Midterm Two Content Flashcards
Types of sensory modalities
Proprioception, light/discriminatory touch, deep/crude touch, vibration, pain, temperature
What are dermatomes
Sensory areas of the body that are innervated by a particular spinal cord segment
What are the main ascending sensory pathways
The posterior column-medial lemniscus (PCML) pathway and the anterolateral pathway
PCML pathway (where and what)
Travels through posterior column of spinal cord and ultimately travels through the medial lemniscus
Made up of larger myelinated afferent fibers and controls mainly:
- Vibration
- Proprioception
- Light/discriminatory touch
Anterolateral pathway (where and what)
Travels through anterolateral region of spinal cord
Made up of smaller unmyelinated afferent fibers and controls mainly:
- Pain
- Temperature
- Deep/crude touch
Where do the primary sensory neuron bodies sit
The dorsal root ganglion
Fasciculus gracilis (where and what)
Located in the medial region of the posterior column
Carries leg and lower trunk (below T6) information
Fasciculus cuneatus (where and what)
Located in the lateral region of the posterior column
Carries upper trunk (above T6), arm, and neck information
What do axons in fasciculus gracilis synapse onto
Nucleus gracilis at the level of the caudal medulla
What do axons in fasciculus cuneatus synapse onto
Nucleus cuneatus at the level of the caudal medulla
Primary somatosensory cortex location
Postcentral gyrus
What are the three ascending pathways that make up the anterolateral pathway
- Spinothalamic tract
- Spinoreticular tract
- Spinomesencephalic tract
Spinothalamic tract (where and what)
Goes from the spinal cord to the thalamus
Mediates discriminative aspects of pain and temperature
Spinoreticular tract (where and what)
Goes from the spinal cord to the reticular formation
Responsible for conveying the emotional and arousal aspects of pain
Spinomesencephalic tract (where and what)
Innervate at the level of the midbrain (periaqueductal gray area)
Participates in the central modulation of pain
Thalamus role
Primary area of integration of sensory information, cerebellar and basal ganglia inputs
PCML sensory neuron order
First-order sensory neurons that have axons in the gracile and cuneate fasciculi synapse onto second-order neurons in the nucleus gracilis and nucleus cuneatus
Axons of second-order neurons cross midline at level of the caudal medulla (internal arcuate fibers) and form/enter the medial lemniscus on the other side of the medulla
The medial lemniscus axons terminate in thalamus and project through the posterior limb of the internal capsule to the primary somatosensory cortex in the postcentral gyrus
Anterolateral sensory neuron order
These axons first synapse in the gray matter of the spinal cord in the dorsal horn
Axons for second-order sensory neurons cross the midline through the anterior commissure (band of white matter) to ascend in the anterolateral white matter
- Takes two to three spinal segments for the fibers to reach the opposite side
Second-order sensory neurons go up the spinal cord and brainstem to synapse on third-order sensory neurons in the thalamus
Third-order sensory neurons project to the somatosensory cortex
Negative symptoms vs. Positive symptoms
Negative = subtraction of normal sensation
Positive = addition of normal sensation
PCML pathway negative symptoms
- Loss of position and vibration sense
- Loss of discriminatory touch
- Astereognosis
- Sensory ataxia
What is astereognosis
The inability to recognize objects by touch
What is sensory ataxia
Unsteady balance and gait/poorly coordinated movement
Characteristics of tabetic/ataxic gait
Due to loss of proprioception of the legs:
- High stepping (excessive knee bending)
- Floot flapping (foot slaps down)
- Unsteady gait (feet cross over + wide leg stance)
What happens when there is primary sensory neuron damage coming into the spinal cord
Loss of deep tendon reflexes (hyporeflexia) occurs. This does not occur when there is primary sensory neuron damage above the spinal cord
Spinothalamic (anterolateral) pathway negative symptoms
- Loss of pain and temperature sensation
- Reduced touch sensation
PCML pathway positive symptoms
- Tingling/numb sensation
- Paresthesia/dysesthesia
What is paresthesia/dysesthesia
Abnormal but not painful sensations
Anterolateral pathway positive symptoms
- Excessive sharpness, burning, or searing pain sensations
- Hyperpathia
- Allodynia
What is hyperpathia
Excessive pain to a normal stimuli
What is allodynia
Pain sensations to stimuli not normally painful
Primary sensory neuron positive symptoms
- Radicular pain, numbness, and tingling sensations that travel down the dermatome
What is CN V
The trigeminal nerve
Trigeminal nerve branches
V1, V2, and V3
What sits in merkels cave
The trigeminal ganglion which contains the cell bodies of the trigeminal nucleus
What is the trigeminal nucleus consist of
Made up of three separate nuclei:
- Mesencephalic
- Chief sensory
- Spinal trigeminal
Chief trigeminal sensory nucleus (what and where)
Receives all nerves and receptors related to fine touch
- Sits in the rostral and medial part of the pons
Spinal trigeminal nucleus (what and where)
Receives information about crude touch, pain, and temperature
- Runs from caudal region of medulla to the rostral region of the spinal cord
Where do somatosensory cortex symptoms occur and what modalities are involved
Contralateral to lesion
- Discriminative touch and joint position sense most affected (but all modalities may be involved)
Where do lateral pons symptoms occur and what modalities are involved
- Body on contralateral side (pain and temperature)
- Face on ipsilateral side (pain and temperature)
Where do thalamus symptoms occur and what modalities are involved
- Body and face on contralateral side (all sensory modalities)
What injuries are involved with transverse cord lesions
- Lower motor neuron symptoms at level of injury on both sides
- Upper motor neuron symptoms below level of the injury on both sides
- PCML damage symptoms for dermatomes at and below level of the injury on both sides
- Anterolateral damage symptoms for dermatomes at and below level of the injury on both sides
What injuries are involved with central cord lesions
Anterolateral damage symptoms for the single dermatome one level below the injury on both sides
What injuries are involved with posterior cord lesions
- PCML damage symptoms for dermatomes at (possibly) and below the injury on both sides
What injuries are involved with anterior cord lesions
- Lower motor neuron symptoms at level of injury on both sides
- Upper motor neuron symptoms below level of injury on both sides
- Anterolateral damage symptoms for dermatomes starting one level below the injury on both sides
What injuries are involved with hemicord cord lesions
- Lower motor neuron symptoms at level of injury on the ipsilateral side
- Upper motor neuron symptoms below level of injury ipsilaterally
- PCML damage symptoms for dermatomes at and below the injury ipsilaterally
- Anterolateral damage symptoms for the dermatome at the level of injury ipsilaterally and possibly all segments starting one to two levels below the injury contralaterally
What are internal arcuate fibers
The region of axons that cross the midline at the level of the caudal medulla
What is syringomyelia
It is a fluid-filled cavity in the spinal cord that causes displacement
What is another name for hemicord lesions
Brown-Sequard Syndrome
Transverse cord lesion causes
- Trauma
- Tumors
- Multiple sclerosis
Central cord lesion causes
- Syringomyelia
- Tumors
- Multiple sclerosis
Posterior cord lesion causes
- Trauma
- Tumors
- Multiple sclerosis
- Vitman B12 deficiency
- Tabes dorsalis
Anterior cord lesion causes
- Trauma
- Tumors
- Multiple sclerosis
- Infarct
Hemicord cord lesion causes
- Penetration trauma
- Compression from tumours
- Multiple sclerosis
Herpes zoster/shingles (what and how)
Sensory disorder that causes allodynia, paresthesia, and rash along specific dermatomes
Caused by dormant chicken pox viruses that lie in the dorsal root ganglion re-emerging and growing down the sensory nerve
Tabes dorsalis (what and how)
Sensory disorder that causes the slow degeneration of the dorsal column, dorsal roots, and ganglia of the spinal cord (typically lumbar regions)
- Proprioceptive loss
- Paresthesia
- Allodynia
- Tabetic/ataxic gait
Cause by prolonged (10-30 years) untreated syphilis
What is a neuropathy
A nerve disorder that can influence the axon, myelin, or both
Mononeuropathy (what)
Involves one nerve (focal)
Polyneuropathy (what)
Involves many nerves (general)
Diabetic neuropathy
Typically affects distal limbs by causing sensation loss in the hands and feet
- Paresthesia/allodynia
- Poor blood supply to fine nerve endings in the distal limbs
- Inflammation of nerves
- Can cause muscle weakness and loss
- Gradual onset
Overdose of pyridoxine (Vitamin B6)
Excessive amounts of Vitamin B6 causes degeneration of nerves across the body
- Impacts large myelinated fibers (PCML pathway)
Anything over 200mg of Vitamin B6 is neurotoxic
- RDA ~1.7mg
Ganglionopathies (what)
Involves damaging the ganglions
- Typically occurs from an autoimmune response
Polyneuritis (what)
Inflammation and infection of multiple sensory nerves
Vestibular system (where)
In the inner ear within the petrous ridge of the temporal bone
Perilymph vs. Endolymph
Peri = around
- Fills the bony labyrinth
Endo = inside
- Fills membranous labyrinth (ducts and sacs)
What are the otolith organs
The utricle and saccule
- Part of the membranous labyrinth
What and where are the three semi-circular canals
- Anterior
- Posterior
- Horizontal
All come off of and return to the utricle
Ampulla (where)
Adjacent to the utricle on the end where the semi-circular canals bulges out
What fills the ampulla
Gelatinous material called the cupola
What is on the floor of the ampulla
Crista ampullaris
What is embedded in the crista ampullaris
Hair cells
What projects from the hair cells/crista ampullaris
Cilia
What makes up a bundle of cilia
- A large and stiff kinocilia
- Stereocilia lined up from smallest to largest with the largest surrounding the kinocilia
What do the kinocilia and stereocilia do
Help determine the direction/motion of the head
What occurs when the stereocilia move toward the kinocilia
Excitation = increased firing rate/impulse frequency
What occurs when the stereocilia move away from the kinocilia
Inhibition = decreased firing rate/impulse frequency
What do the semi-circular canals detect
Angular acceleration
What do the otoliths detect
Linear acceleration and the effects of gravity
What is the resting discharge rate of the cilia at rest
100Hz
What occurs when the stereocilia move toward/away from utricle in the horizontal semi-circular canal
- Hair cells toward the utricle = increased firing rate
- Hair cells away from utricle = decreased firing rate
What occurs when the stereocilia move toward/away from utricle in the anterior/posterior semi-circular canal
- Hair cells toward the utricle = decreased firing rate
- Hair cells away from utricle = increased firing rate
Otolith organ structure
Consists of macula that have hair cells embedded in it.
On top of the macula is the otolithic membrane within which cilia are embedded.
On top of the otolithic membrane are otoconia/otoliths.
The otolith organs detect linear acceleration and head tilt when movement pulls on the otoliths which activate the cilia attached to the hair cells embedded in otolithic membrane
Hair cell receptors have axons projecting to cell bodies in the vestibular ganglion
Orientation of hair cells in utricle vs. saccule
- Utricle = hair cells project vertically (otoliths on floor)
- Saccule = hair cells project horizontally (otoliths on wall)
Where do the cell bodies of vestibular afferents sit
The vestibular ganglion
Where do vestibular afferent axons travel
Via the vestibulocochlear nerve (CN VIII) to the ipsilateral vestibular nuclei in the pons and medulla
What are the four vestibular nuclei
- Lateral VN
- Medial VN
- Superior VN
- Inferior VN
Where do lateral VN axons descend
Ipsilaterally with the lateral vestibulospinal tract
- Controls balance reflexes and extensor tone in limbs
Where do medial and inferior VN axons descend
Bilaterally with the medial vestibulospinal tract
- Controls positioning of head, neck, and upper trunk
- Controls vestibulocollic reflexes
What are vestibulocollic reflexes
The interaction between the vestibular system and the neck muscle to keep your head in space while your body is moving
Where do the superior and medial VN project
They project via the medial longitudinal fascicules to the:
- Oculomotor nucleus
- Trochlear nucleus
- Abducens nucleus
Responsible for controlling eye muscles/reflexes
Where else does the superior VN project
Projects bilaterally to the vestibular cortex via the thalamus
Reciprocal projections with cerebellum control what
Controls largely balance, eye control, and movement coordination
What is the operculum
The primary vestibular cortex
- Located in the inferior part of the parietal cortex deep within the sylvian fissure
What is the vestibuloocular reflex
Eyes move in the opposite direction of head movement but the same direction of the cupula in the semi-circular canals to allow eyes to maintain a stable gaze when moving
What is nystagmus
Continual vestibular stimuli leads to a beating eye effect that consists of:
- Slow phase
- Fast phase
Direction of nystagmus is named after the direction the eyes are moving during fast phase
Different nystagmus tests
- Spinning chair thing
- Head impulse tests
- Caloric irrigation test
What is the caloric irrigation test
Putting either cold or hot water in your ears
- Cold water causes nystagmus in the opposite direction of the ear being irrigated
- Hot water causes nystagmus in the same direction as the ear being irrigated
- COWS
What are vestibular evoked myogenic potentials
Tests for otolith function that utilize short-duration auditory tones to take advantage of the otolith influence on the vestibulospinal and vestiboloocular pathways
What happens with a vestibular evoked myogenic potential
The auditory tones evoke a response in tonically active muscles
- Ipsilateral SCM
- Contralateral eye
- Ipsilateral soleus
What are peripheral vestibular lesions
Damage to either the bony or membranous labyrinths or vestibulocochlear nerve
What are central vestibular lesions
Damage to vestibular nuclei or pathways projecting to brainstem, thalamus, cerebellum, or down the spinal cord
Unilateral vestibular lesions (what)
Lesions to one side of the vestibular system
Unilateral vestibular lesion symptoms
- Vertigo
- Nausea
- Postural instability
- Abnormal vestibuloocular reflex
- Abnormal vestibular evoked myogenic potentials
What is vertigo
True vertigo is the spinning sensation of movement due to spontaneous nystagmus triggered by the unilateral vestibular lesion
What causes nausea
- Sensory mismatch or conflict
- Vestibular autonomic connections
What causes postural instability
- Unbalanced balance reflex
- Loss of awareness or orientaton of body in space
Unilateral vestibular lesion causes
- Tumors
- Vestibular neuritis
- Surgery
- Meniere’s disease
- Perilymph fistula
- Benign paroxysmal peripheral nystagmus/vertigo
What is vestibular neuritis
Viral infection of vestibular cochlear nerve that causes nausea, vertigo, and severe balance issues
Types of unilateral vestibular surgeries
- Labyrinthectomy
- Purposeful chemical or surgical damage to labyrinths or the semicircular canals
- Vestibular nerve section
- Purposefully removing parts of the nerve or nicking the nerve during surgery
What is Meniere’s disease
An episodic disease that causes vestibular and hearing deficits
Potential mechanisms:
- Endolymphatic high drop
- Endolymph fluid cannot get to the endolymphatic sac causing increase endolymph volume and pressure
- Small ruptures of membranous labyrinths
- Mixing of perilymph and endolymph fluid that changes the ionic concentrations
What is a perilymph fistula
Traumatic injury or severe pressure damage
- The round or oval window (membranes that separate the middle and inner ear) ruptures allowing pressure changes to affect inner ear (perilymph fluid leaks out)
- Abnormal nystagmus triggered with additional pressure causing vertigo
What is benign paroxysmal peripheral nystagmus/vertigo
Brief attacks of vertigo or vestibular systems only when there are changes in head position relative to gravity
- Otoconia dislodge from otolith membrane and move to posterior semi-circular canal
- Movement causes a big wave that triggers response
What is the maneuver to identify benign paroxysmal peripheral nystagmus/vertigo
Dix-Hallpike maneuver
- Put person in position that aligns the posterior canal with gravity
- Rapidly drop the person to be laying down
- BPPN happens 10-15s after being laid down
- VOR and nystagmus are torsional and lasts 30-40s
- Rapidly sit them back up and repsonse occurs in the other direction
How is paroxysmal peripheral nystagmus/vertigo treated
The epley maneuver
- Moving the head around through a series of rotations to dislodge the otoconia
What are bilateral vestibular lesions, symptoms, and causes
The complete loss of vestibular function and symptoms include:
- Postural instability (worse without vision)
- Blurry vision (when moving and fixating)
Causes:
- Ototoxic medication (gentamicin)
- Meningitis (in early age <1)
- Meniere’s disease
Testing for central vestibular lesions
Optokinetic reflex
- Eyes normally follow images moving by your eyes going back and forth to keep the images steady
Optokinetic reflex involves medial vestibular nucleus
- Adjusts eye position to reduce retinal slip
Damage to the medial vestibular nucleus will damage reflex and you would not be able to focus on images moving
- No eye movement back and forth
What system is the vestibular nuclei involved with
Both the central and peripheral vestibular system
Damage to vestibular nuclei (peripheral and central damage)
- Abnormal VOR
- Abnormal optokinetic reflex
Only central damage
- Normal VOR
- Abnormal optokinetic reflex
Only peripheral damage
- Abnormal VOR
- Normal optokinetic reflex
What do primary cortical areas process
The basic elements/raw information of a sense or motor function
What does the primary sensory cortex do
Localizes and identifies sensory stimuli
What does the primary motor cortex do
Triggers and executes general movement commands
What are unimodal association areas
Areas responsible for higher-level processing for one modality
What are multi/heteromodal association areas
Higher-level processing that integrates many sensory modalities
Motor association cortex (function and what)
Involved in formulating motor programs for complex movements
Made up of:
- Pre-motor cortex
- Supplementary motor area
Somatotopic organization of motor association cortex
The leg section of these areas are all next to each other:
- Primary motor cortex
- Pre-motor cortex
- Supplementary motor area
Motor association cortex output
Project information primarily to the primary motor cortex for contralateral movements
- Also project to brainstem and spinal cord
Makes up 50% of the corticospinal tracts with direct connections from sensory and motor association areas
Pre-motor cortex (where and what)
Runs down the lateral surface of the brain
Coordinates muscle activity and movement across multiple joints in the same limb
Primarily involved in preparation for voluntary movement
Pre-motor cortex lesions
Causes the inability to initiate an appropriate movement for a given external cue or coordinate multi-joint movement
Supplementary motor area (where and what)
Runs anterior-posterior in the superior and medial surface of the cortex
Involved in planning and performing complex sequences of movement and bilateral coordination of movement
Supplementary motor area lesions
Deficits in bimanual coordination and an inability to perform complex acts requiring sequences of muscle contractions or a planned strategy (apraxia)
Somatosensory association cortex (what)
Gives meaning the the sensory information coming into the brain
Somatosensory association cortex lesions
Causes the inability to prescribe meaning to sensory information coming into the brain
Agnosia
A loss of knowledge or understanding of sensation
Stereoagnosia
Loss of ability to identify objects by touch
Agraphesthesia
Inability to identify numbers, letters, or symbols drawn on the skin
Visual agnosia
Inability to prescribe meaning to visual information coming in
