Cells, Nerve Damage B&B

Question 1

where does tetrodotoxin come from and what is its effect?

Answer 1

toxin from pufferfish, blocks sodium channels in neurons (neurotoxic) —> paralysis

Question 2

what is the role of astrocytes, and what cell marker is specific to them?

Answer 2

remove excess neurotransmitters, repair damage + form scar, major part of reactive gliosis (hypertrophy, hyperplasia)

GFAP (glial fibulary acid protein) is key marker

Question 3

Pt is a 6yo M with a mass in their cerebellum which stains positive for GFAP - what is the diagnosis?

Answer 3

astrocytoma: grow in cerebellum of children

GFAP is astrocyte cell marker

Question 4

JC virus infects which cells of the nervous system?

Answer 4

astrocytes and oligodendyrocytes

causes PML (progressive multifocal leukoencephalopathy) in HIV patients

Question 5

oligodendroglia vs Schwann cells

Answer 5

oligodendroglia: myelinate multiple CNS axons, destroyed in multiple sclerosis

Schwann cells: myelinate PNS axons (only 1), very important for neuron regeneration, destroyed in Guillain-Barre

Question 6

“acoustic neuromas,” aka…

Answer 6

Schwannomas: tumors of Schwann cells, classically affect CN VIII (8) —> interrupt hearing

Question 7

A-alpha vs A-delta vs C nerve fibers

Answer 7

classified by diameter and myelin

A-alpha: large/thick myelinated fibers, most efferent motor fibers + touch/vibration/position

A-delta: small myelinated fibers, sense cold + pain

C fibers: unmyelinated fibers, sense warm + pain

Question 8

Meissner’s corpuscles

Answer 8

touch receptors concentrated in glabrous (hairless) skin like fingers

deformed by pressure —> mechanical nerve stimulation

made of A-alpha (large, myelinated) nerve fibers

Question 9

Pacinian corpuscles

Answer 9

vibration, pressure receptors deep in skin/joints/ligaments

layers of tissue around free nerve ending

deformed by pressure —> mechanical nerve stimulation

A-alpha (large, myelinated) nerve fibers

Question 10

Merkel’s discs

Answer 10

pressure + position receptors found in hair follicles

slowly adapting - provide continuous information for sustained response

made of A-alpha (large, myelinated) nerve fibers

Question 11

mild nerve damage =
moderate nerve damage =
severe nerve damage =
[peripheral nerve damage]

Answer 11

mild nerve damage = neurapraxia (focal demyelination)

moderate nerve damage = axonotmesis (demyelination + axon damage)

severe nerve damage = neurotmesis (axon + myelin sheath irreversibly damaged)

Question 12

mild injury to peripheral nerves resulting in focal demyelination

Answer 12

neurapraxia - axon distal to injury is intact, excellent recovery

Question 13

severe lesions to peripheral nerves resulting in irreversible damage of the axon and myelin sheath

Answer 13

neurotmesis - no significant regeneration occurs, bad prognosis

Question 14

what occurs proximally and distally to lesion in axonotmesis?

Answer 14

axonotmesis: moderate peripheral nerve damage, demyelination + axon damage (endoneurium/perineurium intact)

proximal - axonal reaction (central chromatolysis): cell body swelling + chromatolysis (Nissl bodies disappear) + nucleus pushed to periphery

distal - Wallerian degeneration: axon degenerates and myelin sheath involutes, regrowth possible depending on integrity of Schwann cells

Question 15

describe the central nerve damage that occurs after the following periods of ischemia:
a. 4-5 mins
b. 12-24 hours
c. 24-48 hours
d. days-weeks

Answer 15

a. 4-5 mins: irreversible damage
b. 12-24 hours: microvacuoles in neurons + “red neurons”
c. 24-48 hours: liquefactive necrosis + neutrophil/macrophage infiltration
d. days-weeks: cyst formation + gliosis of astrocytes (multiply/enlarge) which cover cyst

Question 16

how does upper motor neuron (UMN) vs lower motor neuron (LMN) damage present?

Answer 16

UMN (pyramidal signs) —> spastic paralysis (stiff/rigid muscles), hyperreflexia, muscle overactivity, clasp knife spasticity (initial resistance followed by sudden release of movement)

LMN —> flaccid paralysis, fasciculation (spontaneous contractions/twitches), loss of reflexes

Question 17

how would UMN nerve lesions occurring above vs below the decussation present?

Answer 17

above decussation: contralateral dysfunction
below decussation: ipsilateral dysfunction

UMN (pyramidal signs) damage —> spastic paralysis (stiff/rigid muscles), hyperreflexia, muscle overactivity, clasp knife spasticity (initial resistance followed by sudden release of movement)

Question 18

bulbar vs pseudobulbar nerve damage

Answer 18

bulbar palsy = cranial nerve damage (bulbar muscles are those supplied by CN in brainstem) —> LMN damage signs (flaccid paralysis, loss of reflexes)

pseudobulbar = corticobulbar tract damage —> UMN damage signs (spastic paralysis, hyperreflexia)

Question 19

what are the key differences in clinical presentation of bulbar vs pseudobulbar nerve damage?

Answer 19

bulbar palsy = cranial nerve damage —> absent jaw/gag reflexes, flaccid/wasted tongue (LMN signs)

pseudobulbar damage = corticobulbar tract damage —> exaggerated gag reflex, spastic tongue, spastic dysarthria (stop-starting words) (UMN signs)

Question 20

what role do astrocytes play in the tripartite synapse?

Answer 20

contact presynaptic and postsynaptic membranes and regulate glutamate levels (major excitatory NT)

clear glutamate from synaptic cleft, recycle glutamate via conversion to glutamine for reuptake by presynaptic membrane

Question 21

what is the function of satellite cells in the peripheral nervous system?

Answer 21

insulate PNS cell bodies, regulate nutrient/waste exchange for cell bodies in ganglia

Question 22

describe the symptoms of meningismus

Answer 22

meningismus = meningeal irritation

symptoms: headache, nuchal rigidity (stiff neck), photophobia, phonophobia (noise sensitivity), lethargy