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Clinical aspects of upper and lower motor neuron lesions

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Reed O'Brien

Lecture by Prof. Osama Shukir Muhammed Amin FRCP(Edin), FRCP(Glasg), FRCP(Ire), FRCP(Lond), FACP, FAHA about the clinical aspects of upper and lower motor neuron lesions.

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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
Clinical aspects of upper and lower motor neuron lesions
Left corticospinal tract: Note the origin and journey!
Function of the cortico-spinal (pyramidal) tracts? The cortico-spinal tract is involved in the volitional activity of skeletal muscle movements of the contralateral side. 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. Antigravity muscles and movements?
Note: These movements are further controlled/modulated by the extrapyramidal and cerebellar systems, with respect to initiation, coordination, speed, tone, etc.
Lesion(s) of a cortico-spinal 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).
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.
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!
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.
Note the origin, course, and target of lower motor neurons!
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.
Such signs would reflect what? Any lesion from the spinal cords ventral horn alpha motor neurons down to the muscle fibers (i.e., a long pathway).
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.
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.
Rock relief of king Naram-Sin (beloved of moon god Sin), Mountain Qaradagh, Iraq. Circa 2200 BCE. Photo 息 Osama S. M. Amin.

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Clinical aspects of upper and lower motor neuron 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 cortico-spinal (pyramidal) tracts? The cortico-spinal tract is involved in the volitional activity of skeletal muscle movements of the contralateral side. 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. Antigravity muscles and movements?
  • 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 cortico-spinal 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 cords 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 moon god Sin), Mountain Qaradagh, Iraq. Circa 2200 BCE. Photo 息 Osama S. M. Amin.