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Lecture

The Spinal Cord - 2

Dr. Eyad M. Hussein

Ph.D. of Neurology

Consultant & Head of Neurology Department,

Nasser Hospital

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الرجاء تحويل الجوال إلى وضع الصامت مع الشكر

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  • Represent functional pathways that convey sensory information from the periphery to higher levels.
  • Usually consist of a chain of three order neurons.
  • The first-order neuron is always in the spinal ganglion.

I. Ascending Tracts

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  1. Gracile tract (PC): for proprioception & fine touch from lower half of the body.
  2. Cuneate tract (PC): for proprioception & fine touch from upper half of the body.
  3. Lissaurer’s tract: for pain and temperature sensation, lies between the tip of the posterior horn & posterior lateral sulcus.
  4. Dorsal spinocerebellar tract (LC): carries proprioceptive fibers from Clarck’s nuclei to the inferior cerebellar peduncle.
  5. Ventral spinocerebellar tract (LC): carries proprioceptive fibers from spinal border cells to the superior cerebellar peduncle.

Ascending Tracts of the Spinal Cord

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  1. Lateral spinothalamic tract (LC): for pain and temperature pathway.
  2. Ventral spinothalamic tract (AC): for crude touch.
  3. Spinotectal tract (LC): arises from the posterior horn & ends in the superior colliculus (spinovisual reflexes).
  4. Spino-olivary tract (LC): carries proprioceptive impulses to accessory olivary nuclei in the medulla.

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1. Lateral spinothalamic tract:

    • Mediates pain, and temperature sensations.
    • Receives input from free nerve endings and thermal receptors.
    • Receives input from A-delta and C fibers.
    • Somatotopically organized with sacral fibers posterolaterally and cervical fibers anterolaterally.

2. Anterior spinothalamic tract:

    • Concerned with crude touch sensation.
    • Receives input from free nerve endings and from Merkel tactile receptors.

A. Anterolateral System

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1. The first order neuron:

Found in the posterior root spinal ganglion at all levels.

The process divided into:

    • The lateral branch (Dendrite): goes peripherally forming the afferent sensory nerve (the ends of this nerve are receptors of the skin).
    • The medial branch (Axon): enters the spinal cord, forming Lissauer’s tract and make synapse with second order neurons in the posterior horn cells “Substantia Gelatinosa of Rolandi”.

Lateral Spinothalamic Tract

“Pathway of Pain and Temperature Sensations”

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2. The second neuron:

Is the cells of Substantia Gelatinosa of Rolandi and its axon. This axon crosses to the opposite side cross the midline in the ventral white commissure, usually within two to three segments above the level of entry of the peripheral fibers and ascends in the lateral column of the SC as the lateral spinothalamic tract → medulla oblongata → the pons → the mid brain → to relay the sensory impulse at the VPL nucleus of thalamus.

3. The third order neuron:

Starts in the cells of the ventral posterolateral nucleus (VPL) and intralaminar nuclei of the thalamus, its axon ascends to pass through the posterior limb of the internal capsule conducting the impulse to the cortical somatic sensory area (1, 2, 3) in the upper 2/3rd of the postcentral gyrus of the parietal lobe.

Lateral Spinothalamic Tract

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Anterior Spinothalamic Tract

“Pathway of Crude Touch Sensation”

  • Has the same pathway as lateral spinothalamic tract but the second order neuron is main sensory nucleus in posterior horn cells.
  • The axons crosses to the opposite side through the white ventral commissure and ascends in the ventral column of the spinal cord as the Ventral Spinothalamic Tract.
  • Found in the VPL nucleus of the thalamus.

N.B. The spinal lemniscus= lateral spinothalamic tract + ventral

spinothalamic tract

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  • Lesions to the posterior horn cells: Ipsilateral at the same level loss of pain and temperature, and nondiscriminative forms of touch sensations.
  • Lesions to the anterolateral spinothalamic tract: Contralateral loss of pain and temperature, and nondiscriminative forms of touch sensations below the level of lesion.
  • Lesions thalamus and postcentral gyrus: Contralateral loss of pain and temperature, and nondiscriminative forms of touch sensations.

Lesions of the Anterolateral System

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B. Posterior Column Medial Lemniscus System

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  • The posterior column-medial lemniscus system carries general somatic afferent (general sensory) information about discriminative “Fine” touch, pressure, vibration and conscious proprioception.
  • Receives input from Pacinian and Meissner’s corpuscles, joint receptors, muscle spindles, and Golgi tendon organs.
  • Transmitted through the fast-conducting large-diameter fibers (A-Beta fibers).

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1. The first order neuron:

Found in the posterior root spinal ganglion at all levels.

The process divided into:

    • The lateral branch (Dendrite): goes peripherally forming the afferent sensory nerve (the ends of this nerve are receptors of the tendon).
    • The medial branch (Axon): enters the SC and ascends directly in the Gracile and Cuneate tracts “Fasciculus” within the posterior column at the same side to relay in the Gracile and Cuneate nuclei of the medulla.

Pathway of Posterior Column Medial Lemniscus System

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2. The second neuron:

  • Is the cells of the Gracile and Cuneate nuclei in the medulla→ give rise to axons, internal arcuate fibers that decussate to the opposite side of the medulla oblongata ascends as Medial Lemniscus through → the pons → the mid brain → to relay in the “PLV” nucleus of thalamus.

3. The third order neuron:

Starts in the cells of the posterolateral ventral nucleus (PLV) nucleus of the thalamus, its axon ascends to pass through the posterior limb of the internal capsule conducting the impulse to the cortical somatic sensory area (1, 2, 3) in the upper 2/3rd of the postcentral gyrus of the parietal lobe.

Pathway of Deep Sensation

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  • The Gracile Tract: lies more medially and received impulses from the lower part of the body (the lower limbs and lower half of the trunk).
  • Cuneate Tract: lies more laterally and received

impulses from the upper part of the body (the upper limbs

and upper half of the trunk).

  • From medial to lateral side: sacral nerve fibers → lumbar nerve fibers → thoracic nerve fibers → cervical nerve fibers.

Lamination of the Gracile and Cuneate Tracts

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  • Lesions to the posterior columns: Ipsilateral loss of discriminative touch, pressure, vibration and conscious proprioception “Sensitive Ataxia”.
  • Lesions to the medial lemniscus, thalamus and postcentral gyrus: Contralateral loss of discriminative touch, pressure, vibration and conscious proprioception “Sensitive Ataxia”.

Lesions of the Posterior Column Medial Lemniscus System

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1. Posterior spinocerebellar tract:

    • Transmits unconscious proprioceptive information to the cerebellum.
    • Receives input from muscle spindles, Golgi tendon organs, and pressure receptors.
    • Carries unconscious proprioceptive information from ipsilateral lower extremity and trunk.
    • An uncrossed tract.

2. Anterior spinocerebellar tract:

    • Transmits unconscious proprioceptive information to the cerebellum.
    • Carries proprioception from the lower limb to the cerebellum .
    • Receives input from muscle spindles, Golgi tendon organs, and pressure receptors.
    • A crossed tract.

3. Cuneocerebellar tract:

    • The upper-extremity equivalent of the posterior spinocerebellar tract.

C. Spinocerebellar Tracts

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a. First-order neurons:

    • Found in the posterior spinal root ganglia.
    • Project in the posterior thoracic nucleus “Clarck’s nucleus”.

b. Second-order neurons:

    • Found in the posterior thoracic nucleus “Clarck’s nucleus” of (C8–L3).
    • Give rise to axons that ascend in the lateral funiculus and reach the cerebellum via the inferior cerebellar peduncle ipsilateral.

Lesion: Ipsilateral lower limb discoordination “Ataxia”. The patient has difficulty performing the heel-to-shin test.

1. Posterior Spinocerebellar Tract “Flechsig’s Tract”

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Posterior Spinocerebellar Tract

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a. First-order neurons:

    • Found in the posterior spinal root ganglia.
    • Project in the posterior horn cells and make synapse with the spinal border cells.

b. Second-order neurons:

    • Found in the spinal border cells of anterior horns (L1–S2).
    • Give rise to axons that decussate in the anterior white commissure and ascend lateral to the lateral spinothalamic tract in the lateral column.
    • Give rise to axons that enter the cerebellum via the superior cerebellar peduncle contralateral. They then cross the midline again and project the anterior lobe and vermis.

Lesion: Contralateral lower limb discoordination “Ataxia”. The patient has difficulty performing the heel-to-shin test.

2. Anterior Spinocerebellar Tract

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Anterior Spinocerebellar Tract

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a. First-order neurons:

    • Found in the posterior spinal root ganglia “C2 to T7”.
    • Project their axons via the Cuneate tract to the medulla, where they synapse in the accessory cuneate nucleus (similar to Posterior thoracic nucleus “Clarck’s nucleus”).

b. Second-order neurons:

    • Located in the accessory cuneate nucleus of the medulla.
    • Give rise to axons that project ipsilaterally to the cerebellum via the inferior cerebellar peduncle.

3. Cuneocerebellar Tract

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Cuneocerebellar Tract

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  1. Lateral corticospinal (LC): crossed pyramidal tract.
  2. Rubrospinal tract (LC): an extrapyramidal tract.
  3. Lateral reticulospinal tract (LC): an extrapyramidal tract.
  4. Hypothalamospinal tract (LC): the fibers arise from the hypothalamus & end in autonomic cells in the lateral horns.
  5. Olivospinal tract (LC): an extrapyramidal tract.

Descending Tracts of the Spinal Cord

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  1. Sulcomarginal tract (AC): is very close to anterior median fissure.
  2. Anterior corticospinal tract (AC): contains uncrossed corticospinal fibers.
  3. Medial reticulospinal tract (AC): an extrapyramidal tract.
  4. Tectospinal tract (AC): arises from the superior colliculus of midbrain & the fibers end in the A.H.Cs. (spinovisual reflexes ).
  5. Vestibulospinal tract (LC): for equilibrium arises from vestibular nuclei & ends in the A.H.Cs.

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  • The pyramidal tract is a bundle of motor nerve fibers.
  • It begins in the cerebral cortex and ends in:
      • Anterior horn cells of the spinal cord (corticospinal tract).
      • Motor nuclei of the cranial nerves in the brain stem (corticonuclear or corticobulbar tract).
  • The pyramidal tract consists of:
      • Corticospinal tracts (lateral & ventral).
      • Corticonuclear or corticobulbar tracts (Lateral & Medial).

The Pyramidal Tract

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Function:

    • Initiation and control of voluntary motor activity.
    • Inhibition of muscles tone.
    • Inhibition of deep reflexes.

The Upper Motor Neuron System

(Corticospinal Tract)

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  • From Betz cells in motor area 4 ( in the upper 2/3 precentral gyrus of frontal lobe) descends in the corona radiata pass in the posterior limb of the internal capsule descends in midbrain, pons and medulla oblongata.
  • In the medulla the pyramidal fibers collect to form the pyramidpyramidal dicussation.
  1. The Lateral Corticospinal Tract
  2. The Anterior Corticospinal Tract

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  • In the lower medulla:
    1. 85 - 90% of fibers decussate to descends in the lateral column of the opposite side of the spinal cord (indirect or lateral crossed corticospinal tract). The tract gradually diminishes in size and ends about the level of S3 or S4 segment of the SC. For regulation of voluntary movement.

b. 10 - 15% of fibers descend directly in the anterior column of the same side (direct or anterior corticospinal tract) then gives fibers for AHCs at the segmental level in both side. They descend in the spinal cord until they disappear in the midthoracic region.

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  • The motor area of one side of cerebral hemisphere is

responsible for movement of the muscles of the opposite

½ of the body (mainly the limbs).

  • Anterior or direct corticospinal tract end in both

AHCs to supply the trunk and respiratory muscles.

  • The muscles of respiration are received fibers from both

cerebral hemispheres. This explain the absence of

respiratory paralysis in hemiplegic person.

The Corticospinal Tract

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Function:

1. Stimulation of voluntary motor at the level of the same side.

2. Stimulation of muscles tone at the level of the same side.

3. Stimulation of deep reflexes at the level of the same side.

The Lower Motor Neuron System

(Spinomuscular Fibers)

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From AHCs of the spinal cord fibers exit from the spinal cord as the anterior roots of the same side peripheral nerves motor end plate voluntary muscles.

Pathway of the Lower Motor Neuron System

(Spinomuscular fibers)

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  • Arises in the contralateral red nucleus of the midbrain.
  • Plays a role in the control of flexor tone.
  • Crosses to the other side of the midbrain, and descends in the lateral column anterior to the lateral corticospinal tract.

C. Rubrospinal Tract

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  • Arises the ipsilateral lateral vestibular nuclei.
  • Plays a role in the control of extensor tone and head coordination movement.
  • Located in the anterior column.
  • The Medial Vestibulospinal Tract: projects bilaterally from the medial vestibular nucleus within the medial longitudinal fasciculus to the AHCs of the upper cervical cord (C1-C6). It helps with head coordination and eye movement.
  • The Lateral Vestibulospinal Tract: provides excitatory signals to interneurons, which relay the signal to the motor neurons and plays a role in the control of extensor tone.

D. Vestibulospinal Tract

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  • Project to sympathetic (T1–L2) and parasympathetic (S2–S4) centers in the spinal cord.
  • Innervate the ciliospinal center (T1–T2), a pupillary center.
  • Found in the posterior quadrant of the lateral column.
  • Interruption of this hypothalamospinal tract: results in Horner syndrome.

E. Descending Autonomic Tract

“Hypothalamospinal Tract”

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  • Horner’s Syndrome:
    • Partial ptosis “paralysis of the Müller's muscle”.
    • Miosis.
    • Enophthalmus.
    • Anhydrosis.
  • Causes:
    • Brain lesion: (massive ischemic stroke, brain stem lesion).
    • Cervical cord lesion: (syringomyelia and cervical spinal cord tumor),
    • Neck pathology: (Pancost tumor, cervical rib, neck surgery)

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Horner’s Syndrome

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Horner’s Syndrome

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I. According to the location of the lesion:

1. Upper motor neuron lesion (spastic or central paralysis).

2. Lower motor neuron lesion (flaccid or peripheral paralysis).

II. According to the affected limbs:

1. Monoplegia (Rt. UL or LL, Lt. UL or LL): paralysis of one limb.

2. Hemiplegia (Rt. or Lt. sided): paralysis of one side of the body.

3. Paraplegia: paralysis of both limbs.

4. Triplegia: paralysis of three limbs (one upper and two lower limbs).

5. Quadriplegia (tetraplegia): paralysis of four limbs.

6. Bilateral hemiplegia.

Classification of the Motor Neuron Lesion

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  • Result from damage to motor neurons of the anterior horns or motor neurons of the cranial nerve nuclei.
  • Result from interruption of the final common pathway connecting the neuron via its axon with the muscle fibers it innervates (the motor unit).

Lower Motor Neuron lesions (LMNL)

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  1. Flaccid paralysis.
  2. Muscle atrophy (hypotrophy).
  3. Muscle hypotonia.
  4. Areflexia of deep tendon and superficial reflexes.
  5. Muscle fasciculations (visible muscle twitches).
  6. Muscle fibrillations (on electromyography).

Signs of the Lower Motor Neuron lesions (LMNL)

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  1. Anterior horn cells lesion: spinal muscular atrophy, poliomyelitis, and syringomyelia.
  2. Peripheral nerve lesion: mononeuropathy, polyneuropathy.
  3. Motor end plate lesion: myasthenia.
  4. Muscle disease: myopathy.

Diseases of Lower Motor Neuron lesions

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  • Lesions of the corticospinal and corticobulbar tracts “Pyramidal tract lesions”.
  • May occur at all levels of the neuroaxis from the cerebral cortex to the spinal cord.
  • When the lesion above the pyramidal decussation, the motor deficit present below the lesion, on the contralateral side.
  • When the lesion below the pyramidal decussation, the motor deficit present below the lesion, on the ipsilateral side.

Upper Motor Neuron lesions (UMNL)

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  1. Spastic paralysis.
  2. Hyperreflexia of deep tendon reflexes.
  3. Clonus: rhythmic contractions of muscles in response to sudden, passive movements (patellar, or ankle clonus).
  4. Loss of superficial (abdominal and cremasteric) reflexes.
  5. Muscle hypertonia “Clasp-knife spasticity”: when a joint is moved briskly, resistance occurs initially and then fades.
  6. Babinski sign: plantar reflex response that is extensor (dorsiflexion of big toe).

Signs of the Upper Motor Neuron lesions (UMNL)

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Diseases of Upper Motor Neuron lesions

  1. CVA.
  2. Multiple sclerosis.
  3. Brain and spinal cord tumors.
  4. Inflammatory: encephalitis, transverse myelitis.
  5. Traumatic: head trauma, subdural hematoma, spinal cord trauma.
  6. Congenital: cerebral palsy, hereditary spastic paraplegia.
  7. Degenerative: vertebral spondylosis and myelopathy.
  8. Motor neuron disease.

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Differential between the UMNL & LMNL

L.M.N. LESION

U.M.N. LESION

From AHCs until muscles

From area 4 until AHCs

1. Location of lesion

Ipsilateral at the level of lesion

Below the level of lesion: Contralateral (above decussation) and ipsilateral (below decussation)

2. Location of paralysis

Flaccid or peripheral

Spastic or central

3. Paralysis

I. MUSCLES

Wasting occurs early (hypotrophy)

Wasting occurs very late due to disuse

1. State of the muscles

Hypotonia (flaccidity)

Hypertonia (spasticity)

2. Muscle tone

May be present in the irritative lesions of AHCs

Absent

3. Muscle fasciculation

(spontaneous contraction

of muscles group).

II. REFLEXES

Hyporeflexia or areflexia

Hyperreflexia

1. Deep reflexes

Absent

May be present

2. Clonus (Rhythmical series of contraction in response to sudden stretch of muscle tendon).

Absent

+ve (dorsiflexion of big toe + fanning of other toes

3. Pathological reflexes

(Babinski reflex)

Lost if lesion involve the segmental supply of the reflex

Lost if the lesion is above segmental supply of the reflex

4. Superficial reflexes

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  • Complete loss of motor power below the level of lesion.
  • Complete loss of sensation (superficial and deep) below the level of lesion.
  • Atonia and flaccidity with areflexia (in shock stage)
  • Sphincter dysfunction.

Complete Spinal Cord Lesion

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  • Definition: Immediately loss of all SC functions, including the spinal reflexes after sudden transection of the SC.
  • Duration: From two weeks to several months.
  • Mechanism: Due to sudden withdrawal of supraspinal facilitation on the alpha motor neurons.

Spinal Shock

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  1. Quadriplegia or paraplegia (depending on the level of the lesion)
  2. Loss of spinal reflex activity below the level of lesion:
    • Loss of deep and superficial reflexes.
    • Loss of muscle tone with flaccidity of the paralyzed muscles
    • Loss of erection, urination and defecation reflexes
  3. Loss of all sensation below the level of lesion.
  4. Vasodilatation and hypotension below the level of lesion.

Manifestation of the Spinal Shock

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  • DVT and pulmonary embolism.
  • Hypotension (specially in cases of high-level spinal cord lesion).
  • Muscle wasting.
  • Bed sores due to ischemia of the areas are compressed against bed.
  • Urine tract infection due to urine retention and stasis.
  • Sepsis.
  • Decrease of the body temperature due to reduction of the metabolic rate after loss of the muscle tone.

Complication of the Spinal Shock

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If any form of sensation, motor power is preserved below the level of the lesion, spinal cord lesion is considered incomplete:

    • Brown Sequard syndrome (hemicord lesion).
    • Anterior cord lesion.
    • Central cord lesion.
    • Posterior cord lesion.

Incomplete Spinal Cord Lesion

(Partial Transection)

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A. At the level of :

    • Ipsilateral zone of cutaneous anesthesia in the segment of the lesion (due to damage of afferent fibers that entered the cord (PHCs) & have not yet crossed ).
    • Ipsilateral lower motor neuron paralysis in the segment of the lesion( due to damage of the lower motor neuron in the AHCs ).

Brown-Sequard Syndrome

Hemisection Lesion of the Spinal Cord

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B. Below the level of lesion:

  • Ipsilateral loss of proprioception & fine touch below the level of the lesion (due to damage of the dorsal column → cuneate and Gracile Tract).
  • Ipsilateral upper motor neuron paralysis below the level of the lesion( due to damage of the lateral column corticospinal tract ).
  • Contralateral loss of pain, temperature and crude touch sensations below the level of lesion (due to damage of lateral and ventral spinothalamic tract, which has decussated).

Brown-Sequard Syndrome

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  • Lesion of the anterior part of the SC, usually associated with a flexion injury and occlusion in the anterior spinal artery territory.
  • Loss of motor function at lesion and below, decreased superficial sensation, including pain and loss of temperature sensation below the level of lesion.
  • Dysfunction of sphincter tone.
  • Deep and fine sensation is preserved.

Anterior Spinal Cord Syndrome

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  • Lesion of the posterior part of the SC, usually associated with cervical hyperextension injuries, tabes dorsalis (syphilis- tertiary stage), ischemia in the posterior spinal artery territory.
  • Loss of deep sensation, fine touch, and difficulty in coordinating movement.
  • Variable weakness and bladder dysfunction
  • Pain, temperature sensation intact.

Posterior Spinal Cord Syndrome

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  • Often is associated with a cervical region injury in the grey matter of the SC and syringomyelia.
  • Leading to greater weakness in the upper limbs than in the lower limbs and jacket or half jacket loss of Superficial sensation (at the level of lesion).
  • Sparing of deep sensation.

The Central Spinal Cord Syndrome

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  • The lesion involves segments S3–S5.
  • Results in destruction of the sacral parasympathetic nuclei: bladder, fecal incontinence, and impotence.
  • Perianogenital sensory loss in dermatomes S3–S5 (saddle anesthesia).
  • Absence of motor deficits in the lower limbs.

Conus Medullaris Syndrome

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  • Involves the segments L4–S2.
  • Results in sphincter dysfunction.
  • Loss motor and sensation below the level of lesion.
  • Associated with absent achilles tendon reflex.

Epiconus Syndrome

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  • Classically involves spinal roots L2 - S5 below the lower end of the spinal cord.
  • May result from lumbo-sacral intervertebral disk herniation.
  • Produces neurologic deficits similar to those seen in conus or epiconus lesions but presented radicular type loss of sensation.
  • Results in signs that frequently predominate on one side or asymmetrical presentation.
  • Commonly results in severe spontaneous radicular pain (pain that radiates along a dermatome).

Cauda Equina Syndrome

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  1. Poliomyelitis and progressive spinal muscular atrophy.
  2. Multiple sclerosis.
  3. Posterior column disease (Tabes dorsalis).
  4. Amyotrophic lateral sclerosis.
  5. Hemisection of the spinal cord (Brown–Séquard syndrome).
  6. Anterior cord syndrome.
  7. Subacute combined degeneration (vitamin B12 neuropathy).
  8. Syringomyelia.
  9. Charcot–Marie–Tooth disease (hereditary motor–sensory neuropathy type 1).
  10. Posterior cord syndrome.

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