MSC Neuro 2025 P1

6.LumbarCord

Lumbarthickening(L2–S1):

Peripheralparaparesisoflegs+sphincterdisorders.

Epiconuslesion: markedsphincterdysfunction.

7.HalfSpinalCord(Brown-SéquardSyndrome)

Ipsilateral→motorparalysis+deepsensitivityloss.

Contralateral→superficial(pain/temp)loss1–2segmentsbelow.

8.AnteriorHornCells(LMN)

Segmentalperipheralparesis(withfasciculations).

Nosensoryloss.

Example:Poliomyelitis,ALS(LMNpart).

9.PeripheralNerve

Peripheralparalysis+sensorylossinnervedistribution.

10.DRG (Intervertebral Ganglion)

Lossofalltypesofsensationindermatome.

Pain,paresthesias,herpeszostereruptions.

11.PosteriorHorn(SpinalGrey–sensory)

Segmentalanesthesia,pain,tensionsigns.

Dissociatedsensoryloss(lossofpain/temp,preserveddeepsensation).

12.LateralColumnofCord

Contraside→anesthesiaofsuperficialsensations(pain,temperature),beginning ~1–2segmentsbelowlesion(spinothalamicpathway).

Inshort(forexams):

Cortex→Mono/hemiparesis+Jacksonianepilepsy.

Internalcapsule→Classicdense hemiplegia+ CNweakness.

Brainstem→Alternatingparalysis.

Spinalcord→level-dependent(tetraparesis,paraparesis,Brown-Séquard).

Anteriorhorn→LMNonly.

Peripheralnerve→paralysis+sensoryloss.

DRG/posteriorhorn/lateralcolumn→sensorysyndromes.

6.Syndromology of peripheral motor neuron damage at different levels (anterior horns of the spinal cord, anterior roots, plexuses, peripheral nerves).

Peripheralmotorneurondamageat di erentlevels—anteriorhorns,anteriorroots, plexuses,andperipheralnerves—resultsindistinctclinicalsyndromesduetodisruptionin motorpathwaysanddenervationofmuscles.

AnteriorHornsofSpinalCord

Damagehereproduces lowermotorneuronsyndrome: muscleweakness,flaccid paralysis, atrophy,areflexia(lossofdeeptendonreflexes),andfasciculations.

Commonconditions: poliomyelitis, spinalmuscularatrophy,amyotrophiclateral sclerosis.

Sensoryfunctionsarepreservedbecauselesionsaremotor-specific.

AnteriorRoots

Lesionscausesimilarlowermotorneuron symptomsasanteriorhorn lesions: muscleweakness, decreasedtone,atrophy,andareflexia.

Maybeassociatedwithradicularpainbecausetherootscanhavesomemixed

fibers(sensorycomplaintspossibleifbothrootsare a ected).

Oftenseeninradiculopathiesanddemyelinatingdiseases.

Plexuses

Damageleadstomixeddeficits:motorweakness,atrophy,reducedreflexes,and possiblysensorylossdependingontheinvolvedplexus.

Pain,paresthesia,andsometimesautonomicchanges(e.g.,alteredsweating,skin color)maybepresent.

Commonintraumaticorinflammatoryplexopathies(e.g.,Parsonage-Turner syndrome).

PeripheralNerves

Resultsindistalweakness,musclewasting, andreducedreflexes,oftenfollowinga specificnerve’sdistribution.

Sensorysymptomsoftenaccompanymotordeficits(numbness,tingling).

Autonomicsymptomspossible(sweatingchanges, skinchanges,bloodpressure issues).

Damageateachlevelproduceslowermotorneuronsyndromebutvariesinmusclegroups a ected,presenceofsensory/autonomicsymptoms,anddistributionofweakness.

7. Methodology for studying voluntary movements.

Methodology fortheStudyofVoluntaryMovements

1.ObservationofGait&Posture

Wernicke–Mannposture→flexedarm,extendedleg→hemipareticgait (stroke/internalcapsulelesion).

Spastic“scissor”gait→paraparesisfromspinalcordlesions,MS,CP.

Steppage/“cock”gait→footdrop, peronealnerve palsy, polyneuropathy.

2.ActiveMovements

Testfrom toptobottom:armelevation,elbow/wrist/hand,trunkflexion, hip/knee/ankle movements,heel–toe walking.

Detectparesis=incompleterange, slow,awkward.

Testsformildparesis:

UpperBarrétest→armsstretchedforward→weakhanddriftsdown.

LowerBarrétest→lyingprone,kneesflexedat45°→weaklegdrops.

3.MuscleStrength

Graded0–5scale:

0=paralysis,5= normal.

1–2=deepparesis,3=moderate paresis,4 =mildparesis.

4.MuscleTone (passivemovements&palpation)

Hypotonia/atony→flaccid,seeninperipheralparesis,cerebellardisorders.

Hypertonia/spasticity→“clasp-knife phenomenon,”densemuscles=central paralysis.

5.PhysiologicalReflexes

Deepreflexes(proprioceptive):

Upperlimb:biceps,triceps,carpo-radial.

Lowerlimb:patellar,Achilles.

Superficialreflexes(exteroceptive):

Abdominal,cremasteric, plantar.

Changes:

↑=hyperreflexia (UMN lesion).

↓/absent=hyporeflexia/areflexia (LMNlesion).

Asymmetry=anisoreflexia.

Jendrassikmaneuver→reinforcesweakreflexes.

6.PathologicalReflexes(UMNlesionsign)

Lowerlimb:

Babinski(extensorgreattoe).

Upperlimb:

Rossolimo(fingerflexionwithtapping).

(SeeninCNSlesions,normallyabsentinhealthyadults).

7.AtrophyandFasciculations

Inspection+measurementofmuscles.

Atrophy=LMNlesionordisuse.

Fasciculations= twitchingbundles→anteriorhorncelldisease(e.g.,ALS).

Inshort(steps):

1.Posture&gait

2.Activemovements(Barrétests)

3.Strength(0–5scale)

4.Tone(spasticvsflaccid)

5.Reflexes(deep,superficial,comparesides)

6.Pathologicalreflexes(Babinski,Rossolimo)

7.Muscleatrophy&fasciculations

8.Classification of sensitivity in neurology. Types of sensitivity disorders: irritative and destructive disorders (hypesthesia, anesthesia, dysesthesia, paresthesia).

ClassificationofSensitivityinNeurology

Sensationscanbeclassifiedinto:

Exteroceptive:Superficialsensationsfromskin/mucousmembranes(pain, temperature,lighttouch).

Proprioceptive:Deepsensationsfrommuscles,tendons,joints(position,vibration, musclesense).

Interoceptive: Sensationsfrominternalorgans(lesscommonlytested).

Combinedsensations: Requirecorticalintegration(e.g.,stereognosis, graphesthesia).

TypesofSensitivityDisorders

1.IrritativeDisorders

Abnormalorexcessivesensorysensationswithoutlossofsensation.

Examples:

Paresthesia:Spontaneousabnormalsensationsliketingling,crawling.

Dysesthesia:Distortedorunpleasantsensations.

Hyperesthesia:Increasedsensitivitytonon-painfulstimuli.

Hyperalgesia:Increasedsensitivitytopainfulstimuli.

Neuralgia:Intensesharppainalonganervecourse.

Causalgia:Severeburningpainwithtrophicchanges.

Canprecedelesions suchasherpeszosterortrigeminalneuralgia.

2.DestructiveDisorders

Reducedorlostsensationdue todamagetoreceptors,nerves,orpathways.

Examples:

Hypesthesia:Decreasedsensitivitytostimuli.

Anesthesia:Completelossofsensation.

Hypalgesia:Decreasedsensitivitytopain.

Analgesia:Lossofpainsensation.

Thermohypesthesia/Thermoanesthesia:Decreasedorabsenttemperature perception.

Thisclassificationhelpsinclinicaldiagnosis—irritativedisordersreflectnerve irritation, whiledestructiveonesindicatenervedamageorlossoffunction.

9.Syndromesofimpairedsensitivityduetodamage tothe brain:parietalcortex,radiant glow,internalcapsule,thalamus,brainstem.

SyndromesofImpairedSensitivityDuetoBrainDamage

1.ParietalCortex(Postcentral Gyrus)

Sensorydisturbancesonthecontralateralhalfofthebody.

Lossincombinedsensationsrequiringcorticalintegration:

Astereognosis(inabilitytorecognizeobjectsbytouch).

Disordersofbodyschema(impairedspatialandbodypartawareness).

Sensationisdiminishedbutnotcompletelylost(noanesthesia).

Impairmentmainlyofdiscriminativesensationssuchastactilelocalization,twopointdiscrimination,graphesthesia.

Associatedwithsensoryneglect/extinctionanddisorderslikeautotopagnosiaand anosognosia.

2.CoronaRadiata

Contralateraltotalhypoesthesia(conductorytype).

Lossofallsensorymodalitiesduetodensearrangementofsensory fibers.

3.InternalCapsule(PosteriorLimb)

Contralateraltotalhypoesthesiasimilartocoronaradiata.

Severe sensoryloss involvingpain,temperature, touch,proprioception.

Maybedi iculttodistinguishclinicallyfromthalamiclesions.

4.Thalamus

Contralateraltotalhypoesthesia.

Hyperpathiaandthalamicpainsyndrome– severe,intractablepainanddiscomfort inthehypoestheticregion.

Sensoryataxiaoncontralateralsideduetolossofproprioception.

Lossofappreciationforheavytouch,deeppressure,andproprioception.

5.BrainStem(Half)

Alternatingsensorydisturbances:

Ipsilateralsegmentalhypoesthesia (face).