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multiple sclerosis MRI brain periventricular plaques lesions

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Multiple Sclerosis (MS) — All Findings

Overview

MS is a chronic immune-mediated demyelinating disease of the CNS. It occurs 2–2.5× more often in women, typically manifests in the 3rd–4th decade, and has a prevalence of ~309/100,000 in the US (~730,000 Americans; ~2.8 million worldwide).

Clinical Findings

Presenting Symptoms

System	Symptoms
Visual	Optic neuritis — monocular blurring, pain on eye movement, central scotoma (centrocecal), red color desaturation
Sensory	Paresthesias (circumferential, non-dermatomal), bandlike pain around trunk or limb, Lhermitte sign
Motor	Limb weakness, spasticity, hyperreflexia
Cerebellar	Imbalance, incoordination, intention tremor, scanning speech
Bladder	Urgency, frequency, incomplete emptying
Fatigue	Most common symptom overall
Cognitive/Psych	Depression (37–54%), cognitive slowing, euphoria

Key Signs on Examination

Lhermitte sign — electrical sensation down the spine into limbs on neck flexion; indicates cervical cord demyelination
Optic neuritis — afferent pupillary defect (Marcus Gunn), swollen or normal-appearing disc; visual recovery common but often incomplete
Internuclear ophthalmoplegia (INO) — impaired adduction of one eye with nystagmus in the abducting eye; due to MLF demyelination — highly suggestive of MS in a young patient
Sensory levels — incomplete, often asymmetric, may differ by modality (dorsal columns vs. spinothalamic)
Upper motor neuron signs — hyperreflexia, extensor plantar response (Babinski sign), clonus
Charcot triad — intention tremor, scanning speech, nystagmus (classic but rare)
Uhthoff phenomenon — worsening of symptoms with increased body temperature (hot weather, exercise, fever)

MRI Findings (Most Sensitive Investigation — >95% Abnormal in Definite MS)

MS MRI FLAIR Dawson's fingers periventricular plaques

Axial FLAIR/T2 sequences showing classic periventricular MS plaques, including "Dawson's fingers" oriented perpendicular to the ventricles

MS MRI ring-enhancing lesion T1 black holes

T2-FLAIR showing periventricular plaques (A), gadolinium ring-enhancing active lesions (B–C), and T1 "black holes" representing axonal loss (D–E)

T2 / FLAIR — White Lesions (Most Sensitive)

Size: 2 mm – 2 cm (occasionally tumor-like)
Shape: Ovoid, elliptical, discrete borders, no mass effect
Classic locations (McDonald 2017 criteria — lesions in ≥2 of 4 areas):
1. Periventricular — perpendicular to ventricle walls = "Dawson's fingers" (most characteristic)
2. Juxtacortical/cortical
3. Infratentorial — cerebellar peduncles, brainstem
4. Spinal cord — dorsolateral cervical cord

T1 Post-Gadolinium — Active Inflammation

Gadolinium enhancement = blood-brain barrier breakdown = active/new lesion
Pattern: homogeneous, central, or ring-enhancing
Typically persists 2–8 weeks
Provides evidence for dissemination in time (DIT) when concurrent non-enhancing T2 lesions are present

T1 Pre-Contrast — Chronic Damage

"Black holes" = persistent T1 hypointensities = axonal loss and atrophy (irreversible damage)

Spinal Cord MRI

Dorsolateral plaques on sagittal T2; typically <2 vertebral segments (vs. NMO which spans ≥3 segments)

CSF Findings

Test	Finding
Cell count	Mild lymphocytic pleocytosis (usually <50 WBCs/µL); >50 cells or neutrophils is atypical
Total protein	Mildly elevated or normal; >100 mg/dL is unusual for MS
Glucose	Normal
Oligoclonal IgG bands (OCBs)	Present in 85–90% of clinically definite MS (absent in serum = intrathecal production)
IgG index	Elevated (>0.7) — indicates intrathecal immunoglobulin synthesis
Myelin basic protein	May be elevated but non-specific (elevated in any CNS tissue destruction)

CSF is not mandatory when clinical + MRI evidence is sufficient; it is recommended when the diagnosis is uncertain or infection/malignancy must be excluded.

Evoked Potentials

Type	Finding
Visual evoked potentials (VEP)	Prolonged P100 latency — most clinically useful; documents subclinical optic nerve lesion
Brainstem auditory evoked potentials (BAEP)	Delay of central conduction; wave I may be abnormal
Somatosensory evoked potentials (SSEP)	Prolonged central conduction time

Evoked potentials can reveal clinically silent lesions, aiding in demonstrating dissemination in space.

2017 McDonald Diagnostic Criteria (Summary)

The diagnosis requires evidence of dissemination in space (DIS) and dissemination in time (DIT):

DIS on MRI = ≥1 T2 lesion in ≥2 of 4 regions:

Periventricular, juxtacortical/cortical, infratentorial, spinal cord

DIT on MRI = simultaneous presence of:

Asymptomatic gadolinium-enhancing AND non-enhancing T2 lesions, OR
A new T2/enhancing lesion on follow-up scan

CSF shortcut: Positive CSF-specific oligoclonal bands can substitute for DIT in a clinically isolated syndrome (CIS).

Pathological Findings (Gross & Microscopic)

Finding	Description
Plaques	Sharply demarcated areas of demyelination in white matter ± gray matter
Active plaques	Perivascular lymphocytic infiltrates (CD4+/CD8+ T cells, macrophages), myelin stripping
Chronic plaques	Hypocellular, gliotic, axonal loss, "shadow plaques" at edges (remyelination)
Axonal transection	Occurs even in acute lesions; underlies irreversible disability
Cortical demyelination	Common but underdetected by conventional MRI; correlates with cognitive impairment

Disease Course Subtypes

Type	Features
RRMS (85–90% at onset)	Distinct relapses with full or partial recovery; most common
SPMS	Progressive accumulation of disability after initial RR phase
PPMS (~10–15%)	Progressive from onset, no relapses; more spinal cord-dominant
CIS	First demyelinating event; converts to MS if McDonald criteria are later fulfilled

Disability Measurement

Expanded Disability Status Scale (EDSS) (Kurtzke scale) — assesses 7 functional systems:

Pyramidal, cerebellar, brainstem, sensory, bowel/bladder, visual, cerebral

Sources: Goldman-Cecil Medicine 26e, Ch. 380; Harrison's Principles of Internal Medicine 22e, Ch. 50; Bradley and Daroff's Neurology in Clinical Practice

no tell everything about mitral stenosis not multiple sclerosis include images also

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Mitral Stenosis (MS) — Complete Findings

Definition & Aetiology

Mitral stenosis is obstruction to left ventricular inflow at the mitral valve level, causing a persistent diastolic pressure gradient between the left atrium and left ventricle.

Normal mitral valve area: 4–6 cm²

Cause	Notes
Rheumatic fever (most common worldwide)	Commissural fusion + leaflet thickening; 3× more common in women; pure MS in 40% of rheumatic heart disease
Mitral annular calcification (MAC)	Increasing cause in elderly/developed nations
Congenital	Parachute mitral valve, supravalvular ring
Rare	Ball-valve thrombus, LA myxoma, carcinoid, radiation, mucopolysaccharidosis, cor triatriatum (mimics MS)

Pathophysiology

LA–LV pressure gradient in mitral stenosis

The shaded gray area shows the persistent diastolic gradient between LA pressure (red) and LV pressure (yellow) in severe MS — Goldman-Cecil Medicine

Obstructed LV inflow → ↑ LA pressure → pulmonary venous hypertension → dyspnoea / pulmonary oedema
Restricted inflow + reflex vasoconstriction → ↓ cardiac output
Chronic ↑ LA pressure → LA dilatation → atrial fibrillation
AF with MS: rapid rate shortens diastolic filling time → acute decompensation
Progressive pulmonary hypertension → RV pressure overload → RV failure
Symptoms typically appear when MVA < 1.5 cm² (one-third of normal)

Symptoms

Symptom	Mechanism
Dyspnoea on exertion (earliest)	↑ LA & pulmonary venous pressure
Orthopnoea / PND	Pulmonary congestion worsened by recumbency
Haemoptysis	Rupture of bronchial–pulmonary venous anastomoses (high LA pressure); characteristic of MS, uncommon in other causes of LA hypertension
Palpitations	Atrial fibrillation
Ortner syndrome	Hoarseness from compression of left recurrent laryngeal nerve by giant LA
Dysphagia	LA impinging on oesophagus
Systemic embolism / stroke	LA thrombus (especially LAA) from stasis ± AF
Ascites, ankle oedema	Right ventricular failure
Fatigue	↓ cardiac output

Physical Examination Findings

General & Precordium

Malar flush (mitral facies) — peripheral cyanosis with rosy cheeks due to ↓ CO + vasoconstriction
Quiet apical impulse (LV not volume overloaded)
Parasternal lift — if RV hypertrophy from pulmonary hypertension

Heart Sounds

Finding	Mechanism
Loud S1 (most prominent sign)	Transmitral gradient holds valve open; LV systole closes fully open valve forcefully
Opening snap (OS) after S2	Sudden halt of leaflets; only present if leaflets still mobile (absent if calcified)
Short S2–OS interval	High LA pressure; interval 0.04–0.12 sec; closer = more severe
Low-pitched mid-diastolic rumble at apex	Classic murmur; best heard with bell in LLD position; increases in length as severity worsens
Presystolic accentuation	Atrial systole accelerating flow across valve (sinus rhythm only; absent in AF)
Graham Steell murmur	High-pitched early diastolic murmur of pulmonary regurgitation from pulmonary hypertension
Loud P2 (pulmonic component of S2)	Pulmonary hypertension
S3 and S4 absent	Obstruction prevents rapid LV filling

ECG Findings

Finding	Cause
P mitrale — broad, bifid P wave (>0.12 sec) in lead II; biphasic P in V1	LA enlargement (sinus rhythm)
Atrial fibrillation	LA dilatation and rheumatic atrial inflammation
Right axis deviation	RV hypertrophy
RV hypertrophy pattern — tall R in V1, deep S in V5–V6	Pulmonary hypertension

Chest X-Ray Findings

CXR massive left atrial enlargement in mitral stenosis

Chest X-ray showing massively enlarged left atrium in longstanding mitral stenosis — Bailey & Love's Surgery

Feature	Sign
Left atrial enlargement	Double shadow at right heart border; straightening of left heart border; elevation of left main bronchus (carinal angle >70°)
Mitral valve calcification	Visible on lateral film or fluoroscopy
Pulmonary venous hypertension	Upper lobe blood diversion (cephalization); Kerley B lines (horizontal interstitial lines at lung bases)
Pulmonary oedema	Bilateral perihilar haziness in decompensated state
RV enlargement	Filling of retrosternal space on lateral view
Pulmonary artery enlargement	Prominent main pulmonary artery on PA film
Overall cardiac silhouette	May be normal or only mildly enlarged (LV is not dilated)

Echocardiography Findings (Gold Standard — ~100% Diagnostic)

2D / Morphological Findings

Parasternal long-axis echo showing mitral stenosis — thickened leaflets, doming, LA enlargement

Parasternal long-axis view: thickened mitral leaflets with restricted diastolic opening (doming anterior leaflet, white arrow). LA enlargement evident — Grainger & Allison's Radiology

Parasternal short-axis echo showing fish-mouth mitral valve orifice and M-mode diastolic rumble correlation

Left: parasternal short-axis showing stenotic mitral orifice (1.09 cm²). Right: M-mode with phonocardiogram correlating restricted leaflet motion with the classic diastolic rumble — Braunwald's Heart Disease

Feature	Finding
Leaflet morphology	Thickening, calcification, nodularity
Hockey stick deformity	Anterior mitral leaflet bows anteriorly in diastole (posterior leaflet pulled back) — rheumatic
Fish-mouth / buttonhole appearance	Commissural fusion on short-axis view
Commissures	Fusion (anterolateral and/or posteromedial)
Chordae tendineae	Thickening, shortening, fusion
LA enlargement	Chronic pressure overload
LA thrombus	Most commonly in LA appendage; look with TEE
LV	Usually normal size and function; reduced in ~1/3 due to ↓ preload
RV	Dilated + hypertrophied with pulmonary hypertension

Doppler Findings

Measurement	Severe MS
Mean transmitral gradient	≥10 mmHg
Mitral valve area (MVA) — pressure half-time	MVA = 220 / T½ (T½ = time for gradient to fall by 50%)
Severe MVA	< 1.0 cm²
Moderate MVA	1.0–1.5 cm²
Mild MVA	> 1.5 cm²
Peak E-wave velocity	Elevated (>1.5 m/s in significant MS)
E-wave deceleration	Prolonged (slow filling)
TR jet velocity	Elevated if pulmonary hypertension

Grading by Severity

Grade	MVA (cm²)	Mean Gradient (mmHg)
Mild	> 1.5	< 5
Moderate	1.0–1.5	5–10
Severe	< 1.0	> 10

3D Echo Findings

3D TEE fish-mouth mitral orifice with planimetry 0.63 cm²

3D TEE surgical view: fish-mouth mitral orifice, planimetry = 0.63 cm² (critical stenosis)

Echocardiography rheumatic mitral stenosis fish-mouth hockey stick

A: Hockey stick deformity of anterior leaflet (PLAX). B: Fish-mouth orifice (PSAX). C: Dilated LA on apical 4-chamber. D: Color Doppler turbulent flow jet across stenotic valve

Cardiac Catheterisation Findings

Elevated LA / PCWP with persistent LA–LV diastolic gradient
Gorlin formula to calculate MVA from simultaneously measured pressures and cardiac output
Used when echo is inconclusive or when coronary anatomy must be assessed pre-operatively

Cardiac MRI Findings

Cine-MRI showing mitral stenosis flow void from LA to LV

Cine-MRI two-chamber view: small flow void (arrows) from LA to LV indicating mild MS; enlarged LA evident — Grainger & Allison's Radiology

Flow void / turbulent jet across stenotic valve on cine imaging
Direct planimetry of valve orifice
LA enlargement clearly demonstrated
Velocity-encoded MRI allows pressure half-time calculation of MVA

Complications

Complication	Notes
Atrial fibrillation	Most common arrhythmia; precipitates acute decompensation
Systemic thromboembolism / stroke	LA thrombus; most dreaded complication
Pulmonary hypertension	Secondary, initially reactive (reversible); later fixed
RV failure	Late complication of severe pulmonary hypertension
Infective endocarditis	Risk higher in non-calcified, mobile leaflets
Ortner syndrome	Hoarseness from giant LA compressing LRLN
Haemoptysis	Bronchial vein rupture

Management Overview

Scenario	Management
Asymptomatic, sinus rhythm	No therapy needed; serial monitoring
Mild dyspnoea	Diuretics
AF with MS	Rate control (β-blocker, diltiazem, digoxin); warfarin (INR 2.5–3.5) — NOACs are NOT recommended for rheumatic MS with AF
Severe symptomatic MS, suitable anatomy	Percutaneous balloon mitral commissurotomy (PBMC/PTMC) — suitable if pliable, non-calcified valve, no significant MR, no LA thrombus
Unsuitable for PBMC	Open surgical commissurotomy or mitral valve replacement
MAC-related MS	Surgical debridement + MVR (PBMC not effective)
Pulmonary HTN ≥50 mmHg	Indication for mechanical intervention

Wilkins Echo Score (leaflet mobility, thickening, calcification, subvalvular fusion — each 0–4, total 0–16): score ≤8 predicts good outcome with balloon commissurotomy.

Sources: Goldman-Cecil Medicine 26e, Ch. 60; Braunwald's Heart Disease 12e; Grainger & Allison's Diagnostic Radiology; Textbook of Clinical Echocardiography

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