Flashcards in Concepts/Pathways Deck (44):
What is the difference between ischemia and infarction.
Ischemia is the reduction of blood flow to an organ. Below what is needed for normal metabolism.
Infarction is what results from prolonged ischemia. It is the end point where the cells die.
What is an acoustic neuroma?
An acoustic neuroma is a noncancerous growth that develops on the eighth cranial nerve. Also known as the vestibulocochlear nerve, it connects the inner ear with the brain and has two different parts. One part is involved in transmitting sound; the other helps send balance information from the inner ear to the brain.
What is the difference of a focal lesion and diffuse lesion + examples of signs and lesions
A focal lesion is an infection, tumor, or injury that develops at a restricted or circumscribed area of neural tissue. These produce focal neurological signs.
-example of focal lesion signs
1. Loss of pain and temperature on half the face
2. Loss of the ability to repeat a spoken word
3. Loss of vision in one eye
Diffuse or general lesions: Neurodegenerative diseases (advanced Parkinsons disease), psychiatric disorders, inflammatory disorders, infections, malnutrition, genetic disorders, compression of the brain.
examples of non focal:
headache, tiredness, confusion, disorientation.
What are the 6 kinds of time courses and examples?
1. Episodic - migraines, seizures
2. recent onset and episodic - expanding brain tumor
3. Relapsing, remitting - multiple sclerosis
4. Sudden onset, lasting deficits - stroke
5. Slow, progressive - neurodegenerative diseases
6. Progressive over short time period - expanding tumor
Describe the series of events in an action potential
1. Enough graded potentials activate voltage gated sodium channels (-50mV)
2. Sodium influxes, the neuron depolarizes significantly.
3. Then the sodium channels close and potassium channels open, hyperpolarizing until the voltage gated potassium channels close.
4. inactivated sodium channels are no longer inactive.
With all the exocytosis at the nerve terminal, wouldn't the membrane be huge?
There is a process of endocytosis to remove membrane from the nerve terminal.
Adaptor proteins connect clathrin to vesicular membrane forming clathrin coated pits.
Clathrin assemble into coat, curving membrane.
Dynamin ring comes and pinches off membrane.
Coated vesicle is then moved away from terminal along the actin filament
Hsc70/Auxillin - remove the clathrin. Can start storing NT again
How are neurotransmitter regulated?
Can increase (facilitate) or decrease (inhibit) neurotransmitter release
Autoreceptor - feedback regulation – binding of transmitter inhibits its
own further release
Excess released neurotransmitter can be inactivated by:
- Reuptake by specific transporters.
-Degradation by specific enzymes
• Acetylcholine (acetylcholinesterase) • Catecholamines (MAO; COMT) • Neuropeptides
-astrocytes at a tripartate synapse: Metabolize neurotransmitters (GABA, glutamate, serotonin, etc.)
The major excitatory neurotransmitter in the CNS • Contained in approximately 50% of all neurons, and virtually all
• Post-synaptic receptor type:
Metabotropic: May be excitatory or inhibitory, depending on the state of
• Ionotropic: NMDA (N-methyl-D-aspartate), kainate and AMPA. **All
NMDA is both a voltage-gated and ligand-gated Ca2+ ion channel • The receptor is blocked by Mg2+ at resting membrane potential
• Uses the AMPA receptor and influx of Na+ to depolarize the membrane
to remove the Mg2+ block
It is both a voltage-gated and ligand-gated Ca2+ ion channel • The receptor is blocked by Mg2+ at resting membrane potential
• Uses the AMPA receptor and influx of Na+ to depolarize the membrane
to remove the Mg2+ block
NMDA activation in the presence of depolarization, enables
Ca2+ to enter cell.
• Increased intracellular [Ca2+ ] can activate calcium-dependent
• Intracellular signals can produce long-term synaptic changes
that are important for
• development of synapses • regulating neural circuits • learning and memory (Long-term potentiation; LTP)
• Long-term changes include changes in dendritic spines and
insertion of AMPA receptors: Increased responsiveness of post-synaptic neurons after repeated stimulation of neurons (e.g., in hippocampus).
Trauma and disease that impair ATP-generation can cause
increased glutamate release or decreased glutamate reuptake.
• Glutamate NMDA channels allow Ca2+ to leak into cells.
• Increased Ca2+ causes increased water uptake and stimulation of
intracellular enzymes that degrade proteins, lipids, and nucleic acids
• Examples of conditions thought to be associated with
glutamate toxicity: ALS, Alzheimer’s, tumors, oxygen
deficiency, ischemia, trauma, repeated seizures.
Major inhibitory neurotransmitter of the CNS • Contained in about 30% of CNS neurons
• Post-synaptic receptor type:
• Ionotropic: GABAa receptor, GABA gated Cl-channel
• Metabotropic: GABAb functionally linked to potassium or calcium ion channels
Mesolimbic pathway: -Reward pathway (addiction)
Nigrostriatal Pathway: Control of movement
Involved in reward-motivated
behavior and motor pathways
CNS- Neurons originate in
brainstem regions (ventral
tegmental area and substanstia
Drugs that influence dopamine transmission: • Anti-psychotics (-) • Nicotine, cocaine,
methamphetamine (+) • Amphetamines (Adderall) (+) • Methylphenidate (Ritalin) (+)
Main neurotransmitter in the PNS and ANS, but also has
neuromodulator functions in CNS
• PNS- Neuromuscular junctions
• ANS- sympathetic (pre-) & parasympathetic (pre- & post-
• CNS- Neurons originate in the basal forebrain (*nucleus basalis)
and the brainstem (*dorsolateral midbrain-pons) and have
widespread connections to the cortex
• Involved in arousal, attention, memory and motivation • Nucleus basalis degenerates in Alzheimer’s disease
• Associated with memory loss, personality change and dementia
Drugs that influence ACh transmission in the CNS: • Nicotine (on nictotinic
receptors) (+) • Atropine (-) • Scopolamine (-)
Describe the general rules for herniated discs and the nerves they impinge
So in the cervical vertebrae, because the corresponding nerve exits above the vertebrae, a C5-C6 herniated disc impinges on C6 nerve.
In the lumbar its the same but for a different region. The interventricular foramen is large so the corresponding spinal nerve exits above the disc.
So an L4-L5 herniation will not impinge onf the L4 nerve but rather the L5 as it is traveling in the cauda equina. Impinging the L5 nerve.
Terms for weakness, the 4 P's
Paralysis: weakness so severe that a
muscle cannot be contracted.
• Paresis: weakness, or partial paralysis.
• Plegia: severe weakness or paralysis.
– e.g., Diplegia refers to bilateral lower limb
weakness. Quadriplegia to all 4 limbs. – Hemiplegia refers to one side of the body
weakness (arm and leg)
• Palsy: imprecise term for either weakness
or no movement.
Explain the scoring for muscle strength.
Interpret the scoring for spinal cord stretch reflexes
.0/5 No contraction
1/5 Muscle flicker, no movement
2/5 Movement, but not against gravity 3/5 Movement against gravity, but not against resistance
4/5 Movement against some resistance 5/5 Normal
4+ non-sustained clonus
5+ sustained clonus
1-3 can look normal so always refer to opposite side for asymmetry or even with upper and lower
Describe the receptor, circuit and functions of the stretch reflex, golgi-tendon
reflex and flexor withdrawal reflexes.
.Stretch reflex - 1. Muscle stretch receptor excited (connected to Ia afferent) 2. Ia afferent makes an excitatory synapse onto quadriceps motor neurons,
causing muscle contraction
3. Ia afferent also makes an excitatory synapse onto an inhibitory interneuron,
which inhibits hamstring (flexor) motor neurons
Golgi tendon reflex
Stimulus: Muscle tension Circuit: GTO > lb > lb inhibitory interneuron > motor neuron to homonymous muscle
(also excites antagonist muscles)
Flexor withdrawal - stimulated leg flexes to withdraw after cutaneous receptor activated > cutaneous afferent fiber from nociceptor alpha, < activates interneurons which inhibit the extensors and activate flexor in pained foot > for opposite foot the opposite happens, extensor activated, flexor inhibited to stand
Describe the function of a central pattern generator.
Central pattern generators (CPGs) are biological neural networks that produce rhythmic patterned outputs without sensory feedback. ... CPGs have been shown to produce rhythmic outputs resembling normal "rhythmic motor pattern production" even in isolation from motor and sensory feedback from limbs and other muscle targets.
Central pattern generators are neuronal circuits that when activated can produce rhythmic motor patterns such as walking, breathing, flying, and swimming in the absence of sensory or descending inputs that carry specific timing information.
What are the stretch reflexes at these levels
L3-4 – patella (3,4 kick down the door)
C5-6 – biceps
C5-6 – brachioradialis
(5,6 pick up sticks)
(7-8 keep it straight)
S1 – Achilles
(1,2 buckle my shoe)
What are the muscle spindles and the system?
Proprioceptors: providing information about body position/movement.
-Arranged in parallel with skeletal muscles fibers.
• Intrafusal muscle fibers within a
connective tissue capsule.
• Attached to skeletal
Muscle spindle contains this lil capsule, which has efferent (gamma) and afferent nerves. It has two types of sensory nerves, group Ia which responds to rapid, dynamic stretch and
group II which responds to sustained, tonic stretch
Gamma motor neuron: γ-motor neurons are motor neurons that only innervate muscle spindle intrafusal fibers. • DO NOT cause skeletal muscle
fibers to contract. • Increase the excitability of the
Normally both alpha- and gamma-
motor neurons are CO-activated. • Gamma activity increases during
skilled movements and motor
So stretch is going to have a greater response with gamma neuron activity and also picks up slack if muscles are contracted
Describe muscle tone and what is occuring by hypotonia and hypertonia?
Muscle tone is the resting tension in a muscle produced by muscle elasticity.
• Contributes to postural control and ability to store energy
when the muscle is stretched (e.g. during walking or
• Measured by moving around limbs. Flexion-extension,
Hypotonia occurs when spinal nerves are damaged.
Hypertonia occurs with supraspinal lesions because stretch reflexes are increased.
Identify and describe the function of premotor cortical regions.
Ideas about voluntary movement originate in the frontal lobe.
Premotor Cortical Areas (supplementary and premotor cortex) then participate in motor planning (organization of the movement).
-Supplementary motor area
-Primary somatosensory cortex
-Parietal association cortex
Describe the functions of the corticospinal, corticobulbar and reticulospinal tract pathways.
The corticospinal tract is the primary pathway for goal-directed movements.
• Only descending pathway to
project directly to α-motor
neurons of distal muscles.
• It is the only pathway that
generates fine movements of
The corticospinal tract originates in the primary motor cortex as well as the premotor and somatosensory cortex.
*Large Betz Cells in motor cortex (layer 5) project directly to motor neurons
Reticulospinal tracts project mainly ipsilaterally (some bilateral) to medial α-motor neurons throughout the length of the spinal cord. They contribute to posture and gait-related movements.
Generate feedforward preparatory muscle activation. •Contribute to muscle tone.
The corticobulbar tract is a descending pathway responsible for innervating several cranial nerves, and runs in paralell with the corticospinal tract
- Motor cortex (precentral gyrus and anterior part of the paracentral lobule)
Course / Path
- The corticobulbar tracts leave the internal capsule and enter the basilar part of the pons as numerous bundles  The fibres leave the cerebral crus adjacent to the corticospinal tract. The fibres can take several paths and have several different terminations:
i) Termine directly on alpha motor neurones or interneurones innervating alpha motorneurons in the brainstem. These control somatic motor acitivity in the head e.g. muscles that control mastication, expression and eye movement.
ii) Axons that innervate motor nerve cranial nuclei can decussate (cross) before they terminate, resulting in them innervating contralateral muscles. As some decussate and some descend ipsilaterally, it results in bilateral descending control. 
iii) Directly innervate cranial nerves or through interneurones I.E. via the corticospinal tract. 
- Innervates muscles of the face, tongue, jaw, and pharynx, via the cranial nerves.
- The corticobulbar tract directly innervates the nuclei for cranial nerves:
V - Trigeminal- muscles for mastication
VII- Facial- muscles of the face
XI- Accessory- sternocleidomastoid and trapezius
XII- Hypoglossal- muscles of the tongue 
- Cranial nerves motor regions of X (vagus nerve) in the nucleus ambiguus.
Describe the motor deficits that would follow specific upper motor neuron
lesions of the cortex or spinal cord.
1. Generally, the corticospinal tract
2. Trauma to lateral primary motor cortex (face and arm)
3. Trauma to internal capsule
4. What lesions could cause unilateral leg weakness or paralysis? (3) possibilities
Lesions above the spinal cord produce contralateral deficits. Lesions of the spinal cord produce symptoms on the same side of the lesion
Deficits are always below the level of the lesion
Major deficits with CST lesions: •Voluntary motor weakness (distal > proximal) on one side of the body. •Babinski sign
Trauma to lateral primary motor cortex
1. Weakness in right arm and low face 2. UMN (lower face, entire arm).
3. Pathways are CBT and CST
aka. Contralateral Unilateral face and hand hemiparesis.
Trauma to internal capsule
Pure motor hemiparesis with lesion in internal capsule- starting with the lower face.
Trauma to motor cortex (contralateral)
•A lesion affecting the ipsilateral spinal cord—UMN signs
•Peripheral nerve--LMN signs
Contrast the stretch reflex of the bicep and the Golgi tendon reflex
The stretch reflex operates as a feedback mechanism to control MUSCLE LENGTH by causing muscle contraction.
In contrast, the tendon reflex operates as a feedback mechanism to control MUSCLE TENSION by causing muscle relaxation before muscle force becomes so great that tendons might be torn.
Although the tendon reflex is less sensitive than the stretch reflex, it can override the stretch reflex when tension is great, for example, causing a person to drop a very heavy weight. Like the stretch reflex, the tendon reflex is ipsilateral. The sensory receptors for this reflex are called tendon Golgi receptors, which lie within a tendon near its junction with a muscle.
In contrast to muscle spindles, which are sensitive to changes in muscle length, tendon organs detect and respond to changes in muscle tension that are caused by muscular contraction, but not passive stretch.
Define the basic morphology and function of the receptors and axons that mediate cutaneous sensation, proprioception, temperature and pain sensation.
-Meissner corpuscle: surface, motion in dermis
detects edges, indentations, slowly adapting
-Ruffini corpuscle - skin stretch, aligned parallel with stretch lines
-Pacinian corpuscle: deep and with onion like layers, vibration
Proprioception: (1a, II) - the largest, most myelin, fastest
Temperature (Alphadelta, C)
Pain (Alphadelta, C)
Describe the general concept of sensitization along with hyperalgesia, allodynia
Following repeated application of noxious stimuli, neighboring nociceptors that were not responsive now become responsive.
•Hyperalgesia = the phenomenon of stimuli that are normally perceived as slightly painful as significantly more painful
ex. digging fingernail with sunburn
•Allodynia = the induction of pain by what is normally an innocuous stimulus
ex. swallowing with strep throat
Protects injured area, promotes healing and prevents infection.
Results from changes in sensitivity of peripheral nociceptive receptors and/or central targets.
Describe the pathway of peripheral sensitization
The interaction of nociceptors with the “inflammatory soup” of substances to decrease threshold of activation for nociceptors
Prostaglandins: •Increase response of nociceptive fibers.
These nociceptors release substance P which causes vasodilation but also mast cell degranulation releasing histamine as a positive feedback cycle since histamine also activates nociceptors.
Nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g. aspirin and ibuprofen): •Inhibit cyclooxygenase (COX) to prevent synthesis of prostaglandins
Describe the pathway of central sensitization
An immediate, activity dependent increase in the excitability of neurons in
the dorsal horn of the spinal cord following high levels of activity in the
nociceptive afferents to increase pain sensitivity.
Mechanisms of central sensitization
1. Transcription independent (windup) lasts only during stimulation = acute.
2. Transcription dependent (allodynia) outlast stimulus for hours and can be
mediated by COX = chronic.
• Development of or increase in spontaneous activity
• Reduction in threshold for activation by peripheral stimuli
• Expansion of receptive field size (conversion of nociceptive-specific
neurons to wide dynamic neurons that now respond to both innocuous
and noxious stimuli)
-the glutamate channel is open, with repeated stimuli you unblock the NMDA receptor which initiaties a signal cascade. With repeated stimulation, with alot of NT, gene expression changes which permanently changes the neuron
What is sacral sparing?
Many people who suffer incomplete spinal cord injuries experience a phenomenon known as sacral sparing. Sacral sparing means that some movement or sensation is preserved in the sacrum—the region of the spine that is deep in the pelvis, surrounding the pelvic area. Patients with sacral sparing, then, may have fewer problems with bowel functioning and elimination than those with a complete injury.
What is Sacral Sparing?
There are five sacral nerves, each of which plays a role in sensory perceptions in the lower half of the body, particularly deep within the pelvis and along the anus. You may hear your doctor refer to regions associated with a sacral nerve as dermatomes.
A dermatome is simply an area of the body largely controlled by a single nerve, and there are many such regions scattered across the body.
When sacral sparing occurs, the spinal cord is only partially compressed, not fully severed. This allows one or more nerves to continue sending and/or receiving signals though the sacrum. The practical effect is that people with sacral sparing retain some sensation and control though the extent varies depending upon the severity of the injury, the timeliness of treatment, the quality of physical therapy during rehabilitation, and other factors.
Extrinsic vs intrinsic lesions
Extrinsic compression of the spinal cord, e.g. by tumour or prolapsed intervertebral disc, typically produces a pattern of sensory loss in which the sacral dermatomes are involved (saddle anaesthe- sia). This is because the part of the spinothalamic tract closest to the surface of the cord (that convey- ing sensory information from the lumbosacral dermatomes) is most vulnerable to the effects of external compression (Fig. 15.2). By contrast, in- trinsic lesions of the spinal cord tend to damage the more central parts of the spinothalamic tract first (sacral sparing) though this is by no means a strict rule
Feature detection (stereognosis, graphesthesia
On the primary somatosensory cortex - area 2 is important for feature detection.
Principle of cortical processing that allows the brain to find patterns common to stimuli of a particular class
Stereognosis: the mental perception of depth or three-dimensionality by the senses, usually in reference to the ability to perceive the form of solid objects by touch.
Graphesthesia: Graphesthesia is the ability to recognize writing on the skin purely by the sensation of touch. Its name derives from Greek graphē ("writing") and aisthēsis ("perception"). Graphesthesia tests combined cortical sensation; therefore, it is necessary that primary sensation be intact.
What is referred pain and its pathway
Surprisingly, there are few, if any, neurons in the dorsal horn of the spinal cord that are specialized solely for the transmission of visceral pain. Obviously, we recognize such pain, but it is conveyed centrally via dorsal horn neurons that are also concerned with cutaneous pain.
As a result of this economical arrange-
ment, the disorder of an internal organ
is sometimes perceived as cutaneous
pain. A patient may therefore present to the physician with the complaint of pain at a site other than its actual source, a
potentially confusing phenomenon
called referred pain. The most common
clinical example is anginal pain (pain
arising from heart muscle that is not
being adequately perfused with blood)
referred to the upper chest wall, with
radiation into the left arm and hand.
Other important examples are gallblad-
der pain referred to the scapular region,
esophogeal pain referred to the chest
wall, ureteral pain (e.g., from passing a
kidney stone) referred to the lower
abdominal wall, bladder pain referred to
the perineum, and the pain from an
inflamed appendix referred to the ante-
rior abdominal wall around the umbili-
cus. Understanding referred pain can
lead to an astute diagnosis that might
otherwise be missed.
what is Nogo?
It is an inhibitory molecule that with deactivation in mice has been show to lead to long distance regeneration and functional recovery in rats.
Describe the pathway for touch/vibration/pain/temperature for the face
Principal nucleus in PONs - touch and vibration
Spinal nucleus in medulla - pain and temperature
Only the trigeminal lemniscus tract vs trigeminothalamic tract.
Both enter the dorsal horn...
Pain/Temp: descends immediately, synapses at the spinal nucleus and decussates and then travels up the trigemino-thalamic tract to the ventral posterior medial nucleus.
Touch/vibration: synapses at the principal nucleus, decussates with the internal arcuate fibers, travels up the medial leminscus (trigeminal lemniscus) and synapses in the VPM!
-so from the medulla it is traveling in with the DCMLS
At the Ventral posterior complex of thalamus, how does the information travel from there?
VP > (3a, 3b, 1, 2) of the primary somatosensory cortex.
3a, 3b, 1, 2 all go to the secondary somatosensory cortex > amygdala and hippocampus for tactile learning and memory
2 goes to parietal areas 5,7 which then go to motor and premotor cortical areas for association and attention.
Compare LCST, ACST
ACST is 10% of what doesn't decussate at the medullary pyramids
Posterior internal capsule> basis pedunculi > basis pontis > pyramid, decussation> lateral intermediate zone and lateral motor nuclei > distal muscles
Posterior internal capsule > basis pedunculi > basis pontis > ventral column > BILATERAL > medial intermediate zone and medial motor nuclei > proximal trunk muscles
-posture and gait related movements
-premotor cortex > reticular formation > reticulospinal tract > spinal cord separate bilaterally, BOTH MEDIAL
FEEDFOWARD preparatory muscle activation
important in reflex excitability
Lateral and medial vestibulospinal tracts
elaborate sensory system in the inner ear with specialized receptors that monitor head position, movement and acceleration.
Lateral vestibulospinal (balance): projects to the entire spinal cord. It projects **ipsilaterally to medial LMNs to proximal muscles. Especially facilitates extensor muscles in response to deviations from stable balance and upright balance.
Medial vestibulospinal (positioning of head and neck):
projects on to cervical.Projects BILAterally to control head position in response to acceleration "vestibulocervical reflex
important in reflex excitability
orienting movements of the head to visual or auditory stimuli. It also helps to coordinate the eyes and head.
Originates in the superior colliculus and crosses in the MIDBRAIN (not just the one of the only ones to cross in the midbrain but out of the brain stem pathways, the only one to cross at all! ) (tecto and rubro)
Is in the medial motor system.
Generates orienting movements of the head to visual or auditory stimuli. It also helps to coordinate the eyes and head.
Originates in the red nucleus of the midbrain.
Crosses in the midbrain
Travels next to LCST in the spinal cord
Only extends to the *cervical spinal cord
Facilitates FLEXOR muscles>extensors
* this is important because its where a decerebrate - lesion below the midbrain - cause ALL LIMBS to extend vs decorticate which has flexion of the arms.
ONLY pathway that travels and projects lateral!
Lateral: only the LCST and rubrospinal
What is important about these LMN's?
C3-C5: phrenic nerve -diaphragm
S3-S4: Onuf's nucleus - motor neurons innervating urethral and external sphincter which enable voluntary control of urination and defectation
S2-S4: motor neurons to pelvic floor muscles
*very low spinal cord lesions can produce bowel and bladder incontinence
Mesolimbic pathway: -Reward pathway (addiction)
=Control of movement
Which UMN tracts are uncrossed?
1. anterior corticospinal tract
2. Reticulospinal tract
3. Lateral vestibulospinal tract
4. Medial vestibulospinal tract