Diseases Of The Motor Neurons And Corticospinal Tracts Figures 81 and

A. Upper motor neuron (UMN) lesions are caused by transection of the corticospinal tract or destruction of the cortical cells of origin. They result in spastic paresis with pyramidal signs (Babinskis sign).

B. Lower motor neuron (LMN) lesions are caused by damage to the motor neurons. They result in flaccid paralysis, areflexia, atrophy, fasciculations, and fibrillations. Poliomyelitis or Werdnig-Hoffman disease (see Figure 8-2A) results from damage to the motor neurons.

Tabes Dorsal

Dorsal V horn

Ventral . horn

Gracile fasciculus, Cuneate fasciculus

Lateral corticospinal tract-

Ipsilateral loss of tactile discrimination and position and vibration sensation from leg

Ipsilateral loss of tactile discrimination and position and vibration sensation from arm

Ipsilateral spastic paresis with pyramidal signs

Lateral spinothalamic tract

Contralateral loss of pain and temperature sensation one segment below lesion

Ipsilateral flaccid paralysis in affected myotomes

Ventral white commissure

Bilateral loss of pain and temperature sensation within dermatomes of involved segments

Figure 8-1. Transverse section of the cervical spinal cord. The clinically important ascending and descending pathways are shown on the left. Clinical deficits that result from the interruption of these pathways are shown on the right. Destructive lesions of the dorsal horns result in anesthesia and areflexia. Destruction of the ventral white commissure interrupts the central transmission of pain and temperature impulses bilaterally through the lateral spinothalamic tracts.

Tabes Dorsalis TractsTabes Dorsalis

Figure 8-2. Classic lesions of the spinal cord. (A) Poliomyelitis and progressive infantile muscular atrophy (We rd nig-Hoffmann disease). (B) Multiple sclerosis. (C) Dorsal column disease (tabes dorsalis). (D) Amyotrophic lateral sclerosis. (E) 1 lemisecrion of the spinal cord (Brown-S6quard syndrome). (F) Complete ventral spinal artery occlusion of the spinal cord. (G) Subacute combined degeneration (vitamin B,2 neuropathy). (H) Syringomyelia.

Figure 8-2. Classic lesions of the spinal cord. (A) Poliomyelitis and progressive infantile muscular atrophy (We rd nig-Hoffmann disease). (B) Multiple sclerosis. (C) Dorsal column disease (tabes dorsalis). (D) Amyotrophic lateral sclerosis. (E) 1 lemisecrion of the spinal cord (Brown-S6quard syndrome). (F) Complete ventral spinal artery occlusion of the spinal cord. (G) Subacute combined degeneration (vitamin B,2 neuropathy). (H) Syringomyelia.

C. Combined UMN and LMN disease. An example of a combined UMN and LMN disease is amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease) [see Figure 8-21)]. ALS is caused by damage to the corticospinal tracts, with pyramidal signs, and by damage to the LMNs, with LMN symptoms. Patients with ALS have no sensory deficits.

II. SENSORY PATHWAY LESIONS. An example of a condition caused by these lesions is dorsal column disease (tabes dorsalis) [see Figure 8-2C]. This disease is seen in patients with neurosyphilis. It is characterized by a loss of tactile discrimination and position and vibration sensation. Irritative involvement of the dorsal roots results in pain and paresthesias. Patients have a Romberg sign. (Subject stands with his feet together. When he closes his eyes, he loses his balance. This is a sign of dorsal column ataxia.)

Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

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