Term
| Name 2 pathologies that occur due to injury to the neuronal cell body |
|
Definition
|
|
Term
| Moves retrogradely from the GI tract to the cell body of the neuron to attack it. |
|
Definition
|
|
Term
| A viral infection that attacks the cell bodies of alpha motor neurons in the spinal cord. |
|
Definition
|
|
Term
| Where does the polio virus enter the body? |
|
Definition
|
|
Term
| This virus travels up the neuronal axon to the cell body where it interrupts synthesis of neuronal proteins in favor of synthesis of viral proteins. |
|
Definition
|
|
Term
| Can poliomyelitis result in paralyis? |
|
Definition
|
|
Term
| Paralysis caused by this pathology develops 2-5 days post onset of illness or may be delayed as long as 2-3 weeks. |
|
Definition
|
|
Term
| The degree of involvement of this pathology is proportional to the number of motor neurons destroyed. |
|
Definition
|
|
Term
| May occur within 30-40 years following the intial disease of polio. |
|
Definition
|
|
Term
| A slowly progressive weakness in previously affected muscles. |
|
Definition
|
|
Term
| Also known as Lou Gehrig's disease |
|
Definition
|
|
Term
| Name a pathology that occurs because of an injury to action potential conductance mechanism |
|
Definition
|
|
Term
| Produced by puffer fish in their ovaries and liver. Puffer fish is a delicacy in Japan. |
|
Definition
|
|
Term
| This pathology causes blockage of the voltage gated Na+ channels in the neuronal cell membrane so they cannot open. |
|
Definition
|
|
Term
| Causes a failure of action potential with resultant paralysis. Patient can die from respiratory paralysis. |
|
Definition
|
|
Term
| Name 3 pathologies that occur from injuries to synaptic terminals. |
|
Definition
Alpha-latrotoxin
Botulism Toxin
Tetanus Toxin |
|
|
Term
| Produced by black widow spiders |
|
Definition
|
|
Term
| Stimulates excessive release of ACh at the neuromuscular junction |
|
Definition
|
|
Term
| Is alpha-latrotoxin typically fatal? |
|
Definition
|
|
Term
| Causes severe local cramps followed by paralysis secondary to ACh depletion. |
|
Definition
|
|
Term
| A very powerful toxin that is produced by anaerboic bacterium. |
|
Definition
|
|
Term
| Can occur from incompletely sterilized canned foods or inhalation of spores. |
|
Definition
|
|
Term
| A systemic problem if ingested or inhaled. Fine locally. |
|
Definition
|
|
Term
| The most powerful biological poison known. Fatal in very small quantities. |
|
Definition
|
|
Term
| This pathology blocks the release of ACh with resultant paralysis. Patient will die quickly of respiratory failure. |
|
Definition
|
|
Term
| A patient can benefit from this with injection with a few muscles. Dosage depends on the weight of the patient. Useful in CP patients. |
|
Definition
|
|
Term
| Inject __ into spastic agonist muscles to allow for development of full range of motion in joint and allow stregthening of the antagonist. |
|
Definition
|
|
Term
| You inject specific muscles with this for a functional outcome. |
|
Definition
|
|
Term
| Produced by anaerobic bacterium in contaminated puncture wounds |
|
Definition
|
|
Term
| The tetanus toxin is carried to the spinal cord by __ transport up neuronal axons. |
|
Definition
|
|
Term
| Binds to axonal terminals of glycine-secreting inhibitory neurons. |
|
Definition
|
|
Term
| Prevents the release of glycine, causing unopposed excitatory input to motor neurons and uncontrolled muscle contraction. |
|
Definition
|
|
Term
| This is found in fertilized soil or soil contaminated by human or animal waste. The onset of symptoms are 3 days to 3 weeks following injury. |
|
Definition
|
|
Term
| What is the mortality rate of tetanus toxin |
|
Definition
|
|
Term
| How can you prevent tetanus toxin? |
|
Definition
|
|
Term
| Symptoms include asphasia, lock jaw, and spasm of facial neck muscles. |
|
Definition
|
|
Term
| An autoimmune disorder whose etiology is unknown. |
|
Definition
|
|
Term
| Antibodies produced against own ACh receptors which then block the receptors, resulting in muscle weakness. |
|
Definition
|
|
Term
| Causes decreased number of junctional folds which results in decreased ACh receptors. |
|
Definition
|
|
Term
| With this pathology you can have normal activation of a muscle will experience weakness over time. Muscles will have difficulty with fast repetition. |
|
Definition
|
|
Term
| This pathology has decreased number of ACh receptors, sparse, shallow junctional folds, widening of synaptic space. |
|
Definition
|
|
Term
| Patient with this pathology initially presents with weakness of ocular muscles (ptosis and diplopia); oropharyngeal weakness (dysarthria, dysphagia) and limb and neck weakness. |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Weakness with this pathology can be resolved by administeration of cholinesterase blockers such as neostigmine or edrophonium |
|
Definition
|
|
Term
| AChesterase breaks down ACh to reuse it. So if you use a cholinesterase blocker this will inhibit the breakdown and allow for ACh to hang out in the neuromuscular junction longer. What is the problem with this? |
|
Definition
| Receptors may become desensitized |
|
|
Term
| The most common X-linked disorder known. The incidence is 1:3500 live births |
|
Definition
| DMD (Duchenne Muscular Dystrophy) |
|
|
Term
| What is the lifespan of a person with DMD? |
|
Definition
| Late teens to early twenties |
|
|
Term
| What is muscle destruction in DMD due to? |
|
Definition
| abnormal or missing dystrophin (protein) and its effect at the muscle cell membrane |
|
|
Term
| What are PT goals with a patient with DMD? |
|
Definition
| Prevention of contractures and preserevations of mobility |
|
|
Term
| Poisons Schwann cells and causes demyelination fo nerve fibers and loss of nerve function. |
|
Definition
|
|
Term
| An autoimmune disorder preceeded by a viral illness such as mono or flu |
|
Definition
|
|
Term
| Peripheral polyneuropathy. Segmental demyelination of peripheral nerves including cranial nerves. |
|
Definition
|
|
Term
| Causes symmetric limb weakness progressing to paralysis. May or may not experience sensory loss. |
|
Definition
|
|
Term
| Recovery for this pathology can take weeks to months. Two thirds can make a full recovery. |
|
Definition
|
|
Term
| How is cognitive function in a patient with Guillian Barre? |
|
Definition
|
|
Term
| A pathology that is more common in females usually between the ages of 20-40 |
|
Definition
|
|
Term
| Multiple areas of demyelination and sclerosis in the CNS. Unknown etiology, but believed to be a combination of environmental and genetic |
|
Definition
|
|
Term
| A viral infection and autoimmune disorder are the two most common causes of pathogenesis for this. |
|
Definition
|
|
Term
| Symptoms of this pathology very according to location and number of lesions. The disease is characterized by exacerbations and remissions. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Decreased edema and pain making the patient feel better. |
|
Definition
|
|
Term
| This pathology takes a variable and unpredicable course. It has multiple areas of demyelination. There is no functional return or repair. |
|
Definition
|
|
Term
| What are the 3 traumatic injuries to axons and their myelin sheaths that were discussed? |
|
Definition
Neuropraxia
Axonotmesis
Neurotmesis |
|
|
Term
| How are peripheral nerve injuries classified? |
|
Definition
| by their severity of lesion |
|
|
Term
| This peripheral nerve injury results in a temporary slowing or loss of axonal conduction. |
|
Definition
|
|
Term
| This peripheral nerve injury does not have any disruption to the axon or axonal degeneration. |
|
Definition
|
|
Term
| This peripheral nerve injury is usually caused by compression, stretching, or inflammation and a full recovery is expected. |
|
Definition
|
|
Term
| This peripheral nerve injury results in disruption of the axon continuity but no damage to the connective tissue that surrounds the axons. |
|
Definition
|
|
Term
| This peripheral nerve injury may be due to subsequent degeneration of distal axonal segments. |
|
Definition
|
|
Term
| This peripheral nerve injury presents with distal weakness and or sensory loss. It takes time to recover depending on severity and length of the nerve. |
|
Definition
|
|
Term
| Denervation of this peripheral nerve injury may be partial or complete. |
|
Definition
|
|
Term
| What is the peripheral receptor of the Deep Tendon Reflex? |
|
Definition
|
|
Term
| This peripheral nerve injury is caused by axonal disuption and damage to the connective tissue that surrounds the nerve. Must be surgically repaired. |
|
Definition
|
|
Term
| This peripheral nerve injury results in degeneration of distal axonal segments, distal weakness and or sensory loss due to the complete transection of the nerve. |
|
Definition
|
|
Term
| Will a patient with Neurotmesis likely have a full recovery? |
|
Definition
|
|
Term
| The process of axonal degeneration and secondary myelin degeneration following axonotmesis or neurotmesis. |
|
Definition
|
|
Term
| This is where the axon degenerates since it is no longer supported by the neuronal cell body. Then the myelin sheath degenerates. Then macrophages arrive to ingest and remove the dead myelin and axonal fragments. |
|
Definition
|
|
Term
| How long does wallerian degeneration take? |
|
Definition
|
|
Term
| How long does wallerian degeneration take? |
|
Definition
|
|
Term
| Where the nucleus moves to the periphery and there is a loss of nissl substance. |
|
Definition
|
|
Term
| Where do you primarily see axonal degeneration? |
|
Definition
|
|
Term
| Central Chromatolysis of neuronal cell body |
|
Definition
1. cell body swells
2. nissl substance disappears
3. altered metabolism to support regeneration of severed axon |
|
|
Term
| If the nerve sheath is intact, axonal sprouts will grow along it to target organ at an average rate of what? |
|
Definition
|
|
Term
| In axonal regeneration, what is it that sprouts new axons? |
|
Definition
|
|
Term
| Can oligodendrocytes in the CNS regenerate? |
|
Definition
|
|
Term
| Can Schwann cells in the PNS regenerate? |
|
Definition
|
|
