MSC Neuro 2025 P1

Peripheralsensory impairmentsyndromesrefertosensorydisturbancesstemmingfrom lesionsa ectingperipheralnervesandrelatedstructures.Thesecanbeclassifiedinto severaltypesbasedon theanatomicalandclinicalfeatures.

Neural(Mononeuritic)Type

Occurswhenasingleperipheralnerve isa ected.

Sensorylossinvolvesalltypesof sensationwithinthedistributionareaofthe specifica ectednerve.

Sensoryexaminationshowsanesthesia,hypesthesia,analgesia,orhyperesthesia limitedtothenerve'sautonomouszone.

Example:Alesionoftheulnarorradialnerve causinglossoralterationofsensation intheirrespectiveterritories.

Polyneural(Polyneuropathic)Type

Involvesmultipleperipheralnerves,usuallysymmetrically.

Sensoryimpairmenttypicallya ectsthedistalpartsofthelimbs("gloveand stocking"distribution).

Includeslossordecreaseofallormostsensorymodalities—pain,temperature, touch, proprioception.

Frequentlyseeninconditionslikediabeticneuropathy,toxicneuropathies,or hereditarysensoryneuropathies.

Mayinvolvesensoryataxiaduetodeepsensationloss.

RadicularType

Duetolesionsofthedorsal(sensory)rootsofspinalnerves.

Sensorylosscorrespondstothedermatomaldistributionofthea ectednerve roots.

Clinically,canpresent withpain,paresthesias, hypalgesiaorevenanesthesiainthe distributionoftheinvolvedroot.

Irritative lesionscauseradicularpain,oftensharp,stabbing,orlancinating.

SignssuchasNeri's,Lasegue's,and Wassermann'ssymptomsmaybe positive.

Radicularsyndromemaypresentwithdiminishedreflexesifmotorrootsare involved.

PlexusLesions

Lesionsofnerveplexuses(cervical,brachial,lumbosacral)a ectthesensoryand motorfunctionsofmultiplenerves arisingfromthea ectedplexus.

Sensorylossisintheareaofinnervationofthe wholeplexusoritsparts.

Symptomsoftenincludepainandparesthesiasintheplexusdistributionarea.

Signsmightinclude trophicchanges, autonomicdysfunction,andweakness dependingonseverity.

Examples:Brachialplexusinjurycausingsensorylossandparesthesia inthe shoulder,arm,andhand.

Clinicaland DiagnosticAspects

Sensoryexaminationshoulddelineateareasofhypoesthesia,anesthesia,or hyperesthesiarelative tonervedistributionsanddermatomemaps.

Di erentiationbetweenperipheralnerve,root, andplexus lesions isbasedon patternofsensorylossandassociatedmotor/reflexfindings.

Carefultestingofdi erentmodalities(pain,temperature,touch,vibration, proprioception)isessential.

Overlapsinpainand temperaturesensationfieldsmustbeconsidered.

Conditionssuch asneuritismaypresentwithhyperesthesiaandtendernessto nervepalpation.

Radicularpainischaracteristicallyexacerbatedbymovement,coughing,or straining.

Inplexusinjuries,clinicalpresentationsvarydependingontheplexusa ectedand the extentofinvolvement.

12.Methodologyforstudyinggeneralsensitivity.

The methodologyforstudyinggeneral(somatic)sensitivityinvolvesasystematicapproach toassessvarioustypes ofsensorymodalitiestoidentifyabnormalities, localizelesions, anddeterminethenatureofsensorydysfunction.Themainstepsandprinciplesinclude:

1.InitialPatientInterview:

Clarifythepatient’ssubjectivesensorysymptoms,suchaspain,numbness, tingling,burningsensations,andabnormalitiesintemperatureperception.

Notecharacteristicslikeintensity,localization,nature,duration,periodicity, andexacerbatingorrelievingfactors.

Evaluatewhetherthe sensorysymptomsarespontaneousorstimulusevoked.

2.AssessmentofSuperficial(Exteroceptive)Sensation:

Pain:Testedusingpinprickorpin;termslikeanesthesia(loss),hypalgesia (reduced),hyperalgesia(increased)areusedtodescribesensorychange.

Temperature:Evaluatedusingtesttubesormetalobjectswithcoldandhot temperatures.Changesincludethermhypesthesiaorthermhyperesthesia.

Touch:Assessedusinglightstimuli like cotton wool,brush,orfeather; terms include anesthesia,hypesthesia, hyperesthesia.

Conduct testingbilaterallyanduse comparisonbetweena ectedand normalsidefordelineatingdeficitsandborders.

3.AssessmentofDeep(Proprioceptive)Sensation:

Positionsense:Testedbymovingpatient'sfingersortoeswitheyesclosed andaskingfordirectionofmovement.

Vibrationsense:Tested usingatuningforkonbonyprominencessuch as ankles,wrists.

Jointpositionandmovement:Evaluatedtodetectimpairedproprioception.

Abnormalitiesleadtosensory ataxiaifsevere.

4.AssessmentofCombinedorCorticalSensoryFunctions:

Stereognosis:Recognitionofobjectsbytouch witheyesclosed.

Graphesthesia:Abilitytorecognizelettersornumberstracedontheskin.

Two-pointdiscrimination:Abilitytodistinguishtwoclosepointsontheskin.

Barognosis:Abilitytojudgeweightdi erences.

Topesthesia:Localizationoftactilestimuli.

Assessmentofbodyschema:Includingtestsforautotopagnosiaand anosognosia.

Testingthesehelpsdetectcorticalsensorydeficitslikeastereognosis, agraphesthesia.

5.LocalizationofLesions:

Sensorydeficitsconfinedtoperipheralnerveterritoriessuggestperipheral neuropathies.

Segmentalordermatomalsensoryabnormalitiessuggestnerveroot or spinalcordlesions.

Contralateraldeficitspointtocentralnervoussystemlesions,with dissociatedsensorylosspatternshelpingtolocalizespinalcordorbrain lesions.

Associatedneurologicalsignsassistintopographicdiagnosis.

6.AdditionalObservations:

Presenceofallodynia, hyperesthesia,paresthesias,anesthesiadolorosafor painsyndromes.

Useofdiagnosticmaneuvers like painthresholdtesting,sensoryextinction, andassessmentduringvariouspositions.

Insummary,the methodologyforstudyinggeneralsensitivity consists ofadetailedhistory andsystematicexaminationofsuperficial,deep,andcorticalsensory modalities,using qualitativeandquantitativesensory tests,performedbilaterallyandwithattentionto patternandlocalizationofsensorydeficitstoaccuratelydiagnoseand localize neurologicallesions

13.Syndromesofdamagetotheolfactorysystem.

OlfactoryNerve(CNI)

Notatrue cranialnerve–developsfromevagination(outgrowth)ofcerebralvesicle wall,partofolfactorysystem.

OlfactoryPathway(3-neuronsystem)

1.FirstNeurons:

Bipolarcellsinnasalmucosa(uppernasalcavity).

Processesform~20olfactoryfilamentsperside→passthroughcribriform plate→reacholfactorybulb.

2.SecondNeurons:

Mitral&tuftedcellsinolfactorybulb.

Axonsformolfactorytract→terminateinprimaryolfactorycortex(periamygdaloid, prepyriformareas,lateralolfactorygyrus, amygdala).

3.ThirdNeurons:

Locatedinprimaryolfactorycortex.

Axons→entorhinalcortex(parahippocampalgyrus,area28).

Fiberscrossviaanteriorcommissure,linkingbothhemispheres&limbic system.

Connections

Tohypothalamus,thalamus,limbicsystem→emotion&autonomicaspectofsmell.

Viaforebrainbundle,reticularformationnuclei,dorsalvagalnucleus→ visceral/autonomicresponses(e.g.,salivation,nausea).

ClinicalExamination

Testeachnostrilseparatelywithnon-irritantodors(rosewater,camphor,soap).

Avoidirritants (ammonia,vinegar)→stimulatetrigeminalendings.

Ensurenasalpassagesareclear.

DisordersofSmell

Anosmia(lossofsmell):

Bilateral:URTI,rhinitis.

Unilateral:suggestsCNSlesion(e.g.,frontallobetumor).

Hyperosmia:heightenedsmell(hysteria,cocaineabuse).

Parosmia:distortedsmell(schizophrenia,parahippocampalgyruslesion,hysteria).

Olfactoryhallucinations:inepilepsy(uncinate/parahippocampalgyrusseizure focus).

ClinicalImportance

Gatewayforinfections:encephalitis,meningitis,poliomyelitis.

Causesofolfactory impairment:

Nasaldiseases,

Headtrauma,anteriorcranialfossafractures,

Tumors(frontallobe,pituitary),

Hydrocephalus,meningitis,stroke,

Drugintoxication,psychosis,neurosis,congenitaldefects.

SpecificSyndromes

Foster-Kennedysyndrome:Ipsilateralanosmia,opticatrophywith contralateral papilledema(usually frontallobetumor).

Epilepticaura:Olfactorysensation(oftenunpleasantsmell)precedingseizure.

14.Thevisualsystem,signsofitsdamageatdi erentlevels.

OpticNerve(CNII)&VisualPathways

Origin:axonsofganglioncellsofretina.

Course:

Retina→Opticnerve→Opticchiasm(nasalfiberscross;temporalfibersremain)→ Optictracts→Lateralgeniculatebody→Optic radiations(Gratiolet’s radiations) → Primaryvisualcortex(occipitallobe,area17 aroundcalcarinesulcus).

Connections

Pretectalarea→Edinger-Westphalnucleus→direct&consensuallightreflex.

Superiorcolliculi →tectobulbar/spinaltracts→involuntaryeye&headmovements.

Occipitalcortex→othercortical/subcorticalregions→complexvisualprocessing. FieldofVision

Eachhemifieldmappedtooppositeretina:

Temporalvisualfield→nasalretina.

Nasalvisualfield→temporalretina.

Rightvisualfield→lefthalfofbothretinas→leftoptic tract.

Research/Examination

Visualacuity(Snellen,amblyopia =lowvision).

Visualfields(perimetry,campimetry).

Colorvision.

Fundoscopy.

Pupillaryreactions(direct,consensual).

DamageSignsbySite

1.OpticNerve(beforechiasm)

Amaurosis(blindness)ofa ectedeye.

Lossofdirectpupillarylightreflex,butconsensualreflexpreserved.

Scotomas:

Central/paracentral(typicalofopticneuritis).

Positivescotoma(patientperceivesdarkspot).

Negativescotoma(onlyfoundonfieldtesting).

OpticAtrophy:

Primary:directinjury(tumor,toxinslikemethanol,tabesdorsalis).

Secondary:duetopapilledema(tumor,increasedICP,glaucoma, hypertension).

2.OpticChiasm

BitemporalHeteronymousHemianopia(commoninpituitary tumors).

Binasalhemianopia(rare;usuallybilateralperichiasmallesions).

3.OpticTract(post-chiasmuptoLGN)

HomonymousHemianopia(lossofcontralateralhalfofvisualfield).

PupillaryLightReflex:a ectedbecausetractfiberscarrypupillarya erents.

4.OpticRadiation(Gratiolet’sfibers)

Homonymoushemianopiaorquadrantanopia(dependingonlesionsite):

Temporallobe(Meyer’s loop)→UpperQuadrantanopia (“pieinthesky”).

Parietallobe→LowerQuadrantanopia (“pieonthefloor”).

Pupillaryreflexespreserved(fibersseparatedbeforethis level).

5.PrimaryVisualCortex(Occipitallobe,calcarinefissure)

Contralateralhomonymoushemianopia(macularsparingcommonduetodual bloodsupply).

Visualhallucinations:

Simple(photopsias) →flashes,coloredlights.

Complex→figures,faces,scenes(fromoccipital/temporalassociation).

KeyTerms

Amblyopia =reducedacuity.

Amaurosis=completeblindness.

Scotoma=partial fielddefect(positive/negative,central/paracentral/peripheral).

Hemianopia:

Homonymous(samesidehalves lost)→post-chiasmal.

Heteronymous(oppositehalveslost)→chiasmal.

QuickTest Tip:Localizationisbestdonebytype ofvisualfieldloss:

Monocularblindness→Opticnerve.

Bitemporalhemianopia→Chiasm(pituitarytumor).

Homonymoushemianopia→Tract/ radiation /cortex(sideoppositetodefect).

Quadrantanopia→Radiation(temporalorparietallobe).

15.Theimportance ofexaminingthefundusin the clinicofnervousdiseasesand neurosurgery.Variantsofchangesinthefundus oftheeye.

ImportanceofFundusExaminationinNeurologyandNeurosurgery

Non-invasive windowtothecentralnervoussystem:

The fundusrevealstheopticnerveheadandretinalbloodvessels,whichare directextensionsofthebrain’svasculature.

Allowsvisualization ofneurologicalandvascularchangeswithoutinvasive procedures.

Detectionofraisedintracranialpressure:

Papilledema(opticdiscswelling) isanimportantsignindicatingincreased intracranialpressure.

Earlydetectioncanpreventpermanentneurologicaldamageordeathby guidingurgentintervention.

Diagnosisofneurologicalandsystemicdiseases:

Detectsopticneuritis,ischemicopticneuropathy,retinalvascular abnormalities,andhemorrhages.

Revealssignsofsystemichypertension,diabetes,infections,and hematologicaldisordersa ectingthenervoussystem.

Importance:Examiningopticdisc(Z.N.),retina, vesselshelpsdetectintracranialand opticnerve pathology.

NormalDisc

Round, pink,clearborders.

PathologicalChanges

1.CongestiveDisc(Papilledema)–dueto↑intracranialpressure

Signs: blurredborders, red/dark disc,engorgedveins,narrowedarteries,disc swelling, hemorrhages.

Vision:preservedearly, lostlater(secondary atrophy→blindness).

2.OpticNeuritis–inflammatory

Signs: hyperemicdisc,blurrededges,arteries +veinsdilated,noprotrusion aboveretina.

Vision:rapiddecreaseinacuity.

Retrobulbarneuritis: nofundus changesatfirst,butmarkedvisionloss(seen inmultiplesclerosis,arachnoiditis,post-infectiousencephalitis).

3.OpticAtrophy(primary vssecondary)

Primary:pallor,smalldisc,clearmargins→seenintrauma,tumors,syphilis, toxins.

Secondary:discpale+ residualsignsofpastedema/neuritis,blurred margins.

Partialatrophy:temporalpallor(bitemporal)–maybeearlystageoreven normalininfants.

4.SpecialSyndromes

Foster-KennedySyndrome:ipsilateralprimaryatrophy(tumorside)+ contralateralpapilledema.

5.OtherFundusSigns

Toxoplasmosis:chorioretinitis.

Tay-Sachsdisease:“cherry-redspot”.

KeyClinicalValue:

Detectsintracranialhypertension,opticneuritis,andopticnerve/chiasm/tract lesions.

Helpsinlocalizingneurologicalpathologyandmonitoringprogressionto atrophy/blindness.

Forexams→Alwaysrelatediscfindingstocause:

Congestivedisc=raisedICP,

Neuritis=inflammatory/demyelinating(MS),

Primaryatrophy =directinjury/tumor,

Secondary atrophy=consequenceoflongcongestion/neuritis.

16.Pupillaryreflexandsignsofitsdamage;typesandcausesofanisocoria;ArgyllRobertsonsyndrome

PupillaryReflex

MusclesInvolved:

Sphincterpupillae→Circular,parasympathetic(constriction).

Dilatorpupillae→Radial,sympathetic(dilation).

ReflexArc(Lightreflex):

1.A erent→Retina→Opticnerve→Optictract→ Superiorcolliculus.

2.Intercalary neurons→Edinger-Westphalnucleus(bilateral).

3.E erent→Oculomotornerve→Ciliaryganglion→Shortciliarynerves→Sphincter pupillae.

Directreaction: constrictionofstimulatedeye.

Consensual(friendly)reaction:constrictionofoppositepupil.