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Causes of brain injury
What are the types of head injury?
What are their characteristics?
What population are these most common in and why?
What are the two types of CVA?
What are their characteristics?
What population is this more common in?
What are the 2 ways that neurons can cause damage to the brain?
What are other non degenerative causes of brain injury?
- Closed & open
- Open: gunshot wound; damage extending into the brain
- Closed: no penetrating wound; severe blow to the head
- Young adults; more likely to engage in risky behavior
- Ischemic, hemorrhagic
- Ischemic: thrombus/clot that occludes artery and may break off and travel (embolism)
- Hemorrhagic: brain arty ruptures/bleeds
- Older adults
- 1. neurons in direct area being affected by the stroke
- 2. areas that surround the area of direct impact (penumbra) are vulnerable to damage; neurons invade these cortical areas that disrupts normal function
What are factors influencing recovery (4)?
Why is it better to have small lesions?
- Age at time of damage (<2 yr best chance of recovery)
- Size/location of lesion
- Slow-onset vs Rapid-Onset lesions
- Environment (rehab increases likelihood/extent of recovery after TBI)
1. time between lesions gives brain time to recover 2. more collateral sprouting
Regeneration of neurons and axons in the PNS
Survival of certain neurons depends on ___.
____ is secreted by target cells, bound by receptors on the dependent cell, and retrogradely transported down its axon to the cell body.
This trophic substance is produced in which system?
This trophic substance helps maintain health of neuron, but also promotes growth of ___.
- NGF (nerve growth factor)
- neurites (collective term for axons and dendrites)
Neurons in the PNS can regenerate their ___.
Normally, pre- and post-synaptic neurons secrete trophic factor (NGF) to target tissue.
When axons of post-synaptic neurons are injured, presynaptic terminals ___ (no longer receiving trophic substances).
If __ is supplied, the presynaptic terminals are ___.
If anti-NGF antibodies are added near the target tissue, the supply of NGF is ___ and pre-synaptic terminals ___.
- NGF, maintained
- blocked, retract
Both PNS and CNS produce proteins that inhibit growth of neurons, so why does regeneration occur in the PNS but not the CNS?
- PNS: Schwann cells secrete chemicals that override the prohibition of neuron growth
- CNS: Oligos do not produce chemical to override prohibition of neuron growth
__ is required for the regeneration and maintenance of synaptic connection in the ___.
PNS regeneration is a __-__-__ in mammals; CNS neurons have a limited capacity to regenerate.
Following injury, glial cells (e.g. __ cells) in the PNS contribute to axon regeneration by ___ growth-inhibiting proteins, but not in the CNS.
Is recovery in the CNS as extensive as previously thought?
- NGF, PNS
- hit or miss
- Schwann, blocking
No; most recovery is structural in nature; surviving neurons will have structural changes, or may have behavioral compensation
*Ipsilateral connections can be strengthened and children have the ability for the opposite hemisphere to take over functions of injured sites
Plasticity and Neurogenesis (Recovery in CNS)
Plasticity refers to the extent to which the brain can ___ itself.
What is synaptic plasticity?
What is neurogenesis? Where is it studied?
What are stem and progenitor cells?
- reorganize (neural connections)
- Development of new connections (between neurons or different parts of the brain)
- Growth of new neurons from stem or progenitor cells; in hippocampus (also cortex, but only in monkeys)
- Assist in neurogenesis; neither have been fully differentiated into specific types of cells, but can develop into one
Collateral sprouting (Recovery in CNS)
Occurs when intact neurons, near the site of damage, sprout ___ growths that form synapses with neurons that received input s from __ neurons.
Degenerated neurons (one that lost its connection) send out ___ ___. Nearby neurons may sprout new collateral's to take place of empty synapses.
Recovery depends on the __ of 2 axons
- trophic substances
The heightened responsiveness of a denervated postsynaptic neuron to ____ messages from remaining presynaptic neurons.
When a neuron has been deprived of synaptic input, will compensate by becoming more sensitive to ___.
What does this phenomenon explain?
- NT (remaining receptors may get increase in # if receptors in postsynaptic neurons)
- Explains why we can lose 75% of dopamine cells in PD before show symptoms; release of more NT, but will eventually run out
Postsynaptic membrane contains ___ receptors, but no __ receptors. Activation of previously inactive synapses can take over the function of ___ neurons.
Trophic substance ___ binds to receptor, ___ enters. ___ activates proteins that provides signal to ___.
- NMDA, AMPA
- BDNF, Ca+, AMPA receptor
No AMPA (silent)-->BDNF binds, opens NMDA-->Ca+ enters-->inserts AMPA-->synapse no longer silent
The actual extent of neural reorganization after brain damage remains unclear.
Any reorganization occurs because of one of 2 ways:
Strengthens existing connections via experience
Establishes new connections via collateral sprouting (depends on axon's function & similarity)