Sie sind auf Seite 1von 5

Ascending Tracts

Pain, temp & crude touch. Travel in ant &


lat funiculi. Supplied by ant spinal a

Dicriminative touch vibration, propioception &


kinesthesis. Supplied by post spinal a.

Anterolateral

Dorsal Column

Enter cord laterally @ dorsal root entry & synapse in lamina I-V, which then
send axons contralaterally via "ant white commisure" i.e. Crosses to other
side as soon as it gets to cord. Sends collaterals to cord & brainstem making
pthwy resistant to disruption via local lesions

Spinothalamic
Allows for a quick,
direct route to
thalamus

Spinomesencephalic

Spinoreticular

Indirect route to
allow projections
to wide areas of
cortex

Spinocerebellar

Ipsi, unconcious sensation from


receptors in muscle & joints (muscle
spindles, joint capsules & skin). Allows
for coordination of muscle activity by
cerebellum. Sensory info --> DRG -->
nuclei in intermediate horn of grey
matter --> cerebellum (May also go thru
dorsal nucleus of Clark, spinal border
cells & ant cuneate nucleus)

Ipsilateral. Fast,myelinated axons.


Enter cord medially @ dorsal root
entry

Cuneatus

DRG from above T6

Gracilis

DRG from below T6

Cross over & merge @ medulla


to form "Medial Lemniscus"

Sensory info from lower limb to cerebellum

Anterior spinocerebellar

Posterior spinocerebellar

Sensory info from upper limb


to cerebellum

Tract continues thru brainstem & into


thalamus, which then projects to sensory
areas of cerebral cortex, somatotopically

Cuneocerebellar
Ascends contra but recrosses. Carries info from
whole limb

Ascends ipsi & carries info


from individual muscles

Note - Ventral & lateral funiculi supplied jointly. Medial portions by ant spinal a & lateral portions by post spinal a & vasocorona
The boxes over the arrows apply to all the things that those arrows are leading to

Descending tracts

Extensor biased pathways


Major effects on postural m
avtivity related to balance & body
tone

Flexor biased pathways

Pyramidal System

Rubrospinal
tract

Volitional motor tracts. Somatotopic - axons


innervating legs are lateral relative to those
going to arms. Legs = Lateral

Hypothalao
-spinal
tract
Vestibulospinal

Reticulospinal
Corticobulbar

Corticospinal

Controls muscles of the


face, head and neck &
terminates on motor
neurons within brainstem
motor nuclei.

2/3rd of neurons from motor cortex


(frontal lobe & pre-central gyrus).
1/3rd from sensory areas (primary
sensory cortex & parietal lobes) &
terminate in cord.
Innevrate usu via interneurons.
Excite flexors & inhibit extensors.
Fxn is to control fine skilled
movement of extremities.

CST - 90% cross @ foramen


magnum & descend thru dorsal
part of lateral funiculus

Travels close to
CST.
Origin - Red
nucleus of
rostral midbrian.
Does not project
further than
cervical region
Fxn - Flex arm &
forearm. Inhibit
extensors

UMN influence for


visceromotor
activity. Innervate
pre-gang autonomic
neurons of IMLCC.
Can be ipsi or b/l

ACST - 10% remain ipsi- & form "Anterior


corticospinal tract" which descends in anterior
funiculus & then crosses @ spinal level that it
innervates. Innervates crossed or b/l axial
muscles.

Origin - nuclei in
reticular formation
[(pons - ipsi) &
(medulla - b/l)]
Path - Ventral &
ventral lat funiculus
Fxn - Motor neurons
of paravertebral &
proximal extensor m
Unconcious activity
related to posture

Origin - Vestibular
part of vestibulocochlear n
Makes 2 tracts that
maintain posture &
orientation. Medial is
contra, Lateral is ipsi
Fxn - Excite
extensors.
Cerebellar input (not
cerebral)

Note - Extensor or Flexor biased does NOT mean excitatory or inhibitory, just that those tracts innervate those muscles. Can be either excitatory or inhibitory

Lower Motor Neuron


Lesions

Corticonuclear lesions --> death of


brainstem nuclei

Poliomyelitis

ALS
RNA enterovirus --> LMN
death.
95% asymptomatic.
Can produce variety of
symptoms
Can progress to phrenic
nucleus --> respiratory
failure & death

Slow, progressive selective


degeneration of UMN
(corticospinal) & LMN (ant
horn) --> progressive
weakness, problems w/
coordination, swallowing,
breathing.
LMN sxs more noticeable.
NO cognitive deficits.

SYMPTOMS OF LMN LESIONS


Flaccid paralysis --> rapid muscular atrophy
Fasciculations d/t denervation
Hypotonia
Hyporeflexia
(i.e all things go DOWN in lower motor neuron dz)

Werdnig-Hoffman dz
(Spinal Muscular
Atrophy)

Autosomal recessive (1 in 25,000)


Destruction of LMNs --> difficulty
swallowing, breathing etc.
Weakness (hence "floppy baby")
Associated w/ SMN gene on chrom 5 &
NAIP gene

Hypothalamospinal tract

Pyramidal Tract

UMN syndromes in symp & parasym neurons. Usu


sympathetics are more pronounced hence HTN, urinary
retention, piloerection, sweating & dec blood to limbs

Corticospinal tract

If lesion in cord --> Ipsi sxs


If lesion above medulla -->
contra sxs
(+) Babinski
Absence of superficial abdominl
& cremsteric reflex

Corticonuclear
Lesions

Spinocerebellar
Tract

Upper Motor Neuron


Lesions

Will not disrupt reflexes unless


DRG entry zone is messed up
Dorsal Columns /
Medial Lemniscal

Sxs not as apparent d/t


inc amount of bilat
innervation.
Initial weakness
contralaterally followed
by recovery.
Jaw jerk may be
measured.

Isolated lesions are rare & hence no particular


sxs. If near cerebellum then loss of coordinated
movement

If lesion in cord --> ipsi sxs


If lesion above medulla -->
contra sxs
Inability to distinguish 2 point
touch, feel vibration, or tell
position of body part while eyes
are closed

Anterolateral
Tracts

Sensory loss 2 spinal segements


below lesion since axons cross
cord diagonally.
ANY lesion --> contralat sxs

Loss of protopathic touch, pain


& temp

Tabes Dorsalis - Neurosyphilis infxn --> b/l degeneration of large dia axons -->
destruction of dorsal columns (mostly gracilus) --> altered gait, paresthesias, inc
bladder emptying & dec stretch reflexes.

Syringomyelia central canal


cavitation --> b/l loss
of pain & temp at &
below cavitatin level.
Messes w/ ant white
commisure hence
BILATERAL sxs

Sxs of UMN Lesions Spasticity, Hypertonia,


Hyperreflexia, Clonus,
Clasp knife response,
Altered cutaneous
reflexes (Babinski,
Hoffman's, abdominal &
cremasteric), Automnomic
dysreflexia, Slow muscular
atrophy (It's fast in LMN
lesions)
i.e all things go UP in UMN
dz

Syringomyelia central canal


cavitation --> b/l loss
of pain & temp at &
below cavitatin level.
Messes w/ ant white
commisure hence
BILATERAL sxs

Das könnte Ihnen auch gefallen