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Neurology Year 3- K > MS > Flashcards

Flashcards in MS Deck (14):
1

Multiple Sclerosis

Progressive demyelinating D of CNS, affects white matter, disseminated in time and space- anywhere, anytime.
F>M, , genetic componenet as well.

Hx- past focal neurological deficits, remitted w/o therapy-, young otherwise healthy ppl. Esp on younger !
Young healthy adults!
Focal or non responding to singular lesion.

Sx- weakness, paresthesias, bluriness, diplopia, pain on eye moevement( optic neurotis) (MRi- ptic nerve inflammation)

Px- weakness, numbness/tingling, brisk reflexes- MS-UMN , gait disturbances (progressed case)

Dx- MRI-1st line- Required for diagnosis. ⭐️
Other tests- vitamin levels (normal, low vit D), CSF analysis (seen on CSF ologoclonal band) - not so much
VitB12- alcoholics- numbness and tingling on lower limbs.
Evoked response delayed- due to demyelination

2

Progressions

Most- Relapsing- Remitting - sx + severity, baseline w/ episodes of sx exxacerbation- tx for acute sx, then back to baseline. MOST.
Ultimately to 2o progressive disease.
Clearly definingbattacks of worsening eurological function
- remyelination after inflammatory oedema.

Secondary-progressive- followis after the relapsing remitting course
ORIGINALLY HAD relapsing remotting form- hit a point where MS progressively worse- with exacerbations- never bavk to baseline

Primary Progressive- steadyily worsening neuro fx from begining.
Constantly getting worse- minority


Progressive-Relapsing
Start w/ relapses, never go back to baseline.
Least common- no remissions.
Steadily Progressive disease from beginning, with occasional exacerbation.

3

Ddx

Spinal corde neoplasm
Subacute combined degeneration- alcoholics, Long term B12 deficiemcy.

Cryprogenic stroke- elderly- HTN, risk fx- older pt, sudden, not remits ! Permanent damage from stroke

All- lateralised to one side ie lesion, - spinal cord AVM
All will have constanct sx,

Amyotrohic lateral sclerosis- LMn- dierctly affects the muscle !!

4

MRIs

Lesions

Hyperintense lesions

Surround aqueducts, and ventricles.
Always in white matter, and some grey mater atrophy.
White mater disease- demyelination.

T8 hyperintesne region? In spinal cord lesions.

Anywhere where there is white matter.

5

MS tx

Councelled of nature of disease, progressive,
Sx controlled by medications.
Pts concerns!! Answer.

Stress imp of overall wellness. (Dx, let themselves go to hell)
STOP SMOKING- linked to faster progression- cessation clinic
Weight control - weakness and carry more burden
Healthy diet esp vit D

6

Medical tx

1. Tx acute exacerbations-
2. Treat disease progression (long term therapy)
3. Treat complications symptomatically

7

Acute exacerbations

Tx immediately

IV methylprednisolone for 2-3 days, followed by taoer of PO prednisone for 4w.

Pt should feel better 1-2 d

8

Treat disease progression

Long disease modifying therapy
Interferon beta 1 a- IM+ inteferon beta 1B- admn SC- IFN-b1A, INF-b1B
SE- flu like- fever, fatigue, nausea, malaise

Glatiramer- PREGNANCY SAFE , pregnancy class B

Newer drugs- natalizamab, fingolomod- more SE if INF and glatiramer not responding
SE- progressive, multifocal - PML
JC virus,
Fingolomod- w/DM- macular edema, PR prolongation if heart issues.
But its oral.

INF-b1A or glatimier for answers.

Azathiaprine- 3rd line..

9

Tx sx

UMn

Muscle spasticity- Baclofen, Dantrolene, Diazepam (PM) - benzodiazepine- sedation for night time 🌙⭐️

Fatigue and Narcolepsy- Amantadine, Modafanil, Methylphenidate(really serious)

Pain: phenytoin, Carbamazepine, Pregabalin. Usually trigeminal neuralgia pain.

Urinary urgency: tolteromide, Oxybutinin
Stress urinary inconinence meds.

10

Long term management

Reg follow up
At commencment oof INF b or glatiramerA 6M scan, any more white mater lesionsA comsider switching,p drugs !

Ancilarry care- occupational, physical, psychotherapy, social worker to help with emplyoment.

MANDATORY TO STRESS SMOKING CESSATION !!

11

MS extra pints

Disseminated in time and space.
T cells pass BBB- in an autoimmune fashion- destroy the myelin.
Inflammation- lesions- > lead to axon degeneration

12

Brainstem sx

Dysarthria
Nystagmus (CN 3+6)
Dysphagia
Demyelination
Verigo-CN 8
Trigeminal neuralgia- cz many CN start from there.

12

1st episode

Usually young women, flare up, inflammation
Pattern of inflammation: might be sensory and motor dysfx,
After some days it will be better.

13

Neurological patterns

BAM- might die- Vascular
Bad, worse, worse, better, better-> inflammation
Bad, worse, worse, never better-> chronic e.g. Cancer