Motor Lesions

8/20/2019 Motor Lesions

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Motor lesions

Upper and Lower Motor Neurons

The performance of a voluntary act needs the integrity of 2 sets of motor neurons, upper & lowerneurons.

Upper Motor Neurons

These consist of the motor cells of the cerebral cortex & their axons, which relay at the motor nuclei ofthe brain stem & spinal cord, chiefly of the opposite side.

These descending tracts include:

●The corticonuclear tract: which arises from area 8 of the frontal cortex & terminates in the motornuclei of the , !, ! cranial nerves.

●The corticobulbar tract: which arises from the motor area & terminates in the motor nuclei of !, !,", ", " & ".

●The corticospinal tract: #pyramidal tract$: which arises from the motor area & terminates at theanterior horn cells of the spinal cord.

LMN include the followi ng sets:

1.%eurons in the motor nuclei of all the above mentioned cranial nerves & their axons to s' Musclesof the eyes & the head

2. (nterior horn cells of spinal cord & their axons to s' Muscles of the body .

Upper Motor Neuron and Lower Motor Neuron Lesions

Manifestation of UMN lesions (UMNL) ●)"T)%T *+ (-(./00: is wide spread because the pyramidal fibers from a compact bundles which

occupies a small area.

●0T) *+ (-(./00: is opposite to the lesion e'g' hemorrhage into the right internal capsule causeshemiplegia or paralysis of the muscles of the left half of the face & the left upper & lower limbs.

●M10.)

T*%)

: there is hypertonia & hyperreflexia due to bloc of the extrapyramidal inhibitorydischarge on the gamma efferents & hence the excitatory reticular formation because unopposed ' 0o,spasticity is a release phenomenon from the normal inhibitory discharge.

●- )+.)")0: superficial reflexes are absent on the affected side as they receive their facilitatoryinfluence from the pyramidal tracts, while the deep reflexes are exaggerated with appearance ofclonus' 3abinsi4s sign with its center in 05 & 02 is positive.

● 6 (0T%7 *+ T) M10.): is very slight due to exaggerated tone #spasticity$' The slight wastingresults from the lac of voluntary movements.


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●- )0*%0) *+ M10.): to electrical stimulation is normal, with normal excitability .

Lower Motor Neuron Lesions

●)"T)%T *+ (-(./00: is locali9ed depending on the site of the lesion.

●0T) *+ (-(./00: is at the same side of the lesion e'g' damage of the (s on the right side of thespinal cord causes paralysis of the muscle supplied by these (s on the right side.

●T*%) *+ T) M10.): there is hypotonia because the stretch reflex arc is cut.

●- )+.)")0: both superficial and deep reflexes are absent in the affected segments.

● 6 (0T%7 *+ T) M10.)0: is mared due to absence of reflex tone as well as lac of voluntarymovements.

●- )0*%0) *+ M10.)0: the response to electrical stimulation is abnormal' The response is wea

contraction with decreased excitability, then no response when it is transformed into fibrous tissue.

Effect of lesions of the pyramidal tracts at various levels ●.esions of the pyramidal tract cause paralysis of the 1M%. type below the level of the lesion.

●owever, the side affected and the extent of paralysis vary according to the site of the lesion:

○n area : this leads to restricted paralysis in the opposite side e'g' monoplegia # paralysis of onelimb because area is widespread so it is rarely damaged completely $.

○n corona radiate: this leads to contralateral monoplegia or hemiplegia, depending on the extentof the lesion.

○n the internal capsule: this often leads to contralateral hemiplegia because almost all fibers arein;ured.

○n the brain stem: this leads to contralateral hemiplegia and ipsilateral paralysis of the cranialnerve of the .M%. type # due to damage of their nuclei in the brain stem $.

●This condition is called


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● In the spinal cord :

(D Bi la teral lesions: in the upper cervical region are fatal due to interruption of the respiratorypathway' n the lower cervical region, they lead to Cuadriplegia and in the midthoracic region lead toparaplegia.

3D Unilateral lesions: in the cervical region they lead to ipsilateral hemiplegia while in themidthoracic region they lead to ipsilateral monoplegia in the corresponding lower limb' n both

conditions, there is also ipsilateral paralysis of the .M%. type of the muscles at the level of the lesiondue to damage of the spinal motor neurons.

Note:

● (-(.)7( : paralysis of the lower limbs.

●M*%*.)7( : paralysis of one limb.

●)M.)7( : paralysis of half of the body . ●E1(F-.)7( : paralysis of the limbs.

The internal capsule

● The internal capsule is the only subcortical pathway through which nerve fibers ascend to anddescend from the cerebral cortex'

● t is a ! shaped consisting of anterior and posterior limbs and a genu #nee$'

● t is surrounded by the putamen and globus pallidus laterally and the caudate nucleus and thethalamus medially'

The anterior limb

t contains descending fibers from the cerebral cortex to the red nucleus, pons to cerebellum,thalamus, =rd , th , & ?th cranial nerves'

The genu

t contains corticobulbular tract'

The posterior limb

#what is underlined is what we need to memori9e' The anatomy is not important$ contains:

● T) F)0)%F%7 /-(MF(. & )"T-(/-(MF(. +3)-0 in the anterior 2G='


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● T) 0*M(T*0)%0*-/ -(F(T*% that ascends behind the pyramidal fibers from the thalamic nucleito the cortical sensory area'

● T) *T -(F(T*% that ascends behind the somatosensory radiation from the lateral geniculate body to visual areas in the occipital lobe'

● T) (1FT*-/ -(F(T*% that ascends most posteriorly from the medial geniculate body of theauditory areas in the temporal lobe'

Effect of a unilateral lesion in the posterior limb of the internal capsule:

0uch lesion commonly called cerebral stroe is usually caused by thrombosis or hemorrhage oflenticuloDstriate artery #a branch of the middle cerebral artery$' atients pass into an acute thenchronic stage'

cute stage

This lasts a few days up to 2D= wees' t is a stage of acute 1M%. , showing the following

manifestations in the opposite side:

! +.(F (-(./00: including the upper & lower limbs, the lower parts of the face & 5G2 of thetongue'

! )M(%()0T)0( : loss of all sensations

! .*00 *+ T) 01)-+(. -)+.)")0'

! M (/ 3) ( *0T!) 3 (3%0H40 07%'

Notes:

The manifestations of this stage are similar to those of LMNL. Howeer! the" can be differentiated from the LMNL b" the following:

a' The extent of paralysis is much more widespread than in .M%.' b' There is associated hemianaesthesiac' There may be a Ive 3abinisi4s sign'd' 0light absence of muscle atrophy'

"hronic (permanent or spastic) stage

The main manifestations of this stage include the following:

► Contralateral hemiplegia: of the 1M%. type, which is characteri9ed by hypertonia, musclespasticiy of clasp nife type, exaggerated tendon ;ers & clonus, loss of superficial reflexes & apparentIve 3abinisi4s sign'


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Notes

● artial recovery occurs after a variable period by the effect of the ipsilateral corticospinal tract, theextrapyramidal tracts as the corticorubral spinal pathway, so, the patient can stand & even wal, butthe fine silled movements of the fingers & hands are permanently lost'

● ermanent loss of fine sensations in the opposite side, but the crude sensations recover gradually'

● *%T-(.(T)-(. *M*%/M*10 )M(%*( : .oss of vision in the opposite half of the 2 visual fieldsdue to interruption of signals from the temporal part of ipsilateral retina of nasal part of contralateralretina'

● FM%0)F )(-%7 *6)- : n both ears #by about >BJ $, because of damage of auditory radiation

Complete SC transaction

● This result usually from accidents'

● mmediate & everDlasting loss of sensation of voluntary movements occur due to cut of all sensorymotor tracts below the transaction'

● Transaction in the upper cervical regions #above the =rd cervical segment $ result in immediate deathdue to respiratory arrest as in hinging'

● owever, at lower levels, patients pass = stages: spinal shoc, recovery of spinal reflex activity, thenits failure & death'

The following stage follow cord transaction:

■ 0T(7) *+ 0%(. 0*H # wees to months in men$: all cord function are depressed'

● The manifestation of this stage are the following:

- aralysis of all muscle below the lesion #Cuadriplegia or paraplegia $ due to cut of 1M%'

- omplete loss of all sensation below the level of transaction'

- .oss of cord reflexes, as the stretch reflex, hence the paralysed muscle are flaccid & the deepreflexes are absent' The other reflexes are also absent such as the withdrawal flexor reflex'

- (3 #arterial blood pressure $ drops maredly if the transaction is at the level of the 5st

thoracic segment, but slight drop occurs if the lesion is below the 2ed lumber segment' Thisdrop of (3 as well as the vascular !F are due to sympathetic activity bloc' owever, thepressure return to normal within few days'

- .oss of control micturition & defecation reflexes because facilitatory pathway from thehigher centers, responsible for bladder & rectum evacuation are interrupted by thetransaction leading to retention with over flow with dribbling of urine by a full bladder' Thisreturns bac after the 5st few wees'


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- .oss of erection'

● #ause of spinal shoc$:

○ t is due to sudden withdrawal of supraspinal facilitation on spinal alpha motor neurons,namely: the continual tonic discharge transmitted along the excitatory reticalocpinal, vestibulospinal & corticospinal tracts'

● %uration of spinal shoc$:

○ The Furation of spinal shoc differs in different animals according to the degree ofdevelopment of cerebral cortex'

○ t is only a few minutes in rats'

○ n human, the duration last 2D? wees'

● #omplication of spinal shoc$:

○ hypotrension specially in highDlevel spinal cord lesion'

○ ncrease protein catabolism due to lac of movement causing muscle wasting & bonedissolution'

○ schemia of the compresed against bed # upper bac, gluteal region and heels $ which healpoorly due to protein depletion'

○ 1rinary tract infection due to urine stasis'

○ +all of body temp' due to reduction of the metabolic rate after loss of muscle tone'

Management of the Spinal Cord Lesions

● This is aimed at rapid recoer" of the spinal refle& actiit" which can be achieed b" the following:

○ ( huge dose of 7lucocorticoids #5BgGday$ though their antiDinflammatory action couldreduce the death rate from 8BJ to 8J'

○ (ntibiotics & good nursing care prevents infections & reduces the mortality too'

○ 0timulants to the spinal centers as (mphetamines & %eurotrophins'

○ 3ladder catheteri9ation to prevent urine retention & rectal enema #to evacuate the rectum$'

○ revention of bed sore by cleaning sin with an antiseptic & freCuent changing of thepatient4s position in bed'

○ (deCuate nutrition #malnutrition delays recovery$'


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#tages of $ecovery of the #pinal $efle% ctivity

● (fter the stage of spinal shoc, the spinal centers below the level of the lesion recover gradually #butthe sensations & voluntary movements never recover because the tracts in the spinal cord cannotregenerate due to lac of neurolema'

● 'pinal recoer" occurs as the following:

• The static stretch #muscle tone$ recovers spastic paralysis

• t appears first in the flexor muscles #causing paraplegia in flexion$'

• Then a few months later, the extension muscle tone predominates resulting inparaplegia in extension'

• This is followed by other extensor responses e'g' positive supporting reaction so thepatient can stand without support'

• (s a result of recovery of muscle tone the metabolic rate increases, the body temperature

rises towards normal level'

• The activity of the spinal vasomotor centers #lateral horn cells$ is restored, leading to vasoconstriction so the (3 rises #but it remains labile because its precise controlmechanism by the baroreceptors is absent$'

• -eflex micturation and defecation return but are autonomic #as in infants$ due toabsence to voluntary control'

• 0exual reflexes recover #stimulation of the external genitalia in males leading toerection$'

• (ppearances of the mass reflex'

Mass $efle% ● This is a hyperactive spinal reflex response that appears after a few months'

● Mild noxious stimuli applied to the sin below the level of the lesion results in a wide range spreadeffects due to irradiation of signals in spinal cord to involve multiple somatic & autonomic centers'

● 'uch effects includes:

5' )xaggerated withdrawal of the stimulated part2' 1rination & defecation=' 0in pallor & profuse sweating' +luctuation of the (3 #usually rise$

Notes


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● atient can be trained to induce urination or defecation through producing intentional mass reflex#by striing or pinching the thigh sin$'

● The flexor withdrawal reflex & 3abinisi signs are usually the 5st to appear followed by extensorreflex e'g' nee ;er'

Possible mechanisms of The Reappearance of Spinal Reflexes

● Fevelopment of denervation hypersensitivity, the 0pinal neuron becomes hypersensitive tomediators released by remaining excitatory endings'

● 7rowth of new collaterals from preexisting neurons & formation of additional excitatory endings oninterneuron and motor neurons #spinal neurons$'

● -eplace of spinal centers from the normal inhibitory control of the highest centers'

Stage of ailure of Reflex !cti"it#

●This is a terminal #premortal$stage that results from bad management during the recovery stage.

●1rinary tract infection and bed sores infection result in failure of reflex activity and the patient diesfrom renal failure

●The spinal centers below the leel of the lesion are depressed once more leading to:

○.oss of the muscle tone and tendon ;ers then mass reflex,withdrawl reflex and babinisi4s sign

○.oss of the defecation and micturtion reflexes resulting in constipation and urineretention with over flow

○ypotension due to depression of spinal ! center 'T) =-F stage doesn4t now days occur because of perfect nursing and administration of antibiotics, both lines of treatment 'guard against bed source and renal infection

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Motor Lesions