Neuro Midterm Weeks 1 - 5

What are the three nervous systems and their individual subcategories?

Central

• Consists of the cerebral cortex (cerebrum)

  • Subcortical structures

    • Basal Ganglia (Striatum, Subthalamic nucleus, Substantial nigra)

    • Diencephalon (Thalamus, Hypothalamus)

• Brainstem (Midbrain, pons, medulla oblongata)

• Cerebellum

• Spinal Cord

Peripheral

• Cranial nerves (Brainstem)

• Spinal nerves (Peripheral)

Autonomic

• Parasympathetic (Rest ad relax)

  • Cranial-sacral system

  • Conservation of metabolism

• Sympathetic (Fight or flight)

  • Thoracic spinal cord

What are the 6 categories of neurological impairment? Treatment, neurophysiological rational/function (NPR/F) for each?

Weakness (Due to MSK injury or NM pathology. Over or under recruitment)

• Treatment: Strengthening program, isometrics, Bands, weight, and more

• NPR/F: Resetting the spindle, Reciprocal inhibition, Alpha and gamma neurons, UMN vs LMN vs motivation, Motor pathways involved

Abnormal tone (Increased or decreased, hypertonicity, rigidity vs abnormal tone)

• Treatment: Relaxation, positioning, braces, strengthening

• NPR/F: Supra-spinal control, Gamm overdrive, Neurotransmitters (medications), primitive reflexes

Sensory or perception dysfunction (Vestibular deficits, visual deficits, paresthesia)

• Treatment: Vestibular rehab VOR, VCR. Gaze stabilization, Desensitization, approximation

• NPR/F: Vestibular system, cranial nerves, thalamus and internal capsule, somatosensory systems, spinal cord

Lack of coordination (Loss of balance, dysmetria, altered RAM movements)

• Treatment: Static vs dynamic activates, weighted utensils, proprioceptive training, equilibrium reaction

• Cerebellum, basal ganglia pathologies

Balance dysfunctions (Center of gravity, base of support, peripheral vs central)

• Treatment: External vs internal control and feedback, corrective vs compensatory mechanism

• NPR/F: Vestibular vs visual vs perceptual ,Cerebellar vs cerebrum (central), NM vs MSK, peripheral control

Embryological development of the CNS (Not on study guide)

• Where does it arise from? When go limbs generate and bud?

• What are the 4 sections

Arises from a sheet of ectodermal cells that folds over to form the neural tube. Limbs generate and bud close to 5 - 6 weeks.

Prosencephalon (Forebrain)

• Telencephalon

• Diencephalon

Mesencephalon (Midbrain)

Rhombencephalon (Hindbrain)

• Mesencephalon

• Myellencephalon

Spinal chord

What are the anatomical planes of section?

Horizontal, Coronal, Sagittal

In the image below, name the anatomical plane of section for A B C and D

A: Coronal view, Frontal section of cerebrum

• Ventricles are visible

  

B: Horizontal view, cerebellum and brainstem

• cerebellum is physically connected to the rest of the NS at the level of the brainstem

C: Horizontal view, Medulla oblongata

D:Horizontal view, spinal cord.

In the image bellow label the numbers and what each does

1. Dendrites → Reception

   • Receives signals

2 and 3. Cell body and nucleus → Integration/metabolism

• Combines info. Cell metabolism, and houses nucleus

4. Axon hillock → Encoding

   • Maintains membrane potential and is the action potential site. Cone shaped.

5. Axon → Transmission

   • Transits electrical signals (action potential). May or may not be myelinated

6. Myelin sheath → Protection

   • Protects, isolates, and helps increase transmission speed. Composed of proteins and lipids

   • In the CNS myelin is produced in oligodendrocytes ; PNS myelin is produced by Schwann cells. BOTH are glial cells

7. Node of Ranvier → Optimization

   • Optimizes energy consumption and impulse transmissions; increases speed, facilitates movements and ensures signal does not get lost (nerve impulse jump conduction). Gap/spaces between myelin sheaths.

8. Axon terminal → output

   • Creates synapse and links to other neurons. Neurotransmitters are stores here in the synaptic vesicles

What are the three types of neurons and what does each do? How does each look?

Sensory neuron

• Dendrites = receptors

• Cell body = housed in dorsal root ganglion

• activates with sensory mechanisms

  

Projection neuron

• Travels long distances. Myelinated axons

  

Interneuron or local interneuron

• Travels short distances

• Unmyelinated axons

• Changes synergistic muscle activity

Pic of all:

What does glial cells do? What are the 5 types and what does each do?

Glial cells are support cells that help maintain homeostasis in the CNS + PNS

Ependymal cell

• Makes up thin membrane lining in central spinal cord + ventricles. Also makes up CSF fluid and has a big role in the blood brain barrier

Astrocytes

• Facilitates nutrition. Helps maintain normal signaling. Also has connections to both neurons and vasculature.

Microglia

• The clean up crew (the immune cells of the CNS), works with macrophages and limits ecotoxicity. Has a role in promoting plasticity

Oligodendrocytes

• Produces myelin sheath around axons. acts as insulation and increases speed of conduction. Myelinates in CNS.

Schwann Cells

• Produce myelin sheath around axons. Acts as insulation and increases speed of conduction. Nerve regeneration after injury → metabolic support. Myelinates in PNS

What is the blood brain barrier BBB?

BBB

• is a filtration system for the brain. Carries blood to brain spinal cord tissue while blocking certain substances. Vital.

• selective semi-permeable border composed of endothelial cells.

• Protective barrier to CNS from unwanted substances in blood

What is synaptic transmission and how does it work?

This is when neurotransmitters are released from the axon terminal of the presynaptic neuron and bind to receptors in the post synaptic neuron.

• Pre synaptic neuron houses the vesicles (NTs) and gets released in the synaptic cleft.

• Post synaptic neurons accepts the NTs necessary to either excite or inhibit the signal to get relayed.

• Excess NTs in the cleft get reduced, reused or recycles via reuptake, diffusion or enzymes degradation

Membrane potentials are established because? Where are K+, Na+, and Cl-?

What is the resting potential of a neuron?

established because ion concentration gradients across the cell membrane phospholipid bilayer.

• K+ (Potassium ion) Inside neuron

• Na+ (Sodium ion) Outside the neuron

• Cl- (chlorine ion)

Resting potential of the neuron is usually -65 to -70 mV. So the inside of the cell is slightly more negative than the outside.

Pre synaptic neurons can deliver either what two inputs to the post-synaptic cell?

What is graded potentials and how does it relate to action potential?

Excitatory EPSP (+ potential)

• Depolarization TO threshold

Inhibitory IPSP (- potential)

• Hyperpolarization AWAY from threshold

Graded potential: Sum of both potentials

Action potential is the reaction to the sum, exceeding threshold

Active transport mechanism:

What is the sodium potassium pump? Potassium channel is always what?

Sodium potassium pump

• For every 3 Nat+ out of the cell 2 K+ replace inside the cell.

  The inside of the cell is slightly more negative than the outside. , If this is off balance then things like seizers or strokes can occur so this process is vital.

Potassium channel is always open

Sensory potentials

instead of NTs input to dendrites we get signals from tactile sensory modalities (such as pressure, stretch, etc) to the receptor. This is what causes the Stretch Reflex

What is neuroplasticity? Examples?

Neuroplasticity (Practice makes perfect)

• Changes in synaptic efficacy, neuronal function/structure

• Learning and memory; patients change their motor pattern

Examples:

Short term plasticity, reversible

• Habituation: Decrease response to a repeated light stimulus

  • Habituation, getting use to the house smoke alarm going off eventually you don’t hear it.

• Sensitization: Increase response to a repeated stimulus

  • Sensitive to stimulus, bruise starts to hurt/becomes sensitive in that area. Chronic pain

For example: PT should help desensitize a limb so the prosthetic isn’t a noxious stimuli

Long term, learning and memory plasticity

• Active/experience dependent: Persistent, long lasting physiologic changes. Increase strength, sprouting and concentrations of neurons NTs.

• Reinforcements of a specific pattern: Timing, sequence of movements → reward system, increases will to learn.

• Use dependent movement therapies: Increase intensity, increase rep for motor learning. Re-training SCI patients; engages sensory neurons to reconnect communication between feet a brain. Another is body weighted supported treadmill training, constraint induced movement therapy.

Neurotransmitters:

What are ionotropic and metabotropic?

What is the NTs life cycle?

Ionotropic: Positive and negative synaptic inputs convey specific task related info to motoneurons.

Metabotropic: synaptic inputs dramatically impact motoneuron excitability to meet task demands.

Life cycle for NTs:

1. Synthesis: Location is dependent on specific neuron. fabricated in particular region of brain or presynaptic neuron

2. Synaptic action: Diffuses through synaptic cleft and binds to receptor on post-synaptic membrane → ionotropic/metabotropic effects in post synaptic neuron

3. Metabolism: reduce, reuse, and recycle

   • Diffusion → out of synaptic cleft (recycle)

   • Breakdown → inactivation by enzymes (reduce)

   • Reuptake → into pre-synaptic cell (reuse)

What are they types of NTs which associated charges?

Glutamate +

GABA and Glycine -

Acetylcholine AcH +-

Norepinephrine NE +

Serotonin 5-HT +-

Dopamine DA +-

Endorphins

Substance P

What is glutamate function with site of action, transmitters binding effects, and clinical application?

Glutamate +: Important for learning and memory, most common NT in synapse. Regulates development and creation of nerve contacts.

• Site of action: Primary, fast, excitatory NT of CNS ~ 50% of synapses

• Transmitters binding effects: General neuronal signaling. Facilitate learning and development, especially when binging to NMDA receptor in brain.

• Clinical application: Increase levels can cause seizures. Glutamate excitotoxicity can occur in brain injury such as in the case with Tua. Increase concentration of glutamate remaining in synaptic cleft during an ischemic stroke, Post synaptic cell being to become exited to death so to speak. because of slowing energy (decrease O2/glucose)

What is GABA + Glycine function with site of action, transmitters binding effects, and clinical application?

• Site of action: Principle inhibitory NT in CNS (GABA: widespread. Glycine: brainstem and spinal cord)

• Transmitter binding effects: Inhibition of post-synaptic neuron (increase in Cl-). Sedation, anti anxiety, anti-seizure, sleep inducing (GABA). Important for shaping motor commands level of spinal cord

• Clinical application: Baclofen, gabapentin, benzodiazepines, alcohol enhance effects of GABA. Typically given to CP and stroke patients because of the ischemic attacks, helps decrease glutamate action.

What is ACETYLCHOLINE function with site of action, transmitters binding effects, and clinical application?

ACETYLCHOLINE + (?): Major NT in PNS; muscle contraction

• Site of action and → associated transmitter binding effects

  • Somatic: + in all NMJ → Skeletal contraction

  • Autonomic: Ionotropic effects at pre ganglionic receptors → facilitation of post ganglionic autonomic neurons

  • Autonomic: metabotropic effects at parasympathetic post ganglionic muscarinic receptors → increase parasympathetic actions; increase rest actions

  Also present in CNS:

  • Cerebral cortex and ventral striatum (basal ganglia and reward system) → cognitive arousal and feelings of reward

• Clinical application

  • Myasthenia gravis: Autoimmune destruction of AcH receptors at NMJ causing weakness

  • Botox: Inhibits AcH release at NMJ. Used for hypertonia

  • Nicotine binds to ACH receptors in ventral striatum causing the pleasurable and addictive feelings

  • Alzheimer’s: number of AcH receptors in cortex diminish

What is Norepinephrine function with site of action, transmitters binding effects, and clinical application?

• Site of action

  • CNS: cerebral cortex, limbic system, spinal cord

  • PNS: sympathetic NS

• Transmitter binding effects

  • Cortex, limbic system: control of mood

  • Spinal cord: increase excitability of alpha motor neuron and group ll sensory afferents

  • PNS: sympathetic effects (fight/flight)

• Clinical application

  • Important in generation of spasticity and hyperreflexia after NS injury

  • May have vole in chronic pain / central sensitization (partial target of SNRIs drugs)

  • Role in Parkinson's disease

What is Serotonin function with site of action, transmitters binding effects, and clinical application?

• Site of action

  • Brain and spinal cord (from raphe nuclei through cortex)

• Transmitter binding effects

  • Brain: Control of mood, pain perception, increase arousal

  • Spinal cord: increase excitability of ventral horn; decrease excitability of dorsal horn

• Clinical application

  • Alpha motor neuron w metabotropic effects, important in amplifying the effect of ionotropic input → motor command

  • Important in generation of spasticity hyperreflexia after NS injury

  • Lack of 5 HT after Spinal cord injury results in spasms due to adaptive hyperactivity of receptors on alpha motor neuron

  • May have role in chronic pain/central sensitization (partial target of SNRI drugs)

  • Role in Parkinson's disease (Increase in 5-HT can help move and groove on ischemic stroke patients

What is Dopamine function with site of action, transmitters binding effects, and clinical application?

• Site of action

  • Basal ganglia, limbic system, frontal lobe

• Transmitter binding effects

  • Control movements, feelings of pleasure, reinforcement of behaviors (including addiction), decision making, planning

• Clinical application

  • Parkinson’s disease: Loss of dopaminergic neurons (primarily where they are synthesized in substatia nigra of brainstem) is major contributor to motor deficits (tremors). L-DOPA drug increase dopamine. If too high dose, lead to involuntary movements. Too high may also lead to addictive behaviors.

  • Amphetamines and cocaine increase/prolong release

What is Endorphins function with site of action, transmitters binding effects, and clinical application?

• Site of action

  • CNS and spinal cord

• Transmitter binding effects

  • Inhibition of pain signaling (Endogenous opioids)

• Clinical application

  • Decrease signaling and pain perception

  • Descending pain modulation system

  • Pharmacologic agonists; morphine, heroin, oxycodone, etc

What is Substance P function with site of action, transmitters binding effects, and clinical application?

• Site of action

  • PNS: Released by nerve endings in skin, muscles, joints

  • CNS: Brainstem, cortex, hypothalamus, amygdala

• Transmitter binding effects

  • Produce pain sensation

  • Involved with mood, cortical perception of pain

• Clinical application

  • Levels of substance P are excessive in some pathological pain conditions

What view is this?

Superior

What view is on the left and right?

Anterior and posterior

Label. This is considered what for babies?

Coronal suture. Considered a soft spot in babies to allow brain to grow

Fill in the blanks.

Label

Label and state which view is this

Coronal

Orientation of direction in brain vs spinal cord

• Rostral vs caudal

• How does dorsal and ventral differ for the brainstem/spinal cord vs the actual brain

Rostral: towards the nose

Caudal: towards the tail

In the human brainstem/spinal cord

• Dorsal = posterior

• Ventral = anterior

In the human brain

• Dorsal = superior

• Ventral = inferior

Label each based on the correct axis (dorsal, ventral, rostral, caudal)

label the lobes

For each of the four lobes state what they do

Frontal

• Function: Executive functioning, decision making

• Impairment: Ataxia, impulse control

Parietal lobe

• Function: Temperature regulation, touch sensation/pain, proprioception/spatial awareness

• Impairment: Fall risk

Occipital lobe

• Function: vision, perception

Temporal lobe

• Auditory processing

• Broca’s (actually talking) and Wernicke’s (understanding speech)

• Memory storage

• Tailors to motion and motivation

Primary motor is in the precentral gyrus in the frontal lobe: Motor control ect

Primary sensory is in the postcentral gyrus and in the parietal lobe: Processes sensation

Primary visual cortex: Located in the calcarine sulcus in the occipital lobe: vision

Primary auditory cortex located in the Transverse temporal gyrus  in the temporal lobe: auditory interpretation

What is grey matter and what is its cortical and subcortical structures?

Grey matter

• Neuron cell bodies

• Synapses where white matter axons connect with other neurons at the nucleus

• Glial cells (support cells)

Cortical structures

• Lobes

• Specific gyri within lobes

Subcotial structures

• Diencephalon (Thalamus and hypothalamus)

• Limbic system

• Basal ganglia (In telencephalon; motor)

Amygdala: emotional processing center, regulates fear and memories associated with emotions

Hippocampus: critical for memories

What is white matter and its categories of fibers ( (Understand where they connect)?

White matter: Neuron axons surrounded by myelin

Categories of fibers

Projection fibers: Connect cortical, subcortical/brainstem/spinal structure

• Ascend from spinal cord and subcortical structures to cortex (Green)

• Descend from cortex to spinal cord, brainstem, basal ganglia, thalamus (Red)

• Travels through internal capsule

• Travels long distances

Commissural fibers (Between hemispheres): Connect same area between hemispheres like sticky give