Quick Neuro Notes

8/12/2019 Quick Neuro Notes

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The Descending Tracts (Motor)

Tract Origin Decussation Destination Functions

Lateral Tracts travel within the lateral column of the spinal cord. Voluntar movements distal musculature. !ortical control

Corticospinal Motor cortex

Precentral gyrus

Almost all fibres, 80%

in medulla.

Alpha LM in !entral

horn" many !iamonosynaptic path#ays.

!onscious voluntar

muscle control. $apidsilled mo!ements,

predominantly in limbs.

$ubrospinal $ed nucleus. All fibres, most at le!el

of origin in midbrain.

Alpha and gamma LM

in !entral horn.

&nfluences tone of limb

muscles, excitatory toflexors and inhibitory to

extensors.

Venteromedial tracts travel within venteromedial column of spinal cord. "osture and locomotion under #rain stem control.

'ectospinal (uperior colliculus of

midbrain.

All fibres, in midbrain,

close to le!el of origin

Alpha and gamma

motorneurones in !entralhorn, mainly cer!ical.

&nfluences refle$

postural movements

related to visual

stimuli.

)estibulospinal )estibular nuclei of

pons and medulla

one. Alpha and gamma

motorneurones in !entral

horn.

%alance and posture*

reflex postural

mo!ements, excitatoryto extensors and

inhibitory to flexors.$eticulospinal Pontine and medullary

reticular formation. +#idely dispersed groups

of cells.

Pontine mainly

uncrossed, medullarymixed .

Alpha and gamma

motorneurones in !entralhorn.

&nfluence voluntar

movementand reflexacti!ity, particularly of

pro$imal &oints and

a$ial musculature.


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Descending Tract Lesions

"ramidal (corticospinal) tract lesions '$trapramidal tract lesions Lower motor neurone lesions

Loss of fine silled mo!ements.

abinsi sign present. .Alsopresent as a normal feature in first yearof life.

(uperficial abdominal reflex absent.

Cremasteric reflex absent.

(igns contralateral, ipsilateral or

bilateral dependent on le!el of lesion.

Paresis - Paralysis.

o muscle wastingother than that dueto disuse.

pertonicitspasticity/, in!ol!ing

predominantly flexors in upper limb

and extensors in lo#er limb, de!elopso!er se!eral days.

perrefle$iade!elops o!er se!eral

days.

Clasp nife rigidity.

Clonus. (igns contralateral, ipsilateral or

bilateral dependent on le!el of lesion.

Paresis - Paralysis.

Muscle atroph.

asciculation.

potonicitflaccidity/.

porefle$ia- Areflexia.

1&n actual clinical practice the pyramidal and extrapyramidal features of 2M lesions occur together.

1Lesions of the basal ganglia and cerebellum are often described as extrapyramidal but differ from 2M lesions in not in!ol!ingdescending tracts #hich influence motorneurones directly or !ia spinal interneurones.

Lesion in the *nternal !apsulehemorrhagic, embolic infarct/ can cause problems as corticospinal tract passes through here + the

rubrospinal tract may tae o!er functions after a fe# months leading to almost full reco!ery from e.g./ C)A

+pinal +hoc,

1(yndrome of depression or loss of all cord function belo# lesion follo#ing acute se!ere damage to spinal cord.

1laccid paralysis belo# le!el of lesion.

13yporeflexia - areflexia belo# le!el of lesion.

1(ensory loss belo# le!el of lesion.

13ypotension from loss of sympathetic tone if lesion is at high le!el.

14uration up to one month.

1As shoc resol!es spinal neurones regain acti!ity, upper motorneurone signs de!elop and some reco!ery of sensation occurs belo# le!el of lesion.


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The -scending Tracts (+ensor)Tract Origin Decussation Destination Function

Lateral (pinothalamic ree ner!e endings.

A5fast/ and Cslo#/fibres.(ynapse in dorsal horn

substantia gelatinosa/.

&n spinal cord, #ithin one

segment 'hen tra!els inspinal lemniscus

'halamic synapse in

!entral posterolateralnucleus.Posterior limb of internal

capsule.

Pain and temperature

(omatotopic representationin cortex.

Anterior spinothalamic )arious receptors.(ynapse in dorsal horn

substantia gelatinosa/.

&n spinal cordo!er se!eralsegments 'hen tra!els in

spinal lemniscus

'halamic synapse in!entral posterolateral

nucleusPosterior limb of internal

capsule.

Crude touch and pressure(omatotopic representation

in cortex.

4orsal columns Meissner6s corpuscles t#o

point discrimination/"Pacinian corpuscles

!ibration/"muscle, tendon and 7ointreceptors proprioception/.(ynapse in nuclei gracilisand cuneatus

%rain stem

nters medial lemniscus

'halamic synapse in

!entral posterolateralnucleus.

Posterior limb of internalcapsule.

4iscriminatory 'ouch,

)ibrationConcious Proprioception

anterior and posteriorspinocerebellar tracts

Muscle, tendon and 7ointreceptors(ynapse in nucleusdorsalis Clar6s column/..

"osterior tractuncrossedand enters inferiorcerebellar peduncle on #ayto cerebellar cortex.

-nterior tractmainlycrosses at level of snapse

and enters superiorcerebellar peduncle on #ayto cerebellar cortex.Crossed fibres recross viamiddle cere#ellar

peduncles.

o third order neurone&nfo not at conscious le!el

2nconsciousProprioception


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%lood +uppl

Middle cere#ral

"osterior cere#ral

-nterior cere#ral

"osterior cere#ral

-nterior cere#ral


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*shaemia and infarction

1 'hrombotic infarct + occurs in association #ith atherosclerotic pla


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+ome important Fractures

+,ull #ase fractureof (phenoid, temporal and occipital bones * middle cranial fossa floor/ C( otorrhoea if meninges superior to middle ear and tympanic membrane ruptured

4anger of C( infection

Assessment clinical and C'.

+,ull #ase fractureof anterior cranial fossa floor including rontal and ethmoid bones cribriform plate of ethmoid/

(ymptoms-signs related to associated facial and brain in7ury" anosmia"

C( rhinorrhoea

4anger of C( infection should not blo# nose/


Facial +,eleton Fractures

'$ternal ose+ asal bones and septal cartilage in!ol!ed.

(ymptoms-signs cosmetic and functional. Assessment clinical" imaging usually unhelpful.

1gomatic -rch+ Bygomatic, maxilla and temporal bones in!ol!ed.(ymptoms-signs mainly cosmetic.

Assessment clinical, plain *ray and C'.


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Ma$illa+ thmoid, nasal, Dygomatic, palatine and sphenoid bones may also be in!ol!ed.

Le ort classification.

(ymptoms-signs cosmetic and functional.


Mandi#le+ Mandible and temporo*mandibular 7oint in!ol!ed.

(ymptoms-signs functional.

Assessment ortho*pantomography 9PE/ and C'.

%lowout Fracture (intraor#ital fracture)/Caused by an indirect traumatic in7ury e.g. tennis ball/ onto the orbit. 'he sudden rise in

pressure #ithin the orbit can cause the thin bone here to fracture. 2sually this is a FtrapdoorG fracture in the inferior part of the orbit as

this is the #eaest area.

at is displaced into the fracture line + this is not a serious conse


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'pileps

pilepsy has a high pre!alence of % @ in >0/ #ith the most chance of occurring in the !ery young and !ery old. &t is caused by a

change in the excitability of neurones, #hich may result from: meningitis, stroe, trauma or heritable channelopathies.

Tpes of sei2ure

!omple$ partial sei2ure/Abnormal discharge occurs from a focus and spreads locally across a limited area. 'he patient may seemfully a#are but there is an altered state of consciousness. (ymptoms include automatisms che#ing, s#allo#ing etc/. Prior to onset the

patient may experience #arning signals: dH7I !u or 7emais !u may result from in!ol!ement of the hippocampus memory/ #hile

perceptual changes or auras may arise from in!ol!ement of sensory areas.

'hese are generally temporal lobe in origin and may progress to generalised seiDures.

"artial with secondar generalised/'his starts as a simple partial seiDure #ith temporal foci often associated #ith perceptualchanges or auras. Eenerally there is acti!ation of a more central focus and #hole brain generalised/ in!ol!ement. ;ith frontal foci

there are Fmotor seiDuresG + a stiffness and 7ering of the limbs Jacsonian seiDure/. 9ccipital seiDures generally preceded by

hallucinations of light - colour.

-#sence sei2ure (generalised)/this is part of the generalised spectrum. &t is rare in adults, starting in the K*@> year range #ith moregirls than boys affected. 'he patient seems to Fs#itch offG and cannot be alerted or #oen up. $esponds #ell to anti*epileptics.

3eneralised tonicclonic/'here is #hole brain in!ol!ement and so no #arning. &n the tonic phase the #hole body stiffens, breathing

may stop, and there is a loss of bladder control. &n the clonic phase there are muscle 7ers. 'his is follo#ed by loss of consciousnessand muscle relaxation. ;hen consciousness returns, sleepyness, headache and aching limbs are common + there is usually no memoryof the episode.


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"harm/ a4!hannel #loc,ers "harm/ 3-%- (!lchannel) agonists Other/

Phenytoin, carbamaDapine

loc the achannel in its inacti!atedstate + they are therefore use*dependent.

9nly #hen the achannel pool is rapidlyused up seiDure/ #ill the slo# reco!ery

time matter.

enDodiaDepines e.g diaDepam/,

barbiturates e.g phenobarbitone/

'he EAA channels inhibit neuronal

fireing #hen acti!ated + they do this byletting in Cl*#hich hyperpolariDes the cell.

$emo!al of abberent areas guided by M$&

&mplant: !agal ner!e stimulation

-phasia

Tpe Lesion +peech !omprehension Other features

rocaGs Motor association cortex

of frontal lobe

on*fluent, no grammar Eood but not perfect &mpaired repetition and

paraphasic errors

;ernieGs Posterior frontal lobe luent, grammatical, but

meningless

Poor &mpaired repetition and

greater paraphasic errors

rocaGs area may be in!ol!ed in maing grammatical sentences out of #ords, or may contain memories for fine series of motorcontrols re


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!onsciousness/

5e0uires

'he reticular formation of the brainstem spread through pons and medulla/ + responsible for #aefulness. 'he lim#ic sstem+ responsible for affect, mood, attention and moti!ation.

'he cere#ral corte$+ responsible for state of a#areness and for interaction #ith the en!ironment.

Levels of consciousness

ormal+ fully oriented in place, time and person.

Letharg(omnolence" (leepiness/ + a#areness impaired but may become normal or nearly so on arousal" speech slo#"

!oluntary mo!ements diminished and slo#" E mildly abnormal #ith some sleep pattern.

+tupor+ no real a#areness" speech only in response to pain" !oluntary mo!ements minimal or there may be mass mo!ements in

response to pain" E abnormal but distinguishable from normal sleep pattern. !oma2nconsciousness/ + no a#areness" speech absent" mo!ements absent or only reflex in response to pain" E grossly

abnormal or absent.

"ersistent Vegetative +tate

$eticular formation intact but cere#ral corte$

nonfunctional.

Person is a#ae, ie. eyes are open and mo!e

around and sleep*a#ae cycles are present.

A#areness is absent.

$esponse to !erbal command or pain is absent. E contains rhythmic acti!ity resembling

sleep cycles.

'e Opening '

(pontaneous ?

to speech

to pain >

no response @

%est Motor 5esponse M

9beys K

LocaliDes pain + pushes your hand a#ay

lexion*#ithdra#al + mo!es a#ay from the pain ?

lexion*abnormal + upper and lo#er limbs flex

xtension + upper and lo#er limbs extend >

no response @

%est Ver#al 5esponse V

9riented and con!erses

4isoriented and con!erses ?

&nappropriate #ords

&ncomprehensible sounds >

no response @

The 3lasgow !oma +cale (left)

' 4 M 4 V 6 7 to 89

N0% less than or e


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:hat phsiologicall produces coma;

4amage to brain stem reticular formation.

xtensi!e cortical damage, especially if bilateral, but sometimes in!ol!ing only

the dominant hemisphere.

(upratentorial lesion + usually tumour or haemorrhage + not due to infarc + the

area co!ered by an infact is not sufficient.

&nfratentorial lesion + tumour, haemorrhage or infarction affects the reticular

formation of the brainstem/

'oxic-Metabolic disorders + infection, drugs, diabetes, uraemia, etc.

*ntracranial mass lesions

Cause compression and destruction of the brain ad7acent to a lesion + the expansion

of this lesion causes a rise in intracranial pressure. 'his in turn may displace astructure from one place or compartment to another + this is called FherniationG seediagram/

Tpes of herniation

+u#falcine/the anterior cerebral artery may be compressed

Transtentorial/compresses the brainstem

Tonsillar/the tonsils of the cerebellum are pushed through the foramen magnum

!entral/ the brainstem may be pushed to#ards the foramen magnum + ner!es may be compressed esp C&&& + causes papillary signs/.

!ompensation

lood, C( and the brain itself are incompressible substances. &f an expansile mass is present the only #ay to compensate for this is to reduce thelevels of intracranial #lood and !+F. 'his #ors #ell for small lesions but larger lesions may o!ercome this compensation + this problem iscompounded by brain oedema.

Central

Subfalcine

Transtentorial

Tonsillar


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As the intracranial pressure rises, the cerebral perfusion drops. 'his is compensated by a rise in systemic blood pressure and a reflex tachycardiaoccurs also.

+mptomsof mass lesions include: headache, ) pressure on !omiting center/, altered mental state, papilloedema, !isual loss pressure onoptic chiasm - tract etc./ and irregular respiration. Death usuall occurs through ischaemiaas blood flo# drops.

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