair cells are going one way and in the other they are going the opposite direction (excitation & inhibition). If you have more excitation from one side than the other (unbalanced input) |
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Term
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Definition
They contain jelly too (but otolith organs are more like “dinner plates”-a flat layer of jelly rather than a blob)
Made up of our saccule and utricle
A saccule looks like a vertical dinner plate- detects sideways motion & up and down motion.
The utricle lays on the floor and is like a horizontal dinner plate- detects front and backwards movements (linear)
Macula- the dinner plate of jelly that contains hair cells (just like the cupula) But they key difference is the otoconia (sometimes called the otoliths)- little calcium carbonate rocks. They make the macula sensitive to gravity by weighing it down. They are not necessarily floating. |
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Term
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Definition
| looks like a vertical dinner plate- detects sideways motion & up and down motion. |
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Term
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Definition
| lays on the floor and is like a horizontal dinner plate- detects front and backwards movements (linear) |
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Term
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Definition
| the dinner plate of jelly that contains hair cells (just like the cupula) But they key difference is the otoconia (sometimes called the otoliths)- little calcium carbonate rocks. They make the macula sensitive to gravity by weighing it down. They are not necessarily floating. |
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Term
| BPPV (Benign Proximal Positional Vertigo) |
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Definition
If the otoconia (little rocks) get free off the macula they can float into the semicircular canals and bang on the cupula. This will mak it more sensitive to movement and gravity.
The patient will report bending over and they suddenly threw up, got dizzy, or passed out. *You can fix some of these patients in 5 minutes. |
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Term
| signal/pathway vestibulococklear |
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Definition
Signal coming out of the semicircular canals because head is movingunipolar neuronvestibular ganglion (where cell body is found)goes into lower part of pons where most of these neurons that come from vestibular aparatus are going to end on the vestibular nuclei (there are 4 of them on the left and right)Synapse there and another neuron takes over and goes into the superior cerebellar peduncle and end on the floccular nodules (in the cerebellum)
The cerebellum has the info and decides “oh I’m falling to the left”, and sends a neuron from the floccular nodules to the fastigial nucleus which then outputs back to vestibular nuclei.
*See next slide that follows this pathway!!! |
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Term
| The four vestibular nuclei are known as |
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Definition
| Superior, Lateral, Medial, and Inferior |
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Term
| A few fibers don’t go to the vestibular nuclei at all --they bypass and go straight into the |
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Definition
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Term
| The vestibular nuclei are the start of the vestibulospinal tract—which goes down the |
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Definition
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Term
| There are 2 major functions of the vestibular aparatus- |
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Definition
| VSR (vestibular spinal reflex)- posture, balance & VOR (vestibular ocular reflex)- it controls the eyes. |
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Term
| Arising from our vestibular nuclei we have |
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Definition
| 2 vestibulospinal pathways |
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Term
| Arising from the Lateral vestibular nuclei only is the |
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Definition
| lateral vestibulospinal tract. This is an uncrossed or ipsilateral tract.It ends on the lumbar and sacral segments and it causes increased extensor tone in the lower extremities and decreases flexor muscles. (Basically makes you stand up straight) |
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Term
| Arising from the other 3 nuceli (superior, inferior and medial) is the |
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Definition
| the medial vestibulospinal tract. Down the cord but bilateral or crossed tract. It largely ends in the cervical region so it goes to the arms. It increases tone of the extensors and decrease flexor tone |
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Term
| If you cut the brain stem above the vestibular nuclei and below the red nucleus you get |
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Definition
| get de-cerebrate rigidity=Massive increase in extensor tone. |
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Term
| If you destroy the vestibular aparatus in an animal with de-cerebrate rigidity |
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Definition
| the rigidity goes away. This proves that the extensor tone comes from the vestibular aparatus. |
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Term
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Definition
Also coming off of the medial vestibular tract are collaterals. They go upwards through the brainstem in the medial longitudinal fasiculus and into cranial nerves 3,4, and 6 (which control movements of the eyeball).
This is what the vestibular ocular reflex pathways are there for. This stabilizes your vision. So if you are looking at the lines on your hand while moving your head for every 10 degrees you head moves your eyes will move 10 degrees. (your vestibular aparatus detects that your head is moving)
*Remember retinal slip is worthless! |
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Term
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Definition
There are also vestibular cortical connections that are not well known.
The vestibular information can reach consciousness (this is why we sometimes get sick)
The VOR controls the eyeballs in relation to head movement (since visual blurring is worthless). When you move your head to the right your eyes will slowing go left at first then saccade- fast movement of the eyeball, to the right. When you turn your head to the right slowly you get right nystagmus- slow movement to left and fast to right. |
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Term
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Definition
is named in relation to the fast component
We tested this (the horizontal canals) in class with the spinning in the chair. Head tilted 30 degrees down because horizontal canals are tilted 30 degrees upward. If the spinning does not cause nystagmus then the vestibular system is not working correctly!
When you move your head to the right your eyes will slowing go left at first then saccade- fast movement of the eyeball, to the right. When you turn your head to the right slowly you get right nystagmus- slow movement to left and fast to right. |
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Term
| Which way are hair cells knocked to cause left nystagmus?= |
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Definition
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Term
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Definition
tests the lateral (horizontal) canals one ear at a time.
You have patient tilt head 60 degrees backwards to put horizontal (lateral) canal vertical.
You irrigate one ear with warm water which causes a convection current in the horizontal canal. It is making the endolymph nearest the outside to rise upwards and create flow which knocks the hair cells upwards (which is equivalent to knocking it to the left if they were upright).
If you knock hair cell to the left you will see right nystagmus.
This will often cause sickness because one ear says you are moving and other doesn’t.
*Tip: Moving head to the right will normally push hair cells left= right nystagmus.
If pt doesn’t exhibit
If you irrigate with cold water the flow will go downward and the current will go the other way and hair cells will be knocked the other way and you get left nystagmus.
Warm water in patient’s right ear and you see right nystagmus. You put warm water in patient’s left ear and you see nothing.= left horizontal canal is damaged!
This would be called physiological nystagmus= vestibular system doing |
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Term
| warm water in pts right ear you see... |
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Definition
right nystagmus
If warm water in pts left ear and see nothing it means that pats left horizontal canal is damaged. |
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Term
| If you irrigate with cold water the flow will go downward and the current will go the other way and hair cells will be knocked the other way and you get |
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Definition
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Term
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Definition
| caused by visual information changing. No movement of head but eyes still do nystagmus. This would occur when watching a train crossing in front of you. |
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Term
| Can you turn your head to the right without seeing nystagmus?= |
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Definition
| yes because you can fix your eyes by your cerebellum= can override the vestibular system |
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Term
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Definition
any test of balance essentially)
Clinical Test for Sensory Integration and Balance (CTSIB) a.k.a. Foam and Dome test |
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Term
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Definition
Patient will step 50 times with eyes closed and arms out.
Normal- move less than 30 degrees
Vestibular system should keep you there (where you started).
If patient moves a lot then there is vestibular system damage. |
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Term
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Definition
Check-off list
Patient gets a score |
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Term
| Symptoms of vestibular damage |
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Definition
Spontaneous nystagmus
Head tilt
Ataxia
Skew deviations (eyeballs go to the left and the right)
Vertigo
Oscillopsia
Dizziness
Falls
Other types of nystagmus:
Rotational
Up and down |
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Term
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Definition
2 basic principles of treatment: adaptation and habituation
Adaptation= you cure the person (sort of)
Habituation= you basically get sick of it. You do it so many times that you habituate to it. |
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Term
| What part of the brain can influence the vestibular system and reset it?= |
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Definition
| cerebellum- it can dampen down one side or elevate on side to balance things out |
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Term
| In adaptation you are trying to tell the cerebellum that something’s wrong— |
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Definition
| wrong—you emphasize the error and try to get the cerebellum to “reset” the system. |
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Term
| One way to work on the vestibular system using VOR |
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Definition
“Times one” treatment- have patient fixate on something and rotate head left and right slowly with eyes still fixed. For patients with vestibular problems this is difficult.
In patient’s with vestibular problems they will start to have retinal slip and see visual blurring. They won’t be able to focus.
The cerebellum will try to adjust the gain of eye movement to match head movement. |
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Term
“Times two” treatment:
VOR treatment |
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Definition
Patient’s head is turning left and right but the object you are tracking is going in the opposite direction of the head movement. So head goes left and object goes right and vice versa.
This really stresses the system
You are trying to create visual slip so the system will adapt. |
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Term
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Definition
“do what makes it worse”
In this you create the symptoms that make things worse. You do it over and over again until patient is habituated to the signal
Patient won’t like this, because it makes them sick and dizzy
Ex- turn and move head all around. (which is what patient is trying NOT to do)
Not a “nice” treatment |
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Term
Unialteral Vestibular Hypofunction
(vestibular problem) |
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Definition
one side you lose the hair cells (we talked about this last class
At rest there is a background firing which is greater than when there is
At rest there IS firing!
The problem occurs when you get the loss of hair cells from just one side (cuased by things like trauma, aging, MS patients, Parkinson’s patients, diabetics)
This loss of hair cells causes unbalanced input and you can see:
Nystagmus
Oscillopsia (the visual world jumps)
Nausea
Dizziness
Eyes skewed (skew to the side of the lesion, or side where hair cells are lost)
The cerebellum will constantly be trying to adjust the gain |
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Term
Meniere’s Syndrome
(vestibular problem) |
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Definition
Can’t do much for this
Very debilitating situation
Unknown etiology
Patholog- they thing too much endolymph hydrodrops= too much endolymph
You see:
Bouts of dizziness and vertigo
Might last for a minute or two or hour and then go
Nausea
Tinitis- ringing in the ears for no reason
Unilateral most times
SOME bilateral
Most common in males, 40-60 years old
Try salt free diet, dramamine, antihistamines
In sever cases (lasting, and drugs have no effect) they will go in and drill out the vestibular system in the brain (kill it) because it is too debilitating for the person. They can’t function |
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Term
BPPV
(vestibular problem)
(more info) |
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Definition
Benign (won’t kill you) Paraxysmal (sudden burst of it, comes on then it’s gone) Positional (depends on the postion of your head) Vertigo (you get vertigo)
Patient reports nausea & dizziness when they make a sudden head movement (loading dish washer, putting something awway on bottom shelf, making bed, etc.)
The cause is thought to be the otoconia on the utricle and saccule float away and go into the semicircular canals.
One theory says they stay in suspension in canal and bang into it and make hair cells move more than they should
Another says they land and stay stuck on the cupula.
The utricle and saccule ARE sensitive to gravity but the cupula is NOT.
When the otoliths end up on the cupula, the cupula gets weighed down and you start getting signals when you shouldn’t be. |
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Term
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Definition
Hall-Pike Dix Maneuver
You have patient sit up normally and twist head to one side, and quickly move them down and get rotational and movement to one side.
You hold them there and wait for symptoms.
You will start seeing nystagmus or nausea.
*very similar to vertebral artery test. Vertebral artery goes above the vertebral foramen and doing this can shut off the vertebral artery and you might see symptoms. If you deprive blood going to brain stem them you might see vestibular symptoms not actually due to vestibular system.
90% or vast majority of BPPV is found in the posterior canal. |
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Term
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Definition
3 Types:
Brandt’s Exercises: have patient lay on one side and quickly come back up to the other side. Do this repeatedly several times a day.
This is trying to move the rocks out of those canals
The Semont Maneuver #2:
A one treatment approach
One shot
The patient rotates head down looking up on one side, and stay there for three minutes. Next quickly go to other side and look down, then bang on head (vibrate head) hold for 5 minutes. Come back up and stay there for 48 hours. |
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Term
Epley Maneuver:
Treatment for BPPV |
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Definition
A.k.a canal positioning
Free up the rocks by banging while rotating head in various positions, then rotate them back into the right place.
You do this once and the patient stays in upright position for 48 hours.
* See next slide for picture. |
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Term
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Definition
: sound waves come in hit the eardrum vibrates the hammer, anvil and stirrup the stirrup connects to oval window= causes a wave of vibration down the cochlea moves the hair cells in the cochlea (depending on the frequency it moves different ones)
So it travels through the bones (hammer anvil and stirrup) to the cochlea
The sound waves that initially came in turn into vibrations in the fluid and knock over those hair cells and you get the perception of sound
Hair cells coming out of the cochlea stimulate the first order auditory neuron. Cell bodies are going to be found in the spiral ganglion.
Synapses at the dorsal and ventral cochlear nuclei in the pons. As the neurons (first order) come in they bifurcate and go to both dorsal and ventral cochlear nuclei.
Sound waves trigger hair cells to move trigger first order neuron in cochlear nerve cell bodies are in spiral ganglion bifurcates goes to dorsal and ventral cochlear nuclei in pons second order takes over send an ipsilateral and contralateral projection (bilateral tract eminating from EACH nuclei) second orders ascend in lateral lemniscus end in the thalamus in the medial geniculate body 3rd order neuron takes over and goes out to our auditory cortex located in the superior temporal gyrus (41&42) |
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Term
| Stroke in left superior temporal gyrus. Which ear you are not able to hear from |
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Definition
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Term
2 major categories:
DEAFNESS |
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Definition
| Conduction and sensorineural deafness |
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Term
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Definition
middle ear deafness
A mechanical problem. No conduction through the bones (osscicles)
A mechanical impediment that stops sound from getting to the cochlear
Could be caused from
Torn eardrum
Otosclerosis (most common cause)- the stirrup fuses and cannot transmit sound to the oval window (can be surgically fixed) |
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Term
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Definition
A problem with the nerve
Damage to the cochlea or the cranial nerve.
Causes:
Rubella infection (mother has it and baby is born deaf)
Large doses of antibiotics
Cochlea can atrophy with aging
An acoustic neuroma |
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Term
| You can distinguish between the 2 types of deafness by using a |
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Definition
tuning fork
You bang a tuning fork outside of ear and you can’t hear it. You then put the tuning fork on the bone in the skull and you hear it, the cause is conduction. By vibrating the bone you are sending a signal to the cochlear by bypassing the ossicles.
If you do this and STILL can’t hear it then it is probably sensorineural problems. |
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Term
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Definition
Very old and complicated pathways.
We have olfactory cells in the top of the nose
There is a cribifrom plate (ethmoid bone) has holes in it
olfactory receptors
olfactory neurons that are bipolar- on the end of these we have olfactory vessicles and little hairs comes off of the olfactory cells (what actually senses the smell)
Rapidly adapting receptors
The olfactory tract or bulb is connected has extensions of the meninges (he gave example of guy who fell and broke his ethmoid bone and cut meninges and had cerebrospinal fluid coming from his nose) |
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Term
| olfaction has cells that are no where else in the nervous sytem-> |
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Definition
| basal cells= make more neurons (continually regrowing-every 60 days- make new ones) |
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Term
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Definition
| The smell (signal) comes in goes to olfactory neuron then hits olfactory bulb (which is a long tract going back to brain—is actually an extension of the brain) is sampled by the dendrite hairs and goes hit mitral cells carry back deep within the brain then it goes all over the place (not very simple) |
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Term
| smell pathway projected to the |
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Definition
Amygdala and Hippocampus- which are part of the limbic system (nicknamed the emotional brain- short term memory and emotions)
This is why you smell something and it takes you back to a certain memory from years earlier.
To get to consciousness the fibers travel via the medial dorsal nucleus in thalamus projected out to the orbitofrontal cortex (where you consciously perceive smell—is located behind the eye) |
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Term
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Definition
| diminished sense of smell |
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Term
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Definition
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Term
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Definition
|
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Term
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Definition
auditory hallucinations- nasty smells (sometimes associated with seizures of the temporal lobe)
Medial temporal lobe contains a lot of smell tracts= if you have a lesion in here you can get cacosmia. |
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Term
| When do you get diminished sense of smell?= |
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Definition
| when you have a cold, elderly, Parkinson’s patients, if you have head trauma (damage to cribiform plate), frontal lobe glioma (tumor of glial cells), frontal lobe damage |
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Term
| What other signs will you see if frontal lobe damage?= |
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Definition
| behavior/personality changes |
|
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Term
| George Girshman Syndrome- |
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Definition
| had a temporal lobe lesion- he had cacosmia. Which other cranial nerve would be affected here?= optic nerve because Meyer’s Loop goes through temporal lobe= have quadrant anopsia |
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Term
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Definition
| start in motor cortex- cells bodies are found in Layer #5 (NOT SIX |
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Term
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Definition
| actually come out of the pre-motor cortex. |
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Term
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Definition
Huge big pipe coming into head
Little arteries come off of it
Big chunk of fat (red stuff) can go through the big pipe and get sucked into the striate arteries
The striate arteries supply the internal capsule
These are the first arteries a chunk of fat will encounter when coming up from the heart
It gets sucked into there and you get a stroke.
Lacuna stroke- stroke on these small arteries deep within the brain |
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Term
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Definition
lies between the basal ganglia and the thalamus
Corticospinal neurons coming out go through the post. Limb.
The posterior limb is somatotopically organized (Face, Arm, Legs)
Fibers come out the internal capsule and down the cord- at the decussation in medulla 85% cross to toher side and from lateral corticospinal tract and end on the ventral grey horn on our LMN then goes to muscle.
The 10-15% that didn’t cross descend as the anterior corticospinal tract go to segmental level and cross back over
A few don’t cross here and those are the ones that supply trunk muscles |
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Term
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Definition
Spastic paralysis
Clonus
Positive Babinski- can’t do on 3 or 4 month old child because the pathways haven’t been completely myelinated and it will show up anyway!
Hoffmann’s sign
Clasp-knife rigidity
Hyper-reflexia |
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Term
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Definition
Flaccid paralysis
Hypotonia
Areflexia
Fassiculations
Fibrillations
Muscle atrophy |
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Term
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Definition
| This would be a LMN signs and symptoms (the start of the LMN in the cord). |
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Term
| if you wape out half the cord you get |
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Definition
|
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Term
| If you wipe out the section of the cord that has the lateral corticospinal tract it would be |
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Definition
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Term
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Definition
You don’t find this much anymore but can he found in Pakistan, Afghanistan, Nigeria, India. People still getting it here.
It attacks the ventral grey horn. = LMN problem.
Caused by a virus by an insect bite or the GI tract (eat something) then spreads to the blood then the nervous system then eats away at the cord.
High fever, pain, loss of somatic reflexes, flaccidity
Can be confused with meningitis and diphtheria.
Starts with less and less muscle strength then symptoms suddenly stop and a few days later start to regain strength but never get back to original muscle strength.
Once those output neurons are destroyed they can’t be replaced. (and they have been “eaten” by the virus) |
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Term
So how do people get stronger once symptoms are gone?
polio: |
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Definition
within a muscle there are tons of motor units (1 alpha motor neuron to every 1700 muscle fibers, or you might see ratio 1:10 like in eyes)
You get stronger because the remaining alpha motor neurons bud off in the muscle and send collateral branches to the fibers and innervate them. Therefore you get more muscle strength.
Polio can kill (if it invades respiratory muscles)
Who came up with vaccine? Salk- first a needle then later came out with a pill to take |
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Term
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Definition
Patient gets new muscle weakness but polio has NOT come back again
Will also have painful trigger points
What is happening?= The alpha motor neurons that sprouted out are burned out! They die back and only innervate the muscles that they were originally designed to innervate. |
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Term
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Definition
CNS, cerebral problem. UMN problem.
Lots of different types of CP. It affects different parts of the brain.
Any kind of prenatal brain problem is going to be given the name “CP”
Sometimes idiopathic but sometimes caused from toxins in placenta, or oxygen deprivation.
Usually don’t notice to a year or two later after birth.
Spastic paralysis, deafness, blindness, etc. (depends where the lesion is)
Different categories of CP:
Spastic CP: hyper-reflexia, spasticity
Ataxic CP: uncoordinated movement
Hypotonic CP: flaccid issues
Athetoid CP: basal ganglia issue, weird movements of fingers and hands (writhing, twisting movements)
Spastic Diplegia CP: kid walking on tiptoes, spastic paralysis
Quadriplegia CP
Hemiplegia CP
You treat depending on the symptoms you see. Botox, Baclofen, strengthening |
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Term
| ALS- amyotrohpic lateral sclerosis |
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Definition
or Lou Gehrig’s Disease (no muscle nourishment causing scarring or hardening in the lateral corticospinal tract)
UMN problem
Not a cognitive issue
No known cause
Some think it’s an autoimmune disease
Some research suggests it is environmental cause
Usually occurs 40-50 years old
Attacks corticospinal neurons
Men are more likely to get it. About 3 times more likely.
See: muscle weakness, spasticity, muscle atrophy, hyper-reflexia
Usually first appear in forearms and hands (change in hand functioning)
Can progress to difficulty breathing and swallowing (bigger issues)
Can kill in a few years but doesn’t typically
Usally lasts for years and years
Research shows if you get it earlier in life it lasts longer
About 10% of people survive beyond 10 years.
Prevalence in US 1/50,000 |
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Definition
Symptoms that you see
Tried various drugs: latest is Riluzole:
It is a glutamate antagonist. Glutamate is excitatory. Riluzole slows the progression of ALS. |
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Definition
Another tract the eminates in the cortex but doesn’t go to spine—goes to cranial nerves- corticobulbar tract
Starts in cortexbrainsteminnervates those LMN within those cranial nerves (does NOT supply cranial nerves 1, 2 and 8)
This tract is bilateral. Left side supplies the left AND right nerve except for 2 cranial nerves:
the facial N. (bilateral supply to upper face BUT lower face has contralateral supply ONLY-stoke on left side= lower left side damage.
Hypoglossal- contralateral supply only! Left cortex supplies right side of tongue.
The rest of cranial nerves have a bilateral supply! |
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Term
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Definition
“Serious muscle weakness”
Can affect any part of nervous system but typically affects those muscles innervated by bulbar nuclei (cranial nerve muscles)
Symptoms:
Muscle weakness
Bilateral problems particularly late in the day
Ptosis
Diploplia
Strabismus
Females get it way more than males
Most common 20-50 years old
Generally relapsing problem
Start to invade more serious cranial nerves such as vagal nerve.
Idiopathic- some think autoimmune, or some think metabolic problem |
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Definition
Might find abnormality in thymus gland (sometimes take out this gland)
Changes in the neuromuscular junction- the neural endplate-find antibodies here:
2 types- one sits on the nerve and blocks the release of calcium- therefore less ACH being released out of those vessicles
Another antibody blocks the ACH receptors- stop muscle from contracting
Myasthenia Gravis is very similar to curare (blow dart poison) or cobra venim (Bungalow Toxin). Attack in a similar way to this diesease. Bind to the ACH receptors in the muscle.
Research on these has been used to see how severe Myasthenia Gravis is.
They pour Bungalow Toxin into a healthy muscle and see how much comes out. If 100 units in, nothing will come out because those ACH receptors are picking up the venim. If you do this with a muscle with myasthenia gravis, they find it binds only about 33% compared to normal. So for example- 100 units in 66% comes out of muscle. This means 66% of the receptor sites on this muscle must already have a myasthenia gravis antibody on it. No space left for the toxin
This shows how severe the disease is |
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What drug do you use to allow more chance for ACH to get to muscle?=
myasthenia gravis |
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Definition
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Term
| How does this work?= neostigmine |
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Definition
it is a colonesterays inhibitor. This prevents the uptake of ACH so allows more ACH to hang out in cleft for longer so has more chance to bind to receptor sites.
In severe cases people carry around in injectable form of this if they are in respiratory distress. |
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Term
| Immunodepressants are often used if they think it’s an |
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Definition
| autoimmune disease- suppress the immune symptoms (such as Prednisone |
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Term
Another thing used to treat is
Myesthenia gravis |
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Definition
plasmopharesis- filter the blood trying to get rid of the antibodies
In sever cases they can have issues with eating and swallowing. |
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Term
| Facial unilateral problems usually are... |
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Definition
| Bells Palsy; if you see bilateral problems you typically think myasthenia gravis |
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There are many other much older tracts. They do not directly start in the motor cortex. They are extrapyramidal pathways.
4 of the major |
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Definition
Rubrospinal
Tectospinal
Reticulospinal
Vestibulospinal |
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Term
| What kind of stroke affects the deep part of the brain?= |
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Definition
| Lacuna strokes! (they affect the start of these extrapyramidal tracts |
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Term
| We have a lateral and medial vestibulospinal tract, what is the difference? |
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Definition
| lateral is ipsilateral (NOT crossed), the medial is a bilateral (or crossed) tract |
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Term
| What si the most common problem with the basal ganglia?= |
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Definition
1% of the population has Parkinson’s
50,000 new cases a year
Loss of Dopamine
Dopamine is produced by substantia niagra and is circulated through the basal ganglia using axonal transport. There are circuits that go through the basal ganglia. There is a direct and indirect pathway.
Depending on where you are in the US makes a difference on your chances
It’s twice as common in males
High prevalence in the Amish. Some think it is because of pesticides.
Also common in Nebraska.
If you have dark hair you have less chance of getting it. Blondes have 60% more chance of getting it and red hair have even higher chance.
Why is this?= Parkinson’s is caused by dengeneration in substantia niagra (black substance)= makes melanin. The way you color your hair is melanin and it is linked to your ability to make dopamine.
Rate of concordance= 5% (compared to 25% in MS and 65% in schizophrenia) |
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| The direct has what affect on the supplemental motor area?= |
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Definition
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| The indirect is an inhibitory pathway to the |
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Definition
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| Interaction between these two pathways cause |
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Definition
| facilitation and inhibition and end up with Parkinson’s symptoms. |
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Definition
| something that you could do and now can’t |
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Definition
| something that you didn’t have and now do (pill rolling tremor) |
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Definition
Micrographia Cog-wheel rigidity
Pedistle turning
Shuffling gait
Retropulsion
Masked face
Low arm swing
Resting tremor
Stooped posture |
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| Most common treatment: parkinson's |
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Definition
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| Why not dopamine?= as best treatment of parkinson's |
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Definition
| it does not cross the blood brain barrier |
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Term
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Definition
| something you combine with aldopa to prevent the aldopa from being metabolized in other parts of the body. Allows the brain to get more of it. |
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Definition
3 Pure Sensory
Cranial Nerves
4 Pure Motor
Cranial Nerves
5 Mixed (motor
and sensory)
Cranial Nerves |
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