The document discusses the clinical aspects of upper and lower motor neuron lesions with a focus on the functions and disruptions of the corticospinal tracts. It describes the resulting symptoms from upper motor neuron lesions, such as weakness, hypertonia, and exaggerated reflexes, as well as the characteristics of lower motor neuron lesions, including weakness, hypotonia, and atrophy. The clinical presentation varies based on the etiology and location of the lesions.

1. “Clinical Aspects of Upper and
Lower Motor Neuron Lesions”
Osama Shukir Muhammed Amin
MBChB, MD, MRCP, FACP, FAHA, FCCP(USA), FRCP(Edin),
FRCP(Glasg), FRCP(Ire), FRCP(Lond)
Associate Professor of Neurology
School of Medicine, International Medical University,
Malaysia

3. Left
corticospinal
tract:
Note the
origin and
journey!

4. Function of the corticospinal (pyramidal)
tracts?
The corticospinal tract is
involved in the volitional
activity of skeletal muscle
movements of the
contralateral side.
Antigravity muscles and
movements?
• Upper limbs: shoulder
abduction, as well as elbow,
wrist, and fingers extensions.
• Lower limbs: hip and knee
flexion, as well as ankle dorsi-
flexion and planter eversion.

5. Note:
These movements are further
controlled/modulated by the
extrapyramidal and cerebellar
systems, with respect to initiation,
coordination, speed, tone, etc.

6. Lesion(s) of a corticospinal tract?
This would result in loss of
function of that tract with
secondary dominance of
extrapyramidal and other
tracts’ functions; e.g.,
rubrospinal, vestibulospinal,
tectospinal, etc.
The resulting clinical features
depend on the etiology of the
lesion, onset, severity,
multiplicity, and association
with other lesions within and
outside the CNS (i.e.,
peripheral nervous system).

7. Pyramidal system damage would result in…?
Weakness or paresis of the
targeted movement (there
is no complete paralysis).
Monoparesis, hemiparesis,
or quadriparesis.
Reduced control of
volitional movements,
especially of distal fine
dexterity; e.g., buttoning
and unbuttoning.
Hypertonia of clasp-knife
spasticity and “sustained”
clonus.
Exaggerated deep tendon
reflexes.
Extensor planter reflex
(Babinski sign), Hoffman
sign, pronator drift, etc.
No or very minimal
atrophy. Disuse atrophy
occurs in longstanding
cases.

8. That is to say:
Signs of upper motor neuron lesion!
And, this reflects what?
Any lesion from the cerebral cortex down to the anterior
horn cells of the spinal cord!

9. Is it a “patterned” type of weakness?
YES!
The pattern of pyramidal weakness is weakness of upper limbs’
extensors and lower limbs’ flexors.
For instance, left-sided pyramidal weakness, grade 3 power in both
upper and lower limbs.

10. Note the origin,
course, and target
of lower motor
neurons!

11. Lower motor neuron lesions’ signs?
The classical signs are:
Weakness or complete paralysis.
Hypotonia (flaccidity).
Hyporeflexia or areflexia.
Fasciculation (involuntary rippling muscle
movements).
Early and prominent atrophy.

12. Such signs would reflect what?
Any lesion from the spinal
cord’s ventral horn alpha
motor neurons down to the
muscle fibers (i.e., a long
pathway).

13. How would they present clinically?
The presentation depends on the etiology, site of the
lesion, multiplicity of the lesion, onset, and
progression.
And, if there is any coexistent central nervous system
damage.

14. Where, localize?
•Spinal cord anterior ventral horn lesions.
•Radiculopathy.
•Plexopathy.
•Motor-end plate diseases.
•Myopathy/myositis.
PS: Each of them depicts a unique constellation of
symptoms and signs.

15. Rock relief of king
Naram-Sin (beloved of
the moon god Sin),
Mountain Qaradagh,
Iraq. Circa 2200 BCE.
Photo © Osama S. M.
Amin.