Cerebellum/Cranial and Peripheral Nerves Flashcards
The cerebllum regulates muscle activity across multiple joints in anticipation of and adjustment to changing mechanical forces. Describe Cb role in the context of internal vs external forces. What are interaction torques and why do they matter?
The cerebellum adjusts for and controls for INTERACTION TORQUES which are F=M*A.
____ ____ is a stored set of rules that mimics systems and encompasses aspects of [internal / external / both internal and external] forces. . It estimates the interaction between ___ and ____ to yield fluid, successful, automatic movements. This control occurs [ before / during / both before and during ] movement. It is [ static / adaptive ] in the context of varying environmental demands.
An INTERNAL MODEL is a stored set of rules that mimics systems and encompasses aspects of INTERNAL AND EXTERNAL forces. It estimates the interaction between LIMB DYNAMICS and ENVIRONMENT to yield fluid, successful, automatic movements. This control occurs BOTH BEFORE (prediction) AND DURING ongoing movement. It is ADAPTIVE in the context of varying environmental demands.
Visual sampling combines ___ eye movements and ____ to allow for orientation to your visual environment and bring areas of interest into focus. Visual sampling increases during ___ and ____ (movement examples).
Visual sampling combines SACCADIC eye movements and FIXATION to allow for orientation to your visual environment and bring areas of interest into focus. Visual sampling increases during COMPLEX TERRAIN NEGOTIATION (increased feedback reliance on visual feedback e.g. for foot placement!) and TURNING (eyes move, then head then body moves - this is predictive and continuously occurring!).
Eye movements in visual sampling are [reactive / proactive ] (i.e. [feedforward / feedback ] ), which allows for gaze stability! Impaired ____ are shown to interact with foot placement, turning, and gait velocity. If you need to perform multiple corrective ____, you have to move more slowly to account for that!
Eye movements in visual sampling are PROACTIVE (i.e. they’re FEEDFORWARD, seeking info a second BEFORE the action, coordinating w/head/body movement), which allows for gaze stability! Impaired SACCADES are shown to interact with foot placement, turning, and gait velocity. If you need to perform multiple corrective SACCADES, you have to move more slowly to account for that!
Cerebellar lesions impact control of ongoing movement because ___ (i.e. mismatch between internal model vs actual limb properties), ___, and ___ are impaired.
Cerebellar lesions impact control of ongoing movement because PREDICTION (i.e. mismatch between internal model vs actual limb properties), ADAPTABILITY (i.e. difficulty adapting to a change in load or environment), and PRECISION are impaired.
To accurately predict the demands of a movement, the cerebellum has to match the internal model and actual limb properties, which are driven by the limb ___, ___, ____, and ____. When there’s a mismatch, we see ____ clinically!
To accurately predict the demands of a movement, the cerebellum has to match the internal model and actual limb properties, which are driven by the limb SPEED, WEIGHT, MOVEMENT MAGNITUDE / TRAJECTORY, and INERTIA. When there’s a mismatch, we see DYSMETRIA clinically!
In individuals with Cb lesions who showed HYPERMETRIC movements, they tended to [over / under] estimate the limb inertia and start movement with a [high / low ] velocity, then overcorrect resulting in an [over/under] shoot of the movement.
In individuals with Cb lesions who showed HYPOMETRIC movements, they tended to [over / under] estimate the limb inertia and start movement with a [high / low ] velocity, then overcorrect resulting in an [over/under] shoot of the movement.
In individuals with Cb lesions who showed HYPERMETRIC movements, they tended to UNDERestimate the limb inertia and start movement with a LOW velocity, then overcorrect resulting in an OVERshoot of the movement.
In individuals with Cb lesions who showed HYPOMETRIC movements, they tended to OVERestimate the limb inertia and start movement with a HIGH velocity, then overcorrect resulting in an UNDERshoot of the movement.
In cerebellar damage, we see impaired adaptability to changes in the ___ or ____. This results in a bias toward the [INTERNAL/ EXTERNAL ] model representation of limb dynamics; or, the model is “fixed” at a specific value & cannot adapt.
In cerebellar damage, we see impaired adaptability to changes in the LOAD or ENVIRONMENT (e.g. to internal vs external forces). This results in a bias toward the INTERNAL model representation of limb dynamics; or, the model is “fixed” at a specific value & cannot adapt.
In cerebellar damage, we see impaired precision, which results in an [increase / decrease ] in dysmetria most notable with [single / multi] joint movemoents. These individuals [can / cannot ] use feedback (e.g. _____) to compensate, but this results in [slowed / fast ] movement.
In cerebellar damage, we see impaired precision, which results in an INCREASE in dysmetria most notable with MULTI joint movements. These individuals CAN use feedback (e.g. VISION ) to compensate, but this results in SLOW movement.
Clinical features of Cb lesions include [incr/ decr] sway in quiet standing, [gait feature?],, impaired _____ (list ‘em!) eye movements, decreased ____, impaired [explicit/implicit] learning from errors & need to rely on [explicit /implicit] info, and learning/relearning balance/gait activities [is impossible / is faster / takes longer ]
Clinical features of Cb lesions include INCREASED SWAY in quiet standing, GAIT ATAXIA, impaired VORc, SACCADES, SMOOTH PURSUIT, VOR (which can result in dizziness, varied foot placement, less able to use visual feedback even though the Cb lesion makes you more reliant on visual feedback), decreased ADAPTABILITY (may take longer to learn balance or walk under different situations!), impaired IMPLICIT learning from errors & need to rely on EXPLICIT info (i.e. will need to think about movement, use more cognition & attention), and learning/relearning balance/gait activities TAKES LONGER.
What is the impact of Cb dysfunction on proprioception? Are proprioceptive tests intact or impaired w/Cb lesions?
With a pure Cb lesion, classic proprioceptive tests should be INTACT…
BUT…a Cb lesion impairs proprioception with active, self-driven movements, which we cannot clinically test. Pt may have impaired perception of active movement outcomes.
Impact of Cb lesion on endurance?
Cb lesion = pts move SLOWLY and INEFFICENTLY - they have to think about how they move! Impaired endurance can make this worse. 6MWT, monitor RPE & HDR can be helpful!
Gait ataxia is most associated with impaired ____ NOT impaired _____.
Cerebellar lesion + balance deficits -> [gait ataxia / few gait abnormalities ]
Cerebellar lesion + LE coordination deficits but NO balance deficits -> [gait ataxia / few gait abnormalities]
Gait ataxia is most associated with impaired BALANCE NOT impaired LIMB COORDINATION.
Cerebellar lesion + balance deficits -> GAIT ATAXIA
Cerebellar lesion + LE coordination deficits but NO balance deficits -> FEW GAIT ABNORMALITIES!
Anterior cerebellar lesion typically results in [low/high] velocity, [low/high] amplitude sway and [does / does not] improve with visual input.
Vestibulocerebellar lesion typically results in [low/high] frequency, [low/high] amplitude sway and [does / does not] improve with visual input.
Anterior cerebellar lesion typically results in HIGH velocity, LOW amplitude sway and DOES improve with visual input.
Vestibulocerebellar lesion typically results in LOW frequency, HIGH amplitude sway and DOES NOT improve with visual input - high fall risk!
What factors contribute to increased postural sway in Cb dysfunction?
Increased sway due to…
- Faulty muscle scaling: hypermetric balance responses
- Exaggerated and prolonged muscle activity
- Tend to “overshoot” the initial response to an external perturbation
CN I Component Function Attachment to CNS Cranial exit Testing?
CN I - Olfactory Nerve
SENSORY
Smell (olfaction)
Attaches to CNS via telencephalon (cerebrum)
Exits cranium via the CRIBIFORM PLATE of the ETHMOID bone (fracture here w/facial trauma may injure it)
Testing = assess smell (loss of olfactory fibers & decreased smell/taste is common in older adults)
CN II Component Function Attachment to CNS Cranial exit Injury mechanism? Testing?
CN II - Optic Nerve
SENSORY
VIsion
Attaches to CNS via diencephalon via optic chiasm
Exits cranium via the OPTIC CANAL of the SPHENOID BONE
Injury may occur via tumor (e.g. pituitary tumor) aneurysm (often internal carotid), edema, ischemia, inflammation, demyelnation, facial trauma
Test w/visual acuity: Snellen eye chart, book page, test 1 eye at a time, ?corrective lenses; confrontation/fields; color vision; fundus/optic discs
Testing for CN II
- Visual acuity (snellen, Book)
- Visual fields w/confrontation
- Test color vision/color matching
Test fundus (w/fundascope) & optic disc
CN II - why is it unique?
Central of peripheral?
Myelin sheath is formed by [oligodendrocytes / Schwann cells]
It [is / is not] susceptible to demyelinating effects of conditions such as MS.
Fibers [stay on 1 side / decussate and cross to other side]
Central!!! It’s the only central cranial nerve!
Myelin sheath is formed by OLIGODENDROCYTES
It IS susceptible to demyelinating effects of conditions such as MS.
Fibers DECUSSATE - half of fibers remain ipsilateral & other half go contralateral. Specific signs of CN II damage depend on on where in the tract there is damage (think optic tract pathways)
CN III
Component
Function
CN III - OCULOMOTOR
Somatic & visceral MOTOR
Somatic motor: to levator palpabrae superioris (raises eyelid)
Sup/med/inf rectus muscles
Visceral motor: constricts pupil via sphincter mm (efferent response) & accommodates eye (ciliary muscle)
Pupillary light reflex tests the sensory component ([afferent / efferent]) which is carried by CN ___, as well as the motor component ([afferent/efferent]) which is carried by CN ___.
Pupillary light reflex tests the sensory component (AFFERENT) which is carried by CN II (optic), as well as the motor component EFFERENT which is carried by CN III (oculomotor).
CN III
Attachment to CNS?
Cranial exit?
Mechanism of injury?
CN III - oculomotor
Attachment to CNS? MIDBRAIN
Cranial exit? SUPERIOR ORBITAL FISSURE of SPHENOID BONE
Mechanism of injury?
- trauma, tumor, infection, aneurysm increased ICP
Which CNs exit the cranium through the superior orbital fissure of the sphenoid bone?
CNs that exit the cranium through the superior orbital fissure of the sphenoid bone:
- CN III (oculomotor)
- CN IV (trochlear)
- CN V1 (trigeminal)
- CN VI (abducens)
How do you assess CN III?
CN III testing
- Look at symmetry of eye opening (is there ptosis?)
- Pupillary response to light (the motor component is carried by CN III) - both direct response, and consensual response on contralateral eyeball (involves CN II too); could be sluggish or absent, loss of consensual response on opposite response
- Pupil size & shape (mydriasis = blown pupil or enlarged vs other side)
- Test accommodation by focusing from far to near vision
- Visual tracking, look at EOMs
- Pt may endorse diplopia - commonly affected in PD due to impaired coordination between the two eyes, not necessarily a CN III problem
What is mydriasis? If it is present, what does it indicate?
Mydriasis = blown pupil or enlarged vs other side.
Indicates CN III impairment
CN IV Component Function Attachment to CNS? Cranial exit? Mechanism of injury?
CN IV - Trochlear
Component - somatic motor
Function - innervates superior oblique muscle to move eye inferoLATERALLY
Attachment to CNS? via midbrain
Cranial exit? superior orbital fissure of sphenoid bone
Mechanism of injury? Trauma, infection, or tumor
CN IV - how to test? Findings?
Testing: “visually track an object that is moved “down and in”
Abnormal = unable to look inferomedially (though the sup oblique makes the eye look down & OUT, testing with down & IN better isolates superior oblique action from the other extraocular muscles!)
May see upward drift of affected eye as pt looks down (e.g. to try to read)
Pt may report visual disturbance with reading or walking down stairs
Head will often tilt AWAY from involved eye
Talk me through the superior oblique muscle!
Action?
How to test?
What on earth is a trochlea?
CN IV - trochlear nerve, innervates superior oblique
Action: moves eye inferoLATERALLY
Test: have pt look inferoMEDIALLY (to isolate it from other extraocular muscles)
If impaired, may see difficulty looking down, eye may drift up w/attempts to look down
Trochlea = a pulley, which changes the direction of pull!
CN V
V1 = ___ n. (sensory/motor/both)
V2 = ___ n. (s/m/b)
V3 = ___ n. (s/m/b)
CN V: Trigeminal
V1 = Opthalmic nerve (sensory)
V2 = Maxillary nerve (sensory)
V3 = Mandibular nerve (mixed sensory & motor)
CN V1 Component Attachment to CNS Cranial Exit Injury mechanism
CN V1: Opthalmic nerve
Component: general sensoryt o membranes of face, nose, and conjunctiva
Attachment to CNS via PONS
Cranial Exit: superior orbital fissure of sphenoid bone
Injury mechanism: facial trauma, tumor, aneurysm
How do you test CN V
- V1/opthalmic nerve?
- V2/maxillary nerve?
- V3/mandibular nerve?
CN V1 /Trigeminal
- V1/Opthalmic is tested via…
- -> Sensation (sharp/dull or light touch) to skin of the front of the head & nose (terminates in supraorbital nerve)
- -> Corneal reflex
- V2/Maxillary: sensation to skin of upper jaw (terminates in infraorbital nerve)
- V3/Mandibular: sensation to skin of lower jaw; activation of mm of mastication; jaw jerk reflex (terminates in mental nerve)
CN V2 Component Attachment to CNS Cranial Exit Injury mechanism
CN V2: Trigeminal Nerve/Maxillary nerve
Component: general sensory to skin & mucous membranes of upper jaw & maxillary teeth
Attachment to CNS: via midbrain
Cranial Exit: foramen rotundum of sphenoid bone
Injury mechanism: facial trauma, tumor, infection, aneurysm
CN V3 Component Attachment to CNS Cranial Exit Injury mechanism
CN V3: Trigeminal Nerve/Mandibular Nerve
Component: 2 parts:
- General sensory to lower face, mandibular teeth, and tongue
- Special visceral motor (branchial motor) to all muscles of mastication, mylohyoid, anterior belly of digastric mm, tensor veli palatini (in palate), tensor tympani (in auditory canal)
Attachment to CNS via PONS
Cranial Exit: foramen ovale of sphenoid bone
Injury mechanism: facial trauma, tumor, infection, anerysm
Clinical findings for CN V dysfunction?
CN V Trigeminal dysfunction =
- Weakness/paralysis of muscles of mastication w/deviation TOWARD side of lesion (V3)
- Loss of sensation to face (V1,2,3)
- Los of corneal reflex (V1)
Common causes of trigeminal nerve pathology
Common causes of trigeminal nerve pathology
- Dental trauma
- Herpes zoster
- Cranial trauma
- Tumors
Idiopathic trigeminal neuropathy
- Trigeminal neuralgia (aka Tic Douloureaux) - most commonly V2>V3>v1 distribution, cause unknown but maybe related to blood vessel or other pathology of trigeminal ganglia
CN VI Component Function Attachment to CNS Cranial exit Mechanism of injury? Testing/Findings?
CN VI: Abducens Nerve
Component: Somatic motor
Function: Movement of eye via lateral rectus muscle
Attachment to CNS: junction of pons & medulla
Cranial exit: superior orbital fissure of sphenoid bone
Mechanism of injury? Trauma
Testing: visually track laterally
Abnormal = diplopia w/far vision, unable to move eye laterally (lateral rectus palsy)
CN VII
Component
Function
CN VII: Facial
Component: Special visceral motor (branchial motor), special sensory, visceral motor
Function:
- Sensory: taste to anterior 2/3 of tongue & palate
- Special Visceral Motor/Branchial Motor: muscles of facial expression & scalp, stylohyoid muscle, posterior belly of digastric mm, stapedius muscle
- Visceral motor: lacrimal, submandibular, sublingual glands, glands of nose & palate (parasympathetic)
CN VII Attachment to CNS Cranial exit Mechanism of injury? Testing/Findings?
CN VII: Facial
Attachment to CNS: pons & medulla
Cranial exit: a LONG course! via internal acoustic meatus of temporal bone, through facial canal of temporal bone, and ultimately out through the stylomastoid foramen of the temporal bone
Mechanism of injury? trauma, inflamlmation, infection
Testing/Findings? Ask pt to contract mm of facial expression, watch for symmetry (cheek puff, wrinkle forehead, close eyes, purse lips)
CN ___ is the most commonly paralyzed motor cranial nerve! It takes up ~80% of the cross sectional area of the ___ canal, which is why it’s susceptible in ___ palsy.
CN VII (FACIAL) is the most commonly paralyzed motor cranial nerve! It takes up to ~80% of the cross sectional area of the FACIAL canal, which is why it’s susceptible in BELL’S palsy.
Unilateral facial weakness/paralysis is commonly seen in ___ palsy. It indicates a(n) [LMN / UMN ] lesion if ipsilateral to the lesioned side, vs [LMN / UMN] lesion if contralateral to the lesioned side.
Unilateral facial weakness/paralysis is commonly seen in BELL’S palsy. It indicates a(n) LMN lesion if ipsilateral to the lesioned side, vs UMN lesion (e.g. CVA) if contralateral to the lesioned side (often see forehead sparing in UMN lesion due to bilateral innervation, vs no forehead sparing in LMN dz!).
Bilateral facial weakness/paralysis is seen in ___, ____, or ___ (diseases/diagnoses).
Bilateral facial weakness/paralysis is seen in GUILLAIN-BARRE, MYASTHENIA GRAVIS, or LYME DZ (diseases/diagnoses).
Abnormal findings with CN VII Facial nerve
- Weakness/paralysis of facial mm
- Loss/excessive salvation or lacrimation (less common w/LMN injury)
- Loss of taste from anterior 2/3 of tongue (less common w/LMN injury)
- Difficult speech, drooling
- Sensitivity to low frequency sound (stapedius muscle)
CN VIII Component Function Cranial Exit CNS attachment Injury mechanism
CN VIII: Vestibulocochlear Nerve
Special Sensory
Vestibular division: vestibular sensation from semicircular canals, utricle, & saccule
Cochlear division: special sense of hearing from spiral organ
Cranial Exit: internal acoustic meatus of temporal bone
CNS attachment at junction fo pons/medulla
Injured w/trauma, tumor (e.g. acoustic neuroma)
How to test for CN VIII dysfunction?
Test CN VIII via tests for conduction vs sensorineural hearing loss with Rinne and Weber test
Also via:
- Finger rub, whispered speech, watch tick, self-report
The Rinne test assesses [conduction / sensorineural ] hearing loss. A high pitched tuning fork is placed on the ____, then once pt can no longer hear it, the still-vibrating tuning fork is placed next to the ear to test for ____. You should still be able to hear it through the air!
The Rinne test assesses CONDUCTION hearing loss. A high pitched tuning fork is placed on the MASTOID PROCESS, then once pt can no longer hear it, the still-vibrating tuning fork is placed next to the ear to test for AIR CONDUCTION. You should still be able to hear it through the air!
The Weber test assesses [conduction / sensorineural ] hearing loss. A high pitched tuning fork is placed on the ____. You should be able to hear it equally through both ears!
The Weber test assesses SENSORINEURAL hearing loss. A high pitched tuning fork is placed on the TOP OF THE SKULL equidistant from both ears. You should be able to hear it equally through both ears! (vs pt may say one side sounds louder, which would be abnormal)
Abnormal CN VIII findings include…
Tinnitus
Abnormal findings on Rinne and Weber tests - warrant referral to a specialist
Vestibular findings (observation of nystagmus, observation or reports of LOB or vertigo)
CN IX Component Function Attachment to CNS Cranial Exit
CN IX: Glossopharyngela neve
Special visceral Motor /Branchial MOTOR to stylopharyngeus muscle for swallowing
Visceral MOTOR to parasympathetic to parotid gland
Visceral SENSATION to parotid gland, carotid body/sinus, pharynx, middle ear
Special SENSORY: taste to posteior 1/3 of tongue
General SENSORY: cutaneous sensation to external ear
CNS attachment via medulla
Cranial exit via jugular foramen of temporal & occipital bones
CN IX
Mechanism of injury
Of note, isolated CN IX lesions are [common / rare]
CN IX: Glossopharyngeal
Mechanism of injury: it has a large extracranial position which is susceptible to trauma (fractures, stab or gunshot wounds), also via tumor
Of note, isolated CN IX lesions are RARE
CN IX testing
Test CN IX (glossopharyngeal) via taste to the posterior 1/3 of tongue, use tongue depressor to assess position of uvula & gag reflex, assess swallowing
Abnormal CN IX findings include…
Loss of taste to posterior 1/3 of tongue
Loss of sensation on affected side of soft palate
Diminished gag/swallow reflex on affected side
Glossopharyngeal neuralgia: often associated w/swallowing & you see in pain in back of throat, tongue, or ear
CN ___, ___, and ___ are commonly involved together in a condition known as jugular foramen syndrome due to a ____.
CN IX, X, and XI are commonly involved together in a condition known as jugular foramen syndrome due to a TUMOR (or other space-occupying lesion).
CN X
Component & Function
CN X: Vagus
Visceral sensation: base of tongue, pharynx, larynx, trachea, bronchi, heart, esophagus, stomach, intestine to left colic flexure
Visceral motor: parasympathetics to smooth muscle fo trachea, bronchi, digestive tract, cardiac muscle
Branchial motor: motor to constrictor muscles of pharynx (excluding stylopharyngeus) for swallowing
Special sensory: taste from epiglottis & palate
Cutaneous sensory: auricle, external acoustic meatus, dura mater of posterior cranial fossa
CN X
Attachment to CNS
Cranial Exit
CN X: Vagus nerve
Attachment to CNS via medulla
Cranial Exit via jugular foramen of temporal & occipital bones
CN X
Mechanism of Injury
CN X
Mechanism of Injury: has a large extracranial position, susceptible to trauma (fractures, stab or gunshot wounds, neck surgery) or tumor
CN X Testing & abnormal findings
Isolated CN X lesions are [rare / common ]
CN IX & X are commonly tested together due to similar functions
Additional abnormal findings include loss of gag reflex, dysphagia, hoarseness
Isolated CN X lesions are RARE - seen more in conjunction w/ CN IX, X, and XI in jugular foramen syndrome
CN XI Component Function CNS attachment Cranial Exit Mechanism of Injury
CN XI: Spinal accessory nerve
Somatic motor: sternocleidomastoid and trapezius
CNS attachment: cranial root via the medulla, spinal root via the superior spinal cord
Cranial Exit: via the jugular foramen of the temporal and occipital bones
Mechanism of Injury: has a large subcutaneous extracranial position, susceptible to trauma (fractures, stab or gunshot wounds) or tumor
CN XI testing
MMT to sternocleidomastoid and trapezius muscles
Commonly involved al ongside CN IX, X, and XI in condition known as jugular foramen syndrome (tumor)
CN XII Function/component CNS attachment Cranial Exit Mechanism of Injury Testing
CN XII: Hypoglossal
Somatic motor: tongue muscles
Cranial exit via hypoglossal canal
MOI: least common CN injury from head trauma! Most common MOI is neck surgery
Testing: protrude & retract tongue, look for deviations; observe for dysphagia, dysarthria, chewing difficulties
Abnormal CN XII findings
Tongue deviation TOWARD the AFFECTED SIDE on protrusion
Purely sensory CNs include…
SENSORY only:
- CN I/olfactory
- CN II/optic
- CN VIII/vestibulocochlear
Purely motor CNs include…
MOTOR only:
- CN III/oculomotor
- CN IV/trochlear
- CN VI/abducens
- CN XI/spinal accessory nerve
- CN XII/hypoglossal
Mixed sensory and motor CNs include…
MIXED sensory & motor CNs:
- CN V/trigeminal
- CN VII/facial
- CN IX/glossopharyngeal
- CN X/vagus
Spinal nerves... [X] pairs, which include... [X] cervical [X] thoracic [X] lumbar [X] sacral [X] coccygeal
They are [sensory / motor / mixed]
Spinal nerves... [31] pairs, which include... [8] cervical (but recall, only 7 cervical vertibrae!) [12] thoracic [5] lumbar [5] sacral [1] coccygeal
They can be sensory, motor, or mixed!
In upper cervical spine, spinal nerve exits [above/below] vertibrae, then from ___ and down, it exits [above/below] corresponding vertibrae
In upper cervical spine, spinal nerve exits ABOVE vertebrae, then from C8 and down, it exits BELOW corresponding vertebrae (C8 exits below C7, then T1 below T1 vertebra, etc)
Entering the spinal cord, the dorsal ___ and the dorsal ___ ____ carry [SENSORY / MOTOR] information into the dorsal horn of [gray/white] matter of the spinal cord.
The ventral ___ emerges from the ventral ___ of the spinal cord and carries [SENSORY / MOTOR] information out to the periphery.
The ventral and dorsal ___s combine to create the ____.
Leaving the spinal cord, the spinal nerve splits into the dorsal and ventral ___.
Entering the spinal cord, the dorsal ROOT and the dorsal ROOT GANGLION carry SENSORY information into the dorsal horn of GRAY matter of the spinal cord.
The ventral ROOT emerges from the ventral HORN of the spinal cord and carries MOTOR information out to the periphery.
The ventral and dorsal ROOTS combine to create the SPINAL NERVE.
Leaving the spinal cord, the spinal nerve splits into the dorsal and ventral RAMUS.
The spinal nerve is a [one-way / two-way] nerve. [Efferent / afferent / both efferent and afferent ] signals travel through the spinal nerve.
The spinal nerve is a TWO WAY nerve. BOTH EFFERENT & AFFERENT signals travel through the spinal nerve.
The dorsal ramus is a [one-way / two-way] nerve, carrying [efferent / afferent / both efferent and afferent ] signals. Describe what (if any) sensory/motor information it carries.
The dorsal ramus is a TWO-WAY nerve, carrying both EFFERENT & AFFERENT (sensory & motor) signals, including:
- Motor information to the muscles of the deep back
- Sensory information from the skin of the back
The ventral ramus is a [one-way / two-way] nerve, carrying [efferent / afferent / both efferent and afferent ] signals. Describe what (if any) sensory/motor information it carries.
The ventral ramus is a TWO-WAY nerve, carrying both EFFERENT & AFFERENT (sensory & motor) signals, including:
- Motor information to the muscles of the anterior thorax & extremities
- Sensory information from the skin of the anterior thorax & extremities
Peripheral nerve connective tissue coverings are extensions of the spinal meninges. The ___ is an extension of the dura mater that surrounds the entire nerve trunk. The ____ is an extension of the arachnoid that wraps bundles of fibers into fascicles. The ___ surrounds each individual axon.
Peripheral nerve connective tissue coverings are extensions of the spinal meninges. The EPINEURIUM is an extension of the dura mater that surrounds the entire nerve trunk. The PERINEURIUM (inside of the nerve!) is an extension of the arachnoid that wraps bundles of fibers into fascicles. The ENDONEURIUM surrounds each individual axon.
In myelinated peripheral nerve fibers, ___ cells are located between the [nerve connective tissue layer] and the membrane of the axon (aka the ___).
In myelinated peripheral nerve fibers, SCHWANN cells are located between the ENDONEURIUM and the membrane of the axon (aka the AXOLEMMA).
Are peripheral nerves vascularized?
Yes! Each peripheral nerve receives an artery that penetrates THROUGH EACH connective tissue layer to give rich vascular supply
In peripheral nerves, the motor neuron cell bodies are located in the ___. The sensory neuron cell bodies are located in the ___. The autonomic neuron cell bodies are located in the ___, ___, and ___.
In peripheral nerves, the motor neuron cell bodies are located in the VENTRAL HORN OF THE SPINAL CORD. The sensory neuron cell bodies are located in the PERIPHERAL/DORSAL ROOT GANGLIA. The autonomic neuron cell bodies are located in the BRAINSTEM, SPINAL CORD, and PERIPHERAL GANGLIA.
Myelination significantly increases conduction velocity through ____ conduction of ___ at the ____.
Thicker myelinated fibers conduct [faster / slower]. These are involved in [sensation type?] and serve [muscle type?]
Thinner myelinated fibers conduct [faster/ slower] and transmit signals for [sensory type?] as well as [muscle type?]
Myelination significantly increases conduction velocity through SALTATORY conduction of ACTION POTENTIALS at the NODES OF RANVIER.
Thicker myelinated fibers conduct FASTER. These are involved in PROPRIOCEPTIVE SENSE (e.g. to muscle spindle & golgi tendon organ) and serve SKELETAL MUSCLE FIBERS (via alpha motor neurons)
Thinner myelinated fibers conduct SLOWER and transmit signals for PAIN, TEMPERATURE, AND TOUCH as well as AUTONOMIC SIGNALS TO AND FROM THE GANGLIA TO SMOOTH MUSCLE
Age related changes to PNS
- Perineurium and epineurium [thin / thicken ]
- Endoneurium gets ___ with increased ___ content
- Overall [increased / decreased ] number of [myelinated / unmyelinated / both] fibers
- [Ventral (motor) / dorsal (sensory) ] root fibers are more affected.
- We see generalized deterioration of the ___
- Perineurium and epineurium THIN
- Endoneurium gets FIBROTIC with increased COLLAGEN content
- Overall DECREASED number of BOTH myelinated and unmyelinated fibers
- VENTRAL (MOTOR) root fibers are more affected than dorsal (sensory) root fibers.
- We see generalized deterioration of the MYELIN SHEATH (likely r/t decreased protein synthesis as we age)
Age related changes to PNS (continued)
- ___ may occlude vessels supplying nerves, leading to a loss of ___ and development of ___
- Dysfunction of the ___ nervous system, including decline of sympathetic control of ___ , which leads to decreased ___ healing
- Decreased ___ synthesis leads to deterioration of ___ with shorter internode distances, leading to decreased nerve conduction velocity
Age related changes to PNS (continued)
- ATHEROSCLEROTIC PLAQUES may occlude vessels supplying nerves, leading to a loss of NERVE FIBERS and development of PERIPHERAL NEUROPATHIES
- Dysfunction of the AUTONOMIC nervous system, including decline of sympathetic control of DERMAL VASCULATURE (leads to decreased WOUND healing)
- Decreased PROTEIN synthesis leads to deterioration of MYELIN with shorter internode distances, leading to decreased nerve conduction velocity
Peripheral nerve injuries can be the result of ___, ___, or ___ injuries. From least involved to most involved (based on what structures are affected), we call these ___, then ___, then ___.
Peripheral nerve injuries can be the result of ISCHEMIA, COMPRESSION, or STRETCH (ie traction) injuries; transection can also occur. From least involved to most involved (based on what structures are affected), we call these NEURAPRAXIAS, then AXONOTMESIS, then NEUROTMESIS.
Neurapraxia involves segmental ___. It is the [mildest / most severe] type of nerve injury and involves a [permanent /transient ] conduction block usually as a result of [ischemia / compression / stretch ]. It slows or blocks the action potential, and connective tissue coverings of the nerve [remain intact / are severed]. When this occurs in the setting of disease (e.g. MS), we call this a ___. Muscle typically [atrophies / does not atrophy] because action potentials are normally above and below the site of injury. Schwann cells can become ____ active to repair. We [ do / do not] see axonal/Wallerian degeneration. Prognosis/timing?
Neurapraxia involves segmental DEMYELINATION. It is the MILDEST type of nerve injury and involves a TRANSIENT conduction block usually as a result of COMPRESSION. It slows or blocks the action potential, and connective tissue coverings of the nerve REMAIN INTACT.
When this occurs in the setting of disease (e.g. MS), we call this a MYELINOPATHY. Muscle typically DOES NOT ATROPHY because action potentials are normally above and below the site of injury. Schwann cells can become MITOTICALLY active to repair. We DO NOT see axonal/Wallerian degeneration. Prognosis is GOOD! Expect a GRADUAL & FULL RECOVERY of symptoms in DAYS to WEEKS.
Axontomesis involves ____ degeneration. The ___ is damaged but __ ___ coverings remain intact. This most commonly occurs as a result of [compression / stretch / ischemia ], such as ____, but can also happen as a result of __ or ___ type injuries. It leads to ___ and ___. You get degeneration distal to site of the injury where the ___ breaks down, which is known as ____ ___ and begins with in ___ hours/days post-injury. Repair is [impossible / possible] as long as the ___ ___ ___ is intact. New axons sprout from damaged ___, but the [proximal / distal / proximal and distal ] end(s) of the
____ ___ ___ MUST be intact for healing to take place. Prognostically, we expect healing over the course of [days/ weeks/ months/ years] [without / with possibility of / with definite] residual deficits.
Axontomesis involves AXONAL degeneration. The AXON is damaged but CONNECTIVE TISSUE coverings remain intact. Most common via COMPRESSION, (e.g. CARPAL TUNNEL), but can also happen as a result of STRETCH or BLUNT TRAUMA type injuries. It leads to INFARCTION AND NECROSIS. You get degeneration distal to site of the injury where the AXON breaks down, known as WALLERIAN DEGENERATION and begins within 12 HOURS post-injury. Repair is POSSIBLE as long as the NERVE CELL BODY is intact. New axons sprout from damaged AXON, but PROXIMAL AND DISTAL ends of NEURAL TISSUE TUBE must be intact for healing to take place. Can also happen in stretch or blunt trauma type injuries. Prognostically, we expect healing over the course of WEEKS TO MONTHS WITH THE POSSIBILITY OF residual deficits.
Neurotmesis is most severe ___ loss, involving complete severance of the ___ and disruption of one to all of the three ___ ___ coverings. This is common in [compression / stretch / ischemia / trauma], such as ____, ____, and ___-type injuries. Axonal continuity is [maintained / lost], resulting in ___ ____ distal to the site of injury. Muscle fibers innervated by the axon [remain intact / atrophy slowly / atrophy rapidly], which is a process known as ___ ___, with irreversible damage after [X timeframe]. Recovery [involves spontaneous reattachment of / generally requires surgical intervention to reattach ] the proximal & distal ends of the ____, otherwise a ___ will often form. Once the axon has distal contact with the ___ or __ ___, _____ can then begin. Repair process begins with sprouting of a new ___ ___ as new ____ is synthesized. ____ degrade waste tissues, facilitating axonal entry into tissue. ___ and ___ cues guide ___ through the [epineurium / perineurium / endoneurium]. Growth rate is typically ____/day or ___/month. Residual deficits are [uncommon / likely / definite].
Neurotmesis is most severe AXONAL loss, involving complete severance of the AXON and disruption of 1, 2, or all 3 of the CONNECTIVE TISSUE coverings. This is common in TRAUMA such as GUNSHOT, STAB WOUNDS, and AVULSION-TYPE injuries. Axonal continuity is LOST, resulting in WALLERIAN DEGENERATION distal to the site of injury. Muscle fibers innervated by the axon atrophy RAPIDLY, a process known as DENERVATION ATROPHY, after 2 YEARS, those muscle fibers actually undergo irreversible damage. Recovery generally requires SURGERY to reattach the proximal & distal ends of the ENDONEURIUM, otherwise a NEUROMA will often form. Once the axon has distal contact with the MUSCLE or SENSORY RECEPTOR, MYELINATION can then begin. Repair process begins with sprouting of a new GROWTH CONE as new CYTOPLASM is synthesized. PROTEASES degrade waste tissues, facilitating axonal entry into tissue. CHEMICAL and TACTILE cues guide filopodia through ENDONEURIUM. Growth rate is typically 1mm/day or 1”/month. Residual deficits are LIKELY.
Clinical manifestations of peripheral nerve injuries follow those typical of [UMN/LMN] injuries:
- [flaccid paralysis / spasticity ] of muscles distal to the site of the lesion.
- Rapid ____ of involved musculature
- [preservation / loss of ] sensory function distal to the site of the lesion.
Clinical manifestations of peripheral nerve injuries follow those typical of LMN injuries:
- FLACCID PARALYSIS of muscles distal to the site of the lesion.
- Rapid ATROPHY of involved musculature
- LOSS OF sensory function distal to the site of the lesion.
Neurapraxia (1st degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.
Neurapraxia (1st degree): involves ONLY Myelin. Associated with MINOR COMPRESSION injury. There is a conduction BLOCKAGE (though not conduction failure). We see PROFOUND motor loss lasting days to weeks, but no muscle wasting. Normal to minimal sensory involvement.
Axonotmesis (2nd degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.
Axonotmesis (2nd degree) involves the myelin AND axon. Associated with SEVERE COMPRESSION/crush injury. There is a conduction FAILURE. We see COMPLETE motor loss and NO or PARTIAL sensory loss.
Neurotmesis (3rd degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.
Neurotmesis 3rd degree involves the MYELIN, AXON, and ENDONEURIUM. Associated with TRANSECTION, LACERATION, or CHEMICAL injury. There is a conduction FAILURE. We see COMPLETE motor loss and COMPLETE sensory loss.
Neurotmesis (4th degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.
Neurotmesis 4th degree involves the MYELIN, AXON, ENDONEURIUM, and PERINEURIUM. Associated with TRANSECTION, LACERATION, or CHEMICAL injury. There is a conduction FAILURE. We see COMPLETE motor loss and COMPLETE sensory loss.
Neurotmesis (5th degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.
Neurotmesis 4th degree involves the MYELIN, AXON, ENDONEURIUM, PERINEURIUM, and EPINEURIUM (all the layers). Associated with TRANSECTION, LACERATION, or CHEMICAL injury. There is a conduction FAILURE. We see COMPLETE motor loss and COMPLETE sensory loss.
Prevalence of peripheral neuropathy is estimated at ___% in the general population and ___% in those over 55 years of age. There [is only one etiology /are multiple etiologies ] which present with a [consistent/ varied] clinical picture. If you see [acute / chronic] onset, [slow / rapid ] progression, and [mild / moderate / severe ] disability, you need to refer to a specialist.
Prevalence of peripheral neuropathy is estimated at 2.5% in the general population and 8% in those over 55 years of age. There ARE MULTIPLE ETIOLOGIES which present with a VARIED clinical picture. If you see ACUTE onset, RAPID progression, and SEVERE disability, you need to refer to a specialist.
Prevalence of peripheral neuropathy is estimated at ___% in the general population and ___% in those over 55 years of age. There [is only one etiology /are multiple etiologies ] which present with a [consistent/ varied] clinical picture. If you see [acute / chronic] onset, [slow / rapid ] progression, and [mild / moderate / severe ] disability, you need to refer to a specialist given concern for something like ____.
Prevalence of peripheral neuropathy is estimated at 2.5% in the general population and 8% in those over 55 years of age. There ARE MULTIPLE ETIOLOGIES which present with a VARIED clinical picture. If you see ACUTE onset, RAPID progression, and SEVERE disability, you need to refer to a specialist given concern for something like GUILLAN BARRE SYNDROME, which is a medical emergency given risk for respiratory failure.
PNS disorders are classified into two categories: neuropathies involve a pathological condition confined to the ___, whereas myopathies involve a pathological condition confined to the ___.
PNS disorders are classified into two categories: neuropathies involve a pathological condition confined to the NERVE, whereas myopathies involve a pathological condition confined to the MUSCLE.
Peripheral nerves can be impaired at varied sites.
For motor nerves? (4)
For sensory nerves? (3)
Peripheral nerves can be impaired at varied sites.
For motor nerves? Motor neuron cell body, axon motor end plate, and muscle fiber
For sensory nerves? Cell body in the DRG, axon, and sensory receptor
