MSC Neuro 2025 P1

MSC – Neurology and Neurosurgery 2025

PART - 1

1. Methodology for constructing a neurological diagnosis: topical and nosoological diagnoses.

ModernNeurologicalDiagnosis–KeyPoints

A goodneurologicaldiagnosismust:

Be clear,logical,andindividualizedforeachpatient.

Reflectthecourseofthedisease+patient’spersonality.

Directlyguidetherapy,prognosis,andmedicalexpertise.

StepstoDiagnosis

1.Syndromic Diagnosis

Basedonclinicalneurologicalexam.

Identifysymptoms→groupintosyndromes(e.g.,pyramidal,extrapyramidal, cerebellar).

2.TopicalDiagnosis

DeterminesiteoflesionintheNS.

Uses symptom analysis+investigations(MRI,CT,EEG,CSF,etc.).

Aimstoconfirmorexcludeworkinghypothesesanddi erentiatebetween diseases.

3.NosologicalDiagnosis

Finalstage→establishthespecificdiseaseentity(e.g.,MS, Parkinson’s, Stroke).

Allowsforspecifictreatmentplanning.

QuestionsforTopicalDiagnosis

Whenlocalizingthelesion,weask:

1.Natureofdisease:

Structural (tumor,infarct)

Psychogenic

Regulatory/metabolic(e.g.,epilepsy,hypoglycemia).

2.Extentoflesion:

Di use (encephalitis,dementia)

Focal(stroke,tumor)

Partoforganvs.whole organinvolved.

3.Pattern oflesion:

Focalvs.multifocal,

Primaryfocal(stroke,tumor),

Secondary focal(metastases).

4.Characteroflesion:

Locallydestructive(infarct,trauma).

Voluminous(tumor, abscess,hematoma).

5.Dynamicsoflesion:

Progressive (neurodegenerativedisorders,tumors).

Regressing(afterinflammation, trauma recovery).

Stable(oldinfarct,staticencephalopathy).

Inshort:

Syndromic →Topical→Nosological.

Eachstagenarrowsdiagnosis=fromsymptoms→lesionsite→exactdisease.

Alwaysdescribenature,extent,pattern,lesiontype,anddynamics.

2.Classification of neurogenic movement disorders. Definition paresis and paralysis. Classification of paresis by localization, degree of expression femininity.

NeurogenicMovementDisorders–Classification

Byanatomical/functionalbasis:

1.Pyramidaldisorders

2.Extrapyramidaldisorders

3.Cerebellardisorders

Formsofneurogenicmotordisorders:

1.Paresis&Paralysis

2.Pathologicalmusclefatigue

3.Convulsions

4.Ataxia

5.Hypokinesia

6.Hyperkinesia

Definitions

Paresis=partialloss/decreaseofmusclestrengthand restrictionofmovement.

Paralysis=completelossofvoluntarymovement.

ClassificationofParesis

1.ByLocalization(distributioninbody):

Monoparesis–onelimb.

Hemiparesis–halfofthebody(arm+legononeside).

Paraparesis–bothupperorbothlowerlimbs.

Triparesis–three limbs.

Tetraparesis–allfourlimbs.

Biparesis– botharmsorbothlegs.

Akineticmutism–severeglobalreductionofmotoractivitywithmutism.

2.ByMuscleTone:

Spasticparesis–↑tone(centrallesion,UMN).

Flaccidparesis–↓tone(peripherallesion,LMN).

3.ByMechanismofDevelopment:

Central– lesionofcorticospinaltract(UMN).

Peripheral–lesionofmotornerveoranteriorhorncells(LMN).

Mixed.

Psychogenic.

4.ByCourse /Onset:

Acute(e.g.,stroke,trauma).

Regressing(recoveringphase).

Residual(chronic/staticphase).

LesionLocalization&MotorSyndromes

InShortforExams:

Paresis=weakness,Paralysis=nomovement.

Classifyparesisbydistribution,tone,mechanism,andcourse.

Alwayscorrelatewithlesionsite→cortex,capsule,brainstem, spinalcord.

3.Central paralysis. Mechanism and clinical characteristics.

CentralParalysis(SpasticParalysis)

Definition&Mechanism

Causedbydamagetothe centralmotorneuron(UMN)anywhere along:

Motorcortex

Internalcapsule

Brainstem

Spinalcord

Mechanism:Lossofinhibitorycontrolfromcortex→peripheralmotorneurons becomedisinhibited& hyperactive→exaggeratedreflexesandspasticity.

ClinicalCharacteristics

1.Spasticity(↑muscletone)

“Clasp-knife”phenomenon(unevenresistance,thensuddenrelease).

↑tone:flexorsinarms, extensorsinlegs→Wernicke-Mannposture/gait.

2.Hyperreflexia

↑tendonandperiostealreflexes.

3.Clonus

Rhythmic,repetitivecontractionsaftera singlestretch(e.g.,ankleclonus, patellarclonus).

4.PathologicalReflexes

Extensor(UMN signs): Babinski,Oppenheim,Gordon,Schae er.

Flexorsigns:Rossolimo,Bekhterev-Mendel,Zhukovsky-Kornilov.

Hand(carpal)reflexesiflesionabovecervicalcord.

5.ProtectiveReflexes

Spinalautomatism→ involuntarywithdrawal/spontaneousmovementsto stimuli.

6.PathologicalSynkinesis(involuntaryassociatedmovements)

Global:involuntaryflexion/extensionwithe ortor coughing.

Coordinating:appearonlyincomplexmotoracts.

Imitative:mirrormovementsinparalyzedlimb.

7.Nomuscleornervedegeneration(distinguishesfromperipheralparalysis).

Dynamics

Acutephase:flacciditymaybepresentinitially(“spinalshock”), butreflexes↑early (Babinski).

Later→spasticityandUMNsignsdominate.

Topico-DiagnosticOptions(Localization)

Motorcortex/precentralgyrus: contralateralmono-orhemiparesis.

Coronaradiata:contralateralasymmetricalhemiparesis.

Internalcapsule:densecontralateralhemiparesis.

Brainstemlesion:alternatingsyndrome(ipsilateralCNpalsy+ contralateral hemiparesis).

Cervicalcord:tetraparesis,bladderdisturbance.

Thoraciccord:paraparesis oflegs.

Lumbarenlargement:peripherallegparesis.

Inshort(forexams):

Centralparalysis=UMNlesion→spasticparalysis(↑tone,hyperreflexia,clonus, Babinski,synkinesis,noatrophy/degeneration).

Localize bypattern:cortex,capsule, brainstem,orcord.

4.Peripheral paralysis. Mechanism and clinical characteristics. Topical diagnostic options.

Peripheral (Flaccid) Paralysis

Definition

Causedbydamagetoperipheralmotorneurons:

Motornucleiofcranial nerves

Anteriorhorncellsofspinalcord

Axonsofperipheral nerves(radiculopathy,plexopathy, neuropathy)

Neuromuscularjunction(e.g., myastheniagravis,botulism).

Mechanism

Lossofnerveimpulses tomuscle→completedenervation.

Musclecannotcontract,leadingtohypotonia+atrophy.

ClinicalCharacteristics

1.Completeimmobility ofa ectedmuscles.

2.Atony–↓muscletone,limbbecomesflaccid,“pasty,”passivemovementsfree.

3.Areflexia–tendonanddefensivereflexesabsent.

4.Atrophy–progressive musclewasting(20–30%lossin4months; upto70–80% later).

5.Reactionofdegeneration–abnormalresponsetoelectricalstimulation.

Unlikecentralspasticity,herenoactivityatallinmuscle.

6.Pathologicalfatigue(withNMJlesions,e.g., myastheniagravis)→paresisworsens withuse,improveswithrest.

SpecialNotes

ALS(amyotrophic lateralsclerosis):mixedparalysis(UMN+LMNsigns).

Functionalparalysis(neurotic,hysterical,stupor):simulate paralysiswithout organiclesion; varyand lack objectivesigns.

Inshort:

Peripheral=flaccid,atonic,areflexic,atrophic,degenerativereaction.

Central=spastic,hyperreflexic,Babinski+,nodegeneration.

5. Syndromology of the pyramidal tract at different levels (cortex, internal bursa, brainstem, spinal cord).

SyndromologyofPyramidalTractLesions(byLevel)

1.Cortex(PrecentralGyrus–anteriorcentralgyrus)

Lossoffunction→Centralmonoparesis(contralateral,dependingon representation:arm>leg).

Irritative focus→ Jacksonianmotorseizures(focalmotorepilepsywithspread).

2.InternalCapsule

Densecontralateralhemiparesis/hemiplegia.

Involvementofcorticobulbarfibers→centralparesisoffacial&hypoglossal nerves(oppositeside).

3.Brainstem

Alternating(crossed)syndromes:

Ipsilateralcranialnervepalsy(LMNtype).

Contralateralhemiparesis(UMN type).

4.CervicalSpinalCord

Abovecervicalthickening(C1–C4):

Centraltetraparesis+sphincterdisorders.

Cervicalthickening(C5–Th1):

Mixedtetraparesis:

Arms→peripheralparalysis.

Legs→centralparalysis.

Sphincterdisorders.

5.ThoracicCord

Centralparaparesisoflegs+sphincterdisorders.