Lesions of the Spinal Cord

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Lesions of the Spinal Cord

  • Lower Motor Neuron Lesions
    • result from damage to motor neurons of the ventral horns or motor neurons of the cranial nerve nuclei.
    • Neurologic deficits resulting from LMN lesions
      • Flaccid paralysis
      • Muscle atrophy (amyotrophy)
      • Hypotonia
      • Areflexia
        • loss of muscle stretch reflexes (MSRs) (knee and ankle jerks)
        • loss of superficial reflexes (abdominal and cremasteric reflexes).
      • Fasciculations (visible muscle twitches)
      • Fibrillations (seen only on electromyogram)
    • Diseases of LMNs
      • Poliomyelitis
      • Progressive infantile muscular atrophy (Werdnig-Hoffmann disease)
      • Kugelberg-Welander disease (juvenile hereditary LMN disease)
        • affects the large girdle muscles first and then the distal muscles.
  • Upper Motor Neuron Lesions
    • result from damage to cortical neurons that give rise to corticospinal and corticobulbar tracts.
    • calledpyramidal tract lesions.
      • When rostral to the pyramidal decussationof the caudal medulla, they result in deficits below the lesion, on the contralateral side.
      • When caudal to the pyramidal decussation, they result in deficits below the lesion, on the ipsilateral side.
    • Lateral corticospinal tract lesion
      • results in the following ipsilateral motor deficits found below the lesion:
        • Spastic hemiparesis with muscle weakness
        • Hyperreflexia (exaggerated muscle stretch reflexes)
        • Loss of superficial (abdominal and cremasteric) reflexes
        • Clasp-knife spasticity
          • When a joint is moved briskly, resistance occurs initially and then fades (like the opening of a pocketknife blade)
        • Clonus
          • consists of rhythmic contractions of muscles in response to sudden, passive movements (wrist, patellar, or ankle clonus).
        • Babinski sign
          • consists of plantar reflex response that is extensor (dorsiflexion of big toe).
    • Ventral corticospinal tract leision
      • results in mild contralateral motor deficit.
      • Ventral corticospinal tract fibers decussate atspinal levels in the ventral white commissure.
    • Hereditary spastic paraplegia or diplegia
      • is caused by bilateral degeneration of the corticospinal tracts.
      • results in gradual development of spastic weakness of the legs with increased difficulty in walking.
  • Sensory Pathway Lesions
    • Dorsal column syndrome
      • includes the fasciculi gracilis (T6–S5) and cuneatus (C2–T6) and the dorsal roots.
      • is seen in
        • subacute combined degeneration (vitamin B12 neuropathy).
        • neurosyphilis as tabesdorsalis
        • nonsyphilitic sensory neuropathies.
      • results in the following ipsilateral sensory deficits found below the lesion:
        • Loss of tactile discrimination
        • Loss of position (joint) and vibratory sensation
        • Stereoanesthesia(astereognosis)
        • Sensory (dorsal column) dystaxia
        • Paresthesias and pain (dorsal root irritation)
        • Hyporeflexia or areflexia (dorsal root deafferentation)
        • Urinary incontinence, constipation, and impotence (dorsal root deafferentation)
        • Romberg sign (sensory dystaxia) (standing patient is more unsteady with eyes closed)
    • Lateral spinothalamic tract lesion
      • results in contralateral loss of pain and temperature sensation
      • loss is seen one segment below the level of the lesion.
    • Ventral spinothalamic tract lesion
      • results in contralateral loss of light (crude) touch sensation
      • loss is seen three or four segments below the level of the lesion.
    • Dorsal spinocerebellar tract lesion
      • results in ipsilateral leg dystaxia
      • patient has difficulty performing the heel-to-shin test.
    • Ventral spinocerebellar tract lesion
      • results in contralateral leg dystaxia
      • patient has difficulty performing the heel-to-shin test.

 

  • Peripheral Nervous System Lesions
          • may be sensory, motor, or combined.
          • affectspinal roots, dorsal root ganglia, and peripheral nerves.
          • Herpes zoster (shingles)
            • consists of an acute inflammatory reaction in the dorsal root or cranial nerve ganglia.
            • is usually limited to the territory of one dermatome
            • the most common sites are T5 to T10.
            • causesirritation of dorsal root ganglion cell
          • Acute idiopathic polyneuritis (Guillain-Barré syndrome)
            • is also called postinfectious polyneuritis.
            • affects primarily motor fibers
            • causessegmental demyelination and wallerian degeneration.
            • producesLMN symptoms (muscle weakness, flaccid paralysis, and areflexia).
            • results in symmetric paralysis that begins in the lower extremities and ascends to involve the trunk and upper extremities
            • thefacial nerve frequently is involved bilaterally.
            • elevates cerebrospinal fluid (CSF) protein; however, the CSF cell count remains normal (albuminocytologic dissociation).
  • Combined Upper and Lower Motor Neuron Lesions
          • muscle weakness and wasting without sensory deficits.
          • Prototypic disease—amyotrophic lateral sclerosis (AML)
            • is also called Lou Gehrig disease, motor neuron disease, or motor system disease.
            • usually occurs in persons 50 to 70 years of age.
            • involvesboth LMNs and UMNs; either component may dominate the clinical picture.
            • LMN component
              • progressive (spinal) muscular atrophy
              • progressive bulbar palsy
            • UMN component.
              • pseudobulbar palsy
              • primary lateral sclerosis
        • Combined Motor and Sensory Lesions
          • Spinal cord hemisection (Brown-Séquard syndrome)
            • Dorsal column transection
              • results in ipsilateral loss of tactile discrimination, form perception, and position and vibration sensation below the lesion.
            • Lateral spinothalamic tract transection
              • results in contralateral loss of pain and temperature sensation,
              • startingone segmentbelow the lesion.
            • Ventral spinothalamic tract transection
              • results in contralateral loss of crude touch sensation
              • startsthree or four segmentsbelow the lesion.
            • Dorsal spinocerebellar tract transection
              • results in ipsilateral leg dystaxia.
            • Ventral spinocerebellar tract transection
              • results in contralateral leg dystaxia.
            • Hypothalamospinal tract transection rostral to T2
              • results in Horner syndrome.
            • Lateral corticospinal tract transection
              • results in ipsilateral spastic paresisbelow the UMN lesion with the Babinski sign.
            • Ventral corticospinal tract transection
              • results in minor contralateral muscle weakness below the lesion.
            • Ventral horn destruction
              • results in ipsilateral flaccid paralysis of somatic muscles (LMN lesion).
            • Dorsal horn destruction
              • results in ipsilateraldermatomic anesthesia and areflexia.
          • Complete transection of the spinal cord
            • Exituslethalis between C1 and C3
            • Quadriplegia between C4 and C5
            • Paraplegia below T1
            • Spastic paralysis of all voluntary movements below the lesion
            • Complete anesthesia below the lesion
            • Urinary and fecal incontinence, although reflex emptying may occur
            • Anhidrosis and loss of vasomotor tone
            • Paralysis of volitional and automatic breathing if the transection is above C5 (thephrenic nucleus is found at C3–C5)
          • Ventral (anterior) spinal artery occlusion
            • causes infarction of the ventral two-thirds of the spinal cord.
            • usuallyspares the dorsal columns and dorsal horns.
            • results in paralysis of voluntary and automatic respiration in cervical segments
            • it alsoresults in bilateral Horner syndrome.
            • results in loss of voluntary bladder and bowel control, with preservation of reflex emptying
            • results inanhidrosis and loss of vasomotor tone.
            • Ventral horn destruction
              • results in complete flaccid paralysis and areflexiaat the level of the lesion.
            • Corticospinal tract transection
              • results in a spastic paresis below the lesion.
            • Spinothalamic tract transection
              • results in loss of pain and temperature sensations
              • startingone segment below the lesion.
            • Dorsal spinocerebellar tract and ventral spinocerebellar tract transection
              • results in cerebellar incoordination, which is masked by LMN and UMN paralysis.
          • Conusmedullaris and epiconus syndromes
            • neurologic deficits and signs that are most always bilateral.
            • Conusmedullaris syndrome
              • involves segments S3 to Co.
              • is usually caused by small intramedullary tumor metastases or hemorrhagic infarcts.
              • results in destruction of the sacral parasympathetic nucleus, which causes paralytic bladder, fecal incontinence, and impotence.
              • causesperianogenital sensory loss in dermatomes S3 to Co (saddle anesthesia).
              • shows an absence of motor deficits in the lower limbs.
            • Epiconus syndrome
              • involves segments L4 to S2.
              • results in reflex functioning of the bladder and rectum but loss of voluntary control.
              • is characterized by considerable motor disability (external rotation and extension of the thigh are most affected).
              • affects the ventral horns and long tracts.
              • is associated with absent Achilles tendon reflex.
          • Caudaequina syndrome
            • classically involves spinal roots L3 to Co.
            • results in signs that frequently predominate on one side.
            • may result from intervertebral disk herniation.
            • commonly results in severe spontaneous radicular pain.
          • Filumterminale (tethered cord) syndrome
            • results from a thickened, shortened filumterminale that adheres to the sacrum
            • causestraction on the conusmedullaris.
            • results in sphincter dysfunction, gait disorders, and deformities of the feet.
          • Subacute combined degeneration (vitamin B12 neuropathy)
            • associated with pernicious anemia.
            • consists of demyelination of dorsal columns, resulting in loss of vibration and position sensation.
            • consists of demyelination of spinocerebellar tracts, resulting in arm and leg dystaxia.
            • consists of demyelination of corticospinal tracts resulting in spastic paresis (UMN signs).
          • Friedreich hereditary ataxia
            • is the most common hereditary ataxiawith autosomal recessive inheritance.
            • dorsal column, spinocerebellar, and corticospinal tract involve ment.
            • cerebellar involvement (Purkinje cells and dentate nucleus) is frequent with progressiveataxia.
            • commonly leads to cardiomyopathy, pescavus, and kyphoscoliosis.
          • Syringomyelia
            • is a central cavitation of the cervical spinal cord of unknown etiology.
            • results in destruction of the ventral white commissure
            • interruption of decussating spinothalamic fibers, causing bilateral loss of pain and temperature sensation.
            • can result in extension of the syrinx into the ventral horn, causing an LMN lesion with muscle wasting and hyporeflexia.
            • Atrophy of lumbricalsand interosseous muscles of the hand is a common finding.
            • can result in extension of the syrinx into the lateral funiculus, affecting the lateral corticospinal tract and resulting in spastic paresis (a UMN lesion).
            • can result in caudal extension of the syrinx into the lateral horn at T1 or lateral extensioninto the lateral funiculus (interruption of descending autonomic pathways), resulting in Horner syndrome.
          • Multiple sclerosis
            • is the most common form of demyelinating disease.
            • hasasymmetric lesions
            • may affect all tracts of the spinal cord white matter
            • Spinal cordlesions occur most frequently in the cervical segments.
          • Charcot-Marie-Tooth disease (hereditary motor–sensory neuropathy type I)
            • is also called peroneal muscular atrophy.
            • is the most common inherited neuropathy.
            • affects the posterior columns, resulting in a loss of conscious proprioception.
            • affects the anterior horn motor neurons, resulting in muscle weakness (atrophy)
          • Intervertebral Disk Herniation
            • consists of prolapse or herniation of the nucleus pulposusinto the vertebral canal
            • occursthrough the defective annulus fibrosus.
            • The nucleus pulposus impinges on spinal roots, resulting in root pain (radiculopathy) or muscle weakness.
            • may compress the spinal cord with a large central protrusion
            • is recognized as the major cause of severe and chronic low back and leg pain.
            • appears in 90% of cases at the L4–L5 or L5–S1 interspaces
            • usually a single nerve root is compressed,
            • several may be involved at the L5–S1 interspace (caudaequina).
            • appears in 10% of cases in the cervical region, usually at the C5–C6 or C6–C7 interspaces.
            • is characterized by spinal root symptoms, which include paresthesias, pain, sensory loss,hyporeflexia, and muscle weakness.
            • Cervical spondylosis with myelopathy
            • is the most commonly observed myelopathy.
            • consists of spinal cord or spinal cord root compression by calcified disk material extruded into the spinal vertebral canal.
            • presents as painful stiff neck, arm pain and weakness, andspastic leg weakness with dystaxia
            • sensory disorders are frequent.


            Fun with lesions: DCML and spinothalamic pathways
            Anatomy Motor Exam: Spinal Cord Lesions
            Spinal Cord Lesions * Spinal cord lesions often give UMN signs below the level of the lesion (from effect on the corticospinal tract) and LMN signs at the level of the lesion (from effect on the ventral horn or ventral nerve root). * LMN signs are good for locating the level of a spinal cord lesion.
            ipsilateral contralateral
            spinal cord lesion explaining how the terms ipsilateral and contralateral deficits are determined.
            Levels of Function in Spinal Cord Injury
            Spinal cord injuries range from minor to severe, the labeling of these injuries can sometimes be confusing. This video explains the different severities of these labels, as well as exactly what areas are affected by these injuries.
            Head and Spinal Injuries
            MD311 Lecture on Traumatic Head and Brain Injuries and Spinal Cord Injury