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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/
Assessment clinical and C'.
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.
Assessment clinical and C'.
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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