Ms, Demyelinating Diseases Muscle Path, Neurologic Sleep Disorders, And Circadian Rythms

Front 1

define demyelination?

Back 1

myelin destruction out of proportion to axonal damage

Front 2

What is acute disseminated encephalomyelitis? How treat? Optic Neuritis?

Back 2

a single episode of widespread inflammation; treat underlying infections agent/source of inflamm
Optic Nuer- only example of demyelination at a single site

Front 3

MS..Clinical symptoms? 3
Sensory symptoms?

Back 3

Ambulatory problems- loss of spinal cord myelin
Visual Problems- loss os optic nerve
INO- loss of MLF and vestibular reflex
Parathesias and loss of pain/temp in asymetric patterns

Front 4

Etiology of MS: viral or env?
explain in context of epidem
genetic vs env?

Back 4

thought to be EBV or Vit D def, since high prevalence in northern latitudes and northern hemispheres and W>M 2:1
Large genetic influence, but needs trigger env.

Front 5

What are oligoclonal bands? How is CT used in diagnosis?

Back 5

Oligoclonal bands are when plasma cells make specific ABs to CNS anitgens ** only in MS***
CT- get contrast enhancing images (white blobs- plaques) and also see brain atrophy

Front 6

MS; what causes the early prodromal symptoms and what leads to to later stages of disease? Implications for Early therapy?

Back 6

Early- immune mediated problem that leads to demyelination
Later- CNS degeneration of brain atrophy and axonal loss

Treat early with Immunosuppressives (decrease lymphocyte recruitment

Front 7

What is a neurogenic disease? Explain denervation/renervation and how muscle fiber types can change? WHat are type 1? Type 2a and Type 2b?

Back 7

Deterioration of nerve. Get reinnervation by collateral nerves and it alters the type of nerve fiber. Go from mixed assortment to regionally identified based on collateral sprouting.
type 1= slow oxidative
type 2a= fast oxidative/glycolytic
type 2b= fast glycolytic

Front 8

What is MG?
3 other ways to see muscle pathology

Back 8

autoABs to the ACHr at NMJs
Primary muscle diseases DuChennes
myopathies associated with toxins/drugs or vasculitis

Front 9

What is polymyositis? How differ from Dermatomyocytis?
How same?

Back 9

POLY- **Actual PMN infiltration of muscles; muscle fibers necrose and regenerate
DERMATO- perifascicular atrophy, NO Infiltration
Both- proximal muscle weakness and rash

Front 10

Inclusion Body Myositis?
Duchenne's; epi, pathogenesis, what happens molecularly? Long temr prognosis?

Back 10

rimmed vacuoles that appear in muscle fibers
Duchennes- 1/3500 boys; mutation in Dystrophin gene; degeneration and replacement with connective and fatty tissue; lose plasma membrane.. end up in wheelchairs by teenage years.

Front 11

Circadian clock; what cells in retina? where is "Master Clock"? What based on? Input from all over body?

Back 11

Melanopsin cells in retina; project to the superchiasmatic nucleus in hypothalamus; have circadian clocks all throughout body, but master integrates them all; based on 24 hr rotation of earth

Front 12

What is the homeostatic system for sleep and its relation to circadian rythm?

Back 12

Homeostatic- increased pressure to go to sleep the moment we wake up; but circadian rythm can overcome that force; as 16 wake hrs approaches, homeostatic drive takes over

Front 13

What occurs cognitively after 16/18 wake hours? When we are tired, what is the first to go somatically?

Back 13

State instability- delays in brain's response
Eye Movements become slow (CN 3,4,6)

Front 14

Sleep stages? how many?
onger we've been awake, what about staging?

Back 14

4 Non-rem and I rem; the longer we've been awake, the greater demand for more sleep and we have decreased latencies and go right into stage 1/2

Front 15

4 facts about sleep (look at)

Back 15

1. Env factors DONT cause sleepiness..just inattention
2. Individuals vary in their reaction to sleep loss, but can't accurately judge it
3. Humans need 7-9 hrs for optimal performance. Leads to sleep debt that must be made up.
4. WE biologically NEED sleep. Don't adapt to less of it.

Front 16

Vulnerability to the cognitive effects (dim accuracy/speed) of sleep deprivation? Type 1? vs Type 3?

Back 16

Type 1 = MED Students; cognitively resistant to sleep deprivation
Type 3- vulnerable to sleep depriv

Front 17

3 major complaints of sleeping issues?

Back 17

1.. I can't sleep.. Insomnia
2. I sleep too much. Narcolepsy
3. I do weird things in my sleep- Parasomnias

Front 18

Narcolepsy: epi, onset age, sleep architecture boundaries?

Back 18

.o5%, 20/30's first DX; boundaries between wakefulness and REM sleep all day

Front 19

Clinical features of narcolepsy? What is cataplexy?
TX of Narcolepsy?

Back 19

excessive sleepiness, constanly in REM, vivid dreams
Cataplexy= loss of muscle tone; head bobbles; feel weak upon wakening
TX= SSRI's and stimulants

Front 20

Parasomnias
1. Disorders of arousal? What boundary between? What are the symptoms 2?

Back 20

Wake up out of slow wave NREM/WAKE.
Sleep walk- do something purposeful, but don't realize it.
Sleep Terror- wake up and are scared shitless; people don't recall, but generally outgrow it

Front 21

Parasomnia:
2. Treatening Dream disorder? Clinical? REM or NREM? What associated highly with?

Back 21

Fall out of bed and punch wife/injury self; defense in a dream
REM/WAKE issue
Can be scene with drug intoxication/withdrawal
High association with Alzheimer's

Front 22

Parasomnias: Restless Leg syndrome vs. Periodic Limb movements? How differ? Causes/family Hx?

Back 22

Restless leg- a VOLUNTARY motor response due to a sensory disturbance; strong family history and caused by DOPA fluctuations

Periodic Limb Movements: INVOLUNTARY sleep relted motor phenomenon due to loss of supra-spinal inhibition during sleep