Pathology Flashcards
what are the 2 questions you should try to answer?
1- where is the lesion
2- what is (are) the lesions
vascular, tumor, traumatic
what is a lesion?
refers to a zone of localized dysfunction w/in the NS
anatomic- structural damage
physiologic- dysfunction in absence of structural lesions
symptoms=
subjective sensations resulting from the disorder
“I have a headache”
signs=
objective abnormalities detected on exam
“hyperactive reflexes”
syndrome=
a constellation of signs and symptoms associated with each other and suggest a common origin
neurologic manifestations may be ___ or ___
negative- loss of function
position- result from inappropriate excitation (seizure)
diagnosis depends on:
history** observation of behavior ** time course neuroexam neuro imaging techniques
neuro exam:
history
cognitive function
-level of consciousness (confusion, alertness, etc)
gait
requires coordination of sensory, cerebellar, visual and vestibular functions
cranial nerves
motor system
weakness, endurance, side, fine finger movements, reflexes
sensory system
distribution
imaging
CT, MRI, xrays, PET, SPECT, etc
EMG
(PNS- check myotome and dermatome)
(CNS- cranial nerve testing- motor and sensory- some sort of provocative action)
what are the different diseases of the motor unit?
neurogenic diseases
myopathies
muscular dystrophies
myotonic disorders
disease of the synapse
neurogenic diseases tend to be more:
distal (glove- stocking distribution (hands/feet))
what are the 2 types of neurogenic diseases?
1- motor neuron
2-peripheral neuropathies
what are s/s of neurogenic diseases?
muscular spontaneous firing
- fasciculation
- fibrillations
neurogenic in the PNS
neuropathies
myopathies=
diseases of muscle
weakness is primary problem
tends to be proximal
muscular dystrophies=
myopathies with special characteristics
- heredity
- progressive weakness and wasting
**first thing to go that causes death is respiratory system
myotonic disorders:
abnormality of muscle fiber membrane
leads to marked delay in relaxation= increase stiffness
what is myasthenia gravis?
a disease of the synapse
“ALS”
autoimmune disorder-antibodies attack ACh receptors (Ach receptors on post-synaptic side disappear and there is no where for ACh to bind)
slow progressive course
weakness is patchy and does not confirm to the distribution of any single nerve
fluctuating weakness and decrease endurance are the major complaints
any age and more common in females
die from respiratory failure- too weak to breath (diaphragm)
classification of myasthenia gravis:
class I: eye muscle weakness
class II: eye muscle weakness; mild ms weakness
IIa: limb /axial muscles
IIb: bulbar/resp muscles
Class III: eye ms weakness; moderate ms weakness
IIIa: limb/axial ms
IIIb: bulbar/resp ms
Class IV: eye ms weakness; severe ms weakness
IVa: limb/axial ms
IVb: bulbar/resp ms
Class V: intubation needed to maintain airway
peripheral nerve injury:
chromatolysis= dissolution of neuron cell bodies
wallerian degeneration =
- 1 day=neurofilaments break up; axons get shorter
- 10 days= myelin sheaths breaks into lipid droplets around axon
- month= myelin gets denatured chemically
- 3 months= macrophages invade degenerating myelin and phagocytose debris
nerve regeneration:
the single nerve fiber will “sprout” to form a regenerating unit. at the tip of each sprout is a growth cone with multiple filopodia. these filopodia will adhere to the basal lamina of the Schwann cell. the Schwanna cells are intimately associated with the regenerating fibers.
as the regenerating unit matures, the individual sprouts become myelinated. regeneration occurs along the basal lamina of the Schwann cells
CNS and PNS go through same process_____ degeneration
wallerian degeneration
axotomy in the PNS
not only affects injured neuron but also its synaptic partners and neighboring cells
the axon distal to the cut will degenerate and so will the myelin surrounding it. The Schwann cells will stay intact. axon degenerates and breaks down into little pieces; neurolemma sheaths stay intact; from cut to synapse the axon is gone. phagocytes clean out neurolemma sheath so its a clean tube.
proximally, the axon will also regenerate/retract one or 2 internodes and regenerates.
cell body starts producing lots of protein
transneuronal degeneration=
atrophy of certain neurons after interruption of afferent axons or death of other neurons to which they send their efferent output.
anterograde- “dying forward”
retrograde- “dying backward”
transneuronal atrophy
CNS neurons have a trophic effect upon each other
apoptosis=
a mechanism of orderly, genetically programmed cell death
synaptic stripping=
when synaptic terminals withdraw from the neurons and are replaced by the processes of glial cells
peripheral regeneration:
Good
chemotropic factors secreted by schwann cells attract axons
-schwann cells give off facilitory factors that help peripheral nerve regeneration
failure to contract a schwann cell causes a neuroma and cell death
adhesive molecules within the distal stump promote axon growth along cell membranes
inhibitory molecules in the perineurium prevent the regenerating axons from going astray
has neurolemma sheath
surgery-3 weeks
the more proximal the injury the higher the change the nerve will:
die
a lot of length of nerve needs to be regenerated
central regeneration:
poor
glial scare
growth inhibition by oligodentroglia
-neurite growth inhibitors (in myelin)
generally don’t have the trophic factors required for successful regeneration
-no neurolemma sheath
