MSC Neuro 2025 P1

21.Auditoryandvestibularsystems,Syndromology. Meniersyndrome.

Auditoryand VestibularSystems

AuditorySystem(CochlearNerve-CNVIII)

The acousticnerve(CNVIII)consistsofthecochlearnerve (hearing)and the vestibular nerve(balance).

Hearinglossterminology:

Hypacusis:decreasedhearingability.

Anacusis/surditas:totaldeafness.

Hyperacusis:increasedsensitivitytosound.

Typesofhearingloss:

Conductivehearingloss(middleearproblems,e.g.,otitismedia):moreloss oflowfrequencies;bone conductionpreserved;Webertestlateralizesto diseasedear.

Sensorineuralhearingloss(innerear,cochlea,orcochlearnerve):lossof highfrequencies;boneconductionreduced;Webertestlateralizes tohealthy ear.

Irritationofcochlearnerveorauditorycortexmaycause tinnitus,buzzing,or auditoryhallucinations.

VestibularSystem(VestibularNerve -CNVIII)

Consistsofsensoryorgansintheinner ear: semicircularcanals,utricle,and saccule;receptorsarehaircellsrespondingtoheadmovementandspatial orientation.

Signalstransmittedviathe vestibularganglion(Scarpa’sganglion)into the brainstematthecerebellopontineangle,terminatinginthevestibularnuclei.

Vestibularnucleiconnectwith:

Cerebellum(coordination).

Oculomotornuclei(via mediallongitudinalfasciculus foreyemovement coordination).

Thalamusand cerebralcortex(awarenessofbodyposition).

Spinalcord(vestibulospinaltractsforposture).

Autonomiccenters(nausea,vomiting).

Vestibulardysfunction causes:

Vertigo(spinningsensation).

Nystagmus(involuntaryeyemovements).

Imbalance andcoordinationissues.

Autonomicsymptoms: nausea,vomiting, sweating.

Meniere’sDisease(Syndrome)

Innereardisordercausedbyexcessendolymphaticfluidandincreasedpressurein the labyrinth.

Clinicaltriad:

Episodicvertigolasting20minstoseveralhours.

Fluctuatinglow-frequencyhearingloss(progressive),tinnitus.

Feelingsofearfullness andimbalance.

Types:

Classicform:both auditoryandvestibularsymptoms.

Cochlearform:primarilyhearingloss.

Vestibularform:primarilyvertigosymptoms.

Possiblecauses:

Metabolic,allergic,endocrine,vascular,viral,syphilitic,anatomical obstructions, trauma.

Treatment:

Acuteattacksmanagedwithvestibularsedatives(meclizine,diazepam, antihistamines),antiemetics,rest.

Lifestyle:limitphysicalactivityduringattacks, saltrestrictionduring exacerbations.

Surgeryifconservativefails,aimingtorelievesymptomswithoutdamaging hearing.

22.Caudalgroupofcranialnerves. Syndromologyofdamagetothe glossopharyngealand vagusnerves.

CaudalGroupofCranialNerves(IX–XII)

Thesenervesoriginate fromthemedullaoblongataandexitvia thejugularforamen(IX,X,

XI)and hypoglossalcanal(XII).

IX–Glossopharyngealnerve

Fibers:Sensory,Motor,Gustatory,Secretory

Mainfunctions:Taste(posterior1/3tongue),pharyngealsensation,gagreflex, stylopharyngeusmuscle,parasympatheticstoparotid.

Lesion/Syndrome:

Lossoftasteinposterior1/3tongue (hypogeusia,ageusia)

Lossofsensationinupperpharynx,softpalate,tonsils,epiglottis

Absentgag(pharyngeal)reflexona ectedside

Drymouth(from↓parotidsecretions,notreliable)

Motordeficitusuallysilent(stylopharyngeusminorrole)

Irritation→Parageusia(falsetastesensations)

X–Vagusnerve

Fibers:Motor,Sensory,Parasympathetic

Mainfunctions:Phonation,swallowing,palateelevation,visceralregulation(heart,lungs,

GI).

Lesion/Syndrome:

Dysphagia(nasalregurgitationduetopalatalpalsy)

Hoarsenessoraphonia(vocalcordparalysis)

Uvuladeviatestooppositesideoflesion

Lossofgagreflex(a erent=IX,e erent=X)

Voice:nasaltone,hoarse

Cardiace ects:tachycardia(lesion),bradycardia(irritation)

Bilaterallesion→aphonia,severedysphagia,respiratory+cardiacfailure→rapidly fatal

XI–Accessory nerve

Fibers:Motoronly

Mainfunctions:

Sternocleidomastoid(headturn)

Trapezius(shoulderelevation,scapulacontrol) Lesion/Syndrome:

Unilateral:

Headdeviatestolesionside

Weakrotationtoopposite side

Shoulderdroopona ectedside

Di icultyshrugging,armcan’televatewellabovehorizontal

SCM+Trapatrophy

Bilateral:

Headfallsbackward,norotation possible

Irritation:spastictorticollis(tonicheadturn towarda ectedmuscle)

XII–Hypoglossalnerve

Fibers:Motormostly(tongue intrinsic+extrinsicmuscles)

Lesion/Syndrome:

UnilateralLMN lesion:tonguedeviatestowards lesion,atrophy,fasciculations

UnilateralUMN (corticobulbar)lesion:tonguedeviatesawayfromlesion

BilateralLMN lesion (glossoplegia):

Tongueimmobile→anarthria(speech impossible)

Dysarthria(unclearspeech)ifpartial

Severe feeding/swallowingdi iculty

Nucleardamage→wrinkling/atrophy+fasciculations

ClinicalMnemonics

IX–Taste&sensationposterior1/3tongue,gagreflex

X–Swallow,speak,heartbeat(viscera)

XI–Shrug&turnhead

XII–Stickouttongue (lesion="licksthe wound" →tonguepointstolesionsidein LMN)

23.Caudal groupofcranialnerves. Syndromologyoflesionsoftheaccessoryand sublingualnerves. Paresisofthetongue accordingtothe centralandperipheraltype.

Accessory Nerve(XI)– Syndromology

Function:Motor→sternocleidomastoid(SCM)&trapezius

Lesionsigns:

Unilateral:

Headdeviatestowardslesionatrest

Weakrotationtoopposite side

Droopedshoulder,weakshrug,scapuladisplaced

AtrophyofSCM &trapezius

Bilateral:headtiltedback;cannotrotate

Irritation:spastictorticollis(tonicheadturn toa ectedmuscle)

ClinicalPearl: XInervelesion= "weakshrug,weakhead turn,scapulawinging".

HypoglossalNerve (XII)–Syndromology

Function:Motor→intrinsic&extrinsic tongue muscles

Peripheral(LMN)lesion:

Tonguedeviatestowardslesion(onprotrusion)

Atrophy&fasciculationsoftonguemuscles

Speech(dysarthria)andeatingimpaired

BilateralLMN →glossoplegia→immobile tongue,anarthria,severedysphagia Central(UMN)lesion(corticobulbarpathway):

Tonguedeviatesawayfromlesion

Noatrophy,nofasciculations

Oftenpartofpseudobulbarpalsy(bilateralUMNlesion)

KeyClinicalSyndromes(MedullaryAlternatingsyndromesinvolvingXI&XII)

Jackson’ssyndrome:IpsilateralXIIpalsy+contralateralhemiplegia

Schmidt’ssyndrome:IX,X,XI+pyramidaltract. Ipsilateralbulbarparalysis+ contralateralhemiparesis

Avellis’syndrome:IX,X, XIIpalsyipsilaterally+ contralateralhemiparesis

BulbarPalsy:LMNlesionIX,X,XII→dysphagia,nasalspeech, tongue atrophy/fasciculations

PseudobulbarPalsy:BilateralUMN lesion→similarsigns,butspastic,with automatisms&noatrophy

Exam-ReadyTakeaway:

Accessory (XI):weakSCM&trapezius→noshrug,weakheadturn

Hypoglossal(XII):tonguedeviation— towardlesionifLMN,away ifUMN

Bulbar=LMN(atrophy,fasciculations),Pseudobulbar=UMN(spastic, automatisms,emotionallability)

24.Bulbarandpseudobulbarsyndromes.

BulbarPalsy(LMN)

Cause:Peripherallesion=nuclei/rootsofIX,X,XIIin medulla(ornervesthemselves)

Type:Lowermotorneuronparalysis

Clinicalsigns:

Paralysisofsoftpalate,pharynx,larynx,tongue (LMN type)

Voice:nasal,hoarse,weak→aphonia

Speech:slurred(dysarthria)orabsent(anartria)

Swallowingdisturbed→nasalregurgitation, aspiration→dysphagia

Absentpharyngeal+palatalreflexes

Tongue:atrophy,fasciculations,fibrillarytwitching,immobility(glossoplegia ifbilateral)

Extra:Maybeunilateral orbilateral

Commoncauses:ALS(motorneurondisease),syringobulbia,brainstemstroke, tumors

PseudobulbarPalsy(UMN)

Cause:Bilateralcorticobulbartractlesions(centralmotorneuronsofIX,X,XII)

Type:Uppermotorneuronparalysis

Clinicalsigns:

Dysarthria,dysphagia(similartobulbar)butNOmuscleatrophyor fasciculations

Reflexes:increasedpharyngeal&jawjerkreflex,oralautomatismspresent→

snoutreflex

suckreflex

palmomental(Marinescu–Radovici) reflex

Emotionallability:pathologicallaughing&crying

Tongue:spastic, movementsweak,deviatesawayfromlesion,noatrophy

Commoncauses:Bilateralstrokes,vasculardementia,multiplesclerosis

KeyDi erences(QuickTable)

ClinicalPearlstoRemember

Bulbar=LMN→Atrophy,fasciculations,lossofreflexes

Pseudobulbar=UMN→ Spastictongue,exaggeratedreflexes,emotionallability

25.Cerebellarataxiasyndrome. Clinicalcharacteristics,variants,andtestsforthe detectionofstatic-locomotoranddynamic ataxia.

CerebellarAtaxia

Definition:

Disorderofcoordinationofvoluntarymovementsduetocerebellarpathology→inaccuracy, irregularity,disturbedforce &rhythmofmovements.

Vermislesions→truncal(axial)ataxia

Hemispherelesions→limb(appendicular)ataxia

Forms

1)Static-Locomotor(Truncal)Ataxia

Lesion:Cerebellarvermis

Mainproblems:standingandwalking

Stance:wide-based,swaying,imbalance

Walk:“drunkengait”– deviatestoeitherside

Worsewitheyesclosed,headback,narrowbase(Rombergmodifications)

Tests:

Rombergtest→increasedsway,deviation

Tandemgait→poor(legsinline→imbalance)

Flankgaitcheck→poorsidestepping+delayed stop

Asynergypresent→failureofcoordinatedmovementchain(Babinskitestof sittingup:legsriseinsteadoftrunk)

2)Dynamic (Appendicular) Ataxia

Lesion:Cerebellarhemispheres

Mainproblems:voluntarylimbmovements

Clinicalsigns:

Intentiontremor(worse neartarget)

Dysmetria(overshoot/undershoot)

Dysdiadochokinesia(cannotdo rapid alternatingmovements)

Asynergia/dyssynergia(brokensequenceofmovements)

Speech:scanning/chanting,explosive,irregularstressonsyllables

Handwriting:large,irregular(“megalographia”)

Nystagmus: rhythmiceyejerksonlateral/upgaze

Hypotonia:decreasedmuscletone→pendularreflexes

KeyClinicalCharacteristics

Unsteadygait&stance→vermis(truncalataxia)

Uncoordinatedlimbmovements→hemispheres(appendicularataxia)

Otherfeatures:nystagmus,dysarthria,hypotonia,intentiontremor

Rombergtest:deviationseen,but( )unlikesensoryataxia,ataxiapersistseven witheyesopen

Babinski’sasynergytest:risinglegs insteadoftrunkinsupine →cerebellar asynergy