Flashcards in MS Deck (14):
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
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
Start w/ relapses, never go back to baseline.
Least common- no remissions.
Steadily Progressive disease from beginning, with occasional exacerbation.
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 !!
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.
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
1. Tx acute exacerbations-
2. Treat disease progression (long term therapy)
3. Treat complications symptomatically
IV methylprednisolone for 2-3 days, followed by taoer of PO prednisone for 4w.
Pt should feel better 1-2 d
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
Fingolomod- w/DM- macular edema, PR prolongation if heart issues.
But its oral.
INF-b1A or glatimier for answers.
Azathiaprine- 3rd line..
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.
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 !!
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
Nystagmus (CN 3+6)
Trigeminal neuralgia- cz many CN start from there.
Usually young women, flare up, inflammation
Pattern of inflammation: might be sensory and motor dysfx,
After some days it will be better.