Neurology - BMA your career... · Neurology Hollie Wilson. ... Other descending tracts to be aware...

Neurology

Hollie Wilson

Objectives

• Anatomy

• Physiology:• Functional centres of brain• UMN lesion vs. LMN lesion• Spinal cord

• Main tracts – ascending and descending• Nerve roots and peripheral nerves – action potentials

• Pathology

• Quiz

Cortical Organisation

Broca’s and Wernicke’s areas – speech and language

• Broca’s : frontal lobe• Expressive language

• Wernicke’s : temporal lobe• Receptive language

Blood supply to the brain

AnteriorcerebralcirculationINTERNALCAROTIDARTERY

Posteriorcerebralcirculation2VERTEBRALARTERIES

RedundancyAnastomoticconnectionsfacilitatecollateralbloodsupplyintheeventofnarrowingorobstructionofavessel

Threemainpairsofarteriesarising

fromcircleofWillis

•ACA•MCA•PCA

Anterior Cerebral Artery Middle Cerebral Artery Posterior Cerebral Artery

Medial brain Lateral brain Lateral and Medial

Frontal lobe (primary motor cortex) Frontal lobe(Broca’s, primary motor cortex)

Occipital lobe (primary visual cortex)

Parietal lobe (primary somatosensory cortex)

Parietal lobe (primary somatosensory cortex)

Inferior temporal lobe

Superolateral temporal lobe (Wernicke’s area)

Pastquestion1.Areaofbraincontrollingspeech?

• Frontallobeofdominanthemisphere

2.Location?• Broca’s area

3.Bloodsupply?• MCA

Pastquestion

• Distinguishbetweendysarthriaanddysphasia?

• Dysarthriaisaspeechdisordercausedbydisturbanceofmuscularcontrolie aproblemwitharticulation

• Dysphasia/Aphasiaisanimpairmentoflanguageandmaybereceptiveorexpressive.• Expressive(Broca’s area)• Receptive(Wernicke’sarea)

Stroke

• Aetiology• Ischaemic(85%)

• Thrombosis• Embolism• Hypoperfusion

• Haemorrhagic(15%)

RiskfactorsModifiable• Hypertension• DM• AF• Smoking• Hyperlipidaemia

Non‐modifiable• Previousstroke/TIA• Increasingage• FH

ABCD2 score predicts risk of stroke following TIA

Clinicalpresentation• Clinicalpresentationaccordingtovascularterritoryinvolved• MCAmostcommonlyaffectedvessel

• Contra‐lateralhemiparesis• Homonymoushemianopia• Dysphasia

• Clinical• History

• Timeofonset• Ix

• Bloodglucose• CTBrain

Visualfielddefects1.CompletelossofvisionLeye(opticnervelesion)

2.Bitemporal hemianopia (opticchiasmlesion)

3.Righthomonymoushemianopia(optictractlesion)

4.Righthomonymoussuperiorquadrantanopia

5.Righthomonymousinferiorquadrantanopia

6.Righthomonymoushemianopiawithmacularsparing

Agoodworkingknowledgeofthevisualpathwayisimportanttoaidwiththelocalisationofcerebrallesionsfromclinicalfindingsalone.

Upper motor neuron lesions vs. lower motor neuron lesions

• Anuppermotorneuronisamotorneuron,thathasit’scellbodyinthecerebralcortex,andsynapseswithlowermotorneuronsintheanteriorhorncellorcranialnervenuclei

N.B.TheincreasedtoneandhyperreflexiadoesnotdevelopimmediatelyfollowingthedevelopmentofanUMNlesion,duetoaphenomenoncalledSpinalShock.Initiallythetoneandreflexeswillbereduced inanuppermotorneuronlesion.

“Uppersparesupper”

Story so far…

SpinalCordTracts

Thespinalcordtractsruninthewhitematterofthespinalcord

Ascending  Descending

FROM periphery TO brain

Mainly sensoryfeedback

FROM brainTO periphery

Mainly motorcontrol

DescendingSpinalCordTracts

1. Corticospinal Tract (Pyramidal Tract)

Primary Motor Cortex

Internal capsule

Pons & Midbrain

Anterior horn of spinal cord

Crosses over at base of medulla

Other descending tracts to be aware of: 2. Vestibulospinal tract3. Tectospinal tract4. Reticulospinal tract

Corticospinal Tract

• Originatesinthemotorcortex(cortico)andterminatesintheanteriorhorncellsofthespinalcord

• Passesthroughtheinternalcapsule,downthroughtheponsandmidbrain

• Crossesoveratthebaseofthemedulla andformsapyramidalbulgeontheanterioraspectofthemedulla(hencepyramidaltract).

• Fromhere,itdescendsinthelateralaspectofthecorticospinaltracttotheanteriorhornofthespinalcord,whereitsynapseswithmotorneurons

Recap:ActionPotentials

K+ effluxNa+ influx

ActionPotential1• Initiation

• Theintra‐cellularenvironmentoftheaxonisnormallynegativewithrespecttotheextra‐cellularenvironment(restingmembranepotential~‐70mV).

• Allornothingresponse– astimulusmustdecreasethispotential(inotherwordsmaketheinsideoftheaxonlessnegative)inordertobreachthethresholdpotential.

• Oncethethresholdpotentialisbreachedthisresultsinavoltage‐dependentrapidincreaseinmembranepermeabilitytoNa+.TheresultantinfluxofNa+ resultsindepolarisationwhichreversesthepotentialacrosstheneuronalcellmembrane(theinsideisnowtransientlypositiveandtheoutsidenegative).

ActionPotential2

• Propagation• Actionpotentialstravelalonganaxonbysaltatory conduction

• GapsinthemyelinsheathformnodesofRanvier alongtheaxonwhichallowtheactionpotentialtojumpfromnodetonode

• Conductionvelocityisthereforeincreasedbymyelination andisalsoproportionaltotheaxondiameter.

ActionPotential3• Repolarisation

• Thesamevoltage‐dependentincreasewhichfacilitatedNa+influxalsofacilitatesaslowerK+ efflux

• Thislossofpositivechargerestoresthenormalnegativerestingmembranepotential(repolarisation)

• Refractoryperiod– asecondstimulusduringthisperiodwillnotresultindepolarisationduetotransientinactivationofNa+ channels

K+ efflux

ActionPotential4• Synaptictransmission

• Neuronsareconnectedfunctionallybysynapsesbetweentheaxonofoneneuroneandthedendritesofanother.

• Depolarisationofthepre‐synapticmembraneresultsinincreasedpermeabilitytoCa2+ bytheopeningofvoltage‐gatedCa2+ channels.

• SubsequentCa2+ influxcausesfusionofsynapticvesicleswiththepre‐synapticmembraneandneurotransmitterreleaseacrossthesynapticcleft.

• Bindingoftheneurotransmittertoreceptor‐operatedionchannelsonthepost‐synapticmembraneallowsexcitationorinhibitionofthepost‐synapticneurone.

The Neuromuscular Junction

• Terminalboutonofnervefibres sitsininfolding ofsarcolemma(musclecellmembrane)calledajunctionalfold

• TheAcetycholinereceptorsfoundattheneuromuscularjunctionarenicotinicacetylcholinereceptors

NeuromuscularTransmission1. Actionpotentialtravelsdowntheaxonoftheneuroninnervatingthemusclefibre,leadingtotheopeningof

VoltageGatedCalciumChannels2. ThisleadstoinfluxofCa 2+3. Byanunknownmechanism,theincreasedCa 2+causesbindingofvesiclescontainingacetylcholinetothe

pre‐synapticmembrane,causingreleaseofacetylcholineintothesynapticcleftviaaprocesscalledexocytosis

4. Thisacetylcholinebindstoacetycholine receptorsontransmittergatedionchannels,thatopeninresponsetothebindingofacetylcholine

5. ThiscausesNa+influxintothemusclefibre6. Thisdeplolarises themusclefibre,leadingtothegenerationofanactionpotentialwithinthemuscle.Thisis

knownasanexcitatorypost‐synapticpotentialorEPSP7. Inaprocessknowasexcitation‐contractioncoupling,theactionpotentialspreadstothesarcoplasmic

reticulumviaT‐tubules,andthearrivalofanactionpotentialtothesarcoplasmicreticulumleadstoCa2+releasefromtheorganelle.ThisCa2+bindstoTroponinC,andthisleadstoaconformationalchangethatmeansthattropomyosin movesawayfromitsnormalbindingsiteontheactinfilament,allowingthemyosinheadstobindtotheactinfilamentandcausemuscularcontraction

SpinalCordTracts

Thespinalcordtractsruninthewhitematterofthespinalcord

Ascending  Descending

FROM periphery TO brain

Mainly sensoryfeedback

FROM brainTO periphery

Mainly motorcontrol

AscendingSpinalCordTracts

1. ThePosteriorColumn:finetouch,vibrationandproprioception.Thesetractscrossoverinthemedulla,beforeterminatinginthethalamus.Fromhere,neuronsleavethethalamustoascendintotheparietallobe(primarysomatosensorycortex)

2. TheSpinothalamicTract:anterior(crudetouch)andlateral(painandtemperature)

Thesetractscrossoveratthelevelofthespinalcordatwhichtheyenterthroughthedorsalhorn.Ascendinthespinalcordtoreachthethalamus,fromwherethereareprojectionstotheparietallobe

3. Thespinoreticular tracts4. Thespinocerebellartracts (unconsciousproprioception)

AscendingSpinalCordTracts

Fine touchVibrationProprioception

Crude touchPainTemperature

Question: 

A 21 year old man was involved in a street fight and brought to ED. He sustained a knife wound to the left side of his neck which damaged his spinal cord unilaterally. What sensory and motor impairment will he have following this injury?

Objectives

• Anatomy

• Physiology:• Functional centres of brain• UMN lesion vs. LMN lesion• Spinal cord

• Main tracts – ascending and descending• Nerve roots and peripheral nerves – action potentials

• Pathology: strokes, spinal cord damage

• Quiz

QUIZ

Additional notes 

SpinalReflexArc

MuscleSpindle• Musclemechanoreceptorsthatdetectstretchingofmusclefibres

• Composedofintrafusal fibresthatruninparalleltoextrafusalfibres thatformthemusclebulk

• Acttoregulatemuscletoneandmediatetendonreflexes Action Potentials

MuscleStretchvs MuscleTension

• Musclestretch:changeinlength ofamuscle(usuallyanincreaseinlength).Thisisdetectedbythemusclespindlethatlieswithinthemuscle.Spindlesalsodetecttheratethatthelengthofthemuscleischanging(dynamicinformation).

• Muscletension:weight/force appliedtotheendofamuscle,andisdetectedbytheGolgiTendonOrgan,thatlieswithinthemuscletendon.

GolgiTendonOrgan• Alsoinvolvedinmuscleproprioception,butinsteadofsignallingchangesinmusclelength,theysignalchangesinmuscletension

• Unlikemusclespindles,the1bafferentfibres synapsewithinterneuronsinthespinalcord,thatinturnsynapsewithalphamotorneurones,toinhibit them

• Acttomediatetheforceofmusclecontraction‐i.e graspingapintglasshardenoughtostopitfalling,butnotsohardthattheglasssmashes

GolgiTendonReflex