Spinal cord lesions

H. Z. Mwale
may be classified according to the area of origin or the area affected.
A. Lower motor neuron (LMN) lesions
B. Upper motor neuron (UMN) lesions
C. Sensory pathway lesions
D. Peripheral nervous system (PNS) lesions
E. Combined upper and lower motor neuron lesions
F. Combined motor and sensory lesions
G. Herniations of the intervertebral disk
LMN
• result from damage to motor neurons of the ventral 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).
A. Neurologic deficits resulting from LMN lesions
1. Flaccid paralysis
2. Muscle atrophy (amyotrophy)
3. Hypotonia
4. Areflexia
• consists of loss of muscle stretch reflexes (MSRs) (knee and ankle jerks) and loss of superficial reflexes
(abdominal and cremasteric reflexes).
5. Fasciculations (visible muscle twitches)
6. Fibrillations (seen only on electromyogram)
Diseases of LMNs
• Diseases of LMNs
1. Poliomyelitis
• is an acute inflammatory viral infection affecting
the LMNs; it is caused by an enterovirus.
• results in a flaccid paralysis
2. Progressive infantile muscular atrophy
(Werdnig-Hoffmann disease)
• is a heredofamilial degenerative disease of
infants that affects LMNs.
3. Kugelberg-Welander disease (juvenile
hereditary LMN disease)
• appears at 3 to 20 years of age.
• affects the large girdle muscles first and then
the distal muscles.
Upper motor neuron lesions
• are lesions of the corticospinal and corticobulbar tracts, called
pyramidal tract lesions.
• may occur at all levels of the neuraxis from the cerebral cortex to the
spinal cord.
• When rostral to the pyramidal decussation of 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.
• A. Lateral corticospinal tract lesion
• results in the following ipsilateral motor deficits found below the lesion:
1. Spastic hemiparesis with muscle weakness
2. Hyperreflexia (exaggerated muscle stretch reflexes)
3. Clasp-knife spasticity-When a joint is moved briskly, resistance occurs initially
and then fades
4. Loss of superficial (abdominal and cremasteric) reflexes
5. Clonus- consists of rhythmic contractions of muscles in response to sudden,
passive movements (wrist, patellar, or ankle clonus).
6. Babinski sign - consists of plantar reflex response that is extensor (dorsiflexion
of big toe)
• B. Ventral corticospinal tract lesion
• results in mild contralateral motor deficit.
• Ventral corticospinal tract fibers decussate at spinal levels in the
ventral white commissure.
• C. 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.
Anterior Horn Lesions
• Anterior horn contain LMN
• Lesions of the Ventral Roots abolish
motor functions of the muscles
innervated by the affected segment.
• For example, section of the ventral
root of C8 will result in paralysis of
the muscles of the hand.
• Similarly, section of thoracic ventral
roots will result in disturbances in
the function of visceral organs
innervated by them.
Symptoms Causes
• Lesion maybe symmetric or
asymmetric
• Poliomyelitis
Flaccid paralysis • West Nile virus- fever, rash
Muscle atrophy (amyotrophy) meningitis/encephalitis
Hypotonia • Acute onset
Areflexia • Spinal muscular atrophy
consists of loss of muscle stretch • Amyotropic lateral syndrome
reflexes (MSRs) (knee and ankle jerks)
and loss of superficial reflexes
(abdominal and cremasteric reflexes).
Fasciculations
Fibrillations
Posterior horn syndrome
• Posterior cord syndrome is a rare
type of incomplete spinal cord
injury
• responsible for the perception of
fine-touch, vibration, sense of
self-movement and body
positioning (proprioception).
• Causes:
• Damage to dorsal columns
• Demyelinating Disorders e.g Vitamin B12
Deficiency, multiple sclerosis, tertiary
syphilis infection- Tabes dorsalis,
Friedreich hereditary ataxia
• External compression e.g
tumors,
mechanical degeneration of cervical
spine,
hereditary neurodegenerative disorders
Blockage in posterior spinal artery
• results in ipsilateral dermatomic anesthesia and areflexia
• Impaired position and vibration sense in LL
• Tactile and postural hallucinations can occur
• Numbness or paresthesia
• Sensory ataxia
• Positive rhomberg sign
• Positive sink sign
• Abadies sign of (tabes dorsalis) positive
• Urinary incontinence
• Areflexia, Hypotonia
• Miotic and irregular pupil not reacting to light Argyl Robertson Pupil
 Central cord syndrome
• Central cord syndrome (central cervical cord syndrome) is the
most common form of an “incomplete spinal cord injury”
• it is associated with damage to tracts that carry information
directly from the brain's cerebral cortex (involved with muscle
movement in the body) to the spinal cord.
• These nerves are particularly important for hand and arm
function.
• CCS usually occurs in people with existing arthritis changes in
the bones of the neck.
• Canal through which the spinal cord travels can be narrow, so
that if the neck is forcefully extended (head tilted back), such
as in a car accident, the spinal cord can be squeezed.
• When the spinal cord is squashed, bruising, bleeding and
swelling can occur, particularly in the center or central portion
of the spinal cord.
Central cord syndrome
• Since the spinal cord is organized with the nerves
that control the movement of the arms in the
center
• Then nerves going to the legs more toward the
outside, the arms are affected more than the
legs in this situation.
• As a result, patients with CCS tend to be weaker
in the arms than in the legs.
• Many patients with CCS regain use of their legs
and can often walk, but cannot effectively use
their arms and hands.
• The overall amount and type of functional loss is
dependent upon the severity of nerve damage.
• Symptoms may include:
• Paralysis or loss of fine control of
movements in the arms and
hands, with relatively less
impairment of leg movements
• Loss of or change in sensation
below the site of the injury
• Loss of bladder control
• Painful sensations such as
tinging, burning, or dull ache
• Commonest cause is
Syringomyelia
• Other causes:
• Hyperextension injuries of neck
• Intramedullary tumors
• Trauma
• Associated with Arnold Chiari
type 1 and 2
• Dandy walker malformation
• Sensory: pain and temperature
are affected
• Touch and proprioception are
preserved
• Dissociative anaesthesia
• Shawl (cape-like) distriburion of
sensory loss
• Motor:
• Upper limb weakness >lower limb
Spinal cord hemisection (Brown-Séquard syndrome)

• Spinal cord hemisection (Brown-Séquard syndrome) also known as

transverse hemisection.
• lesion involving one lateral half of spinal cord
• BSS may occur as a result of spinal cord damage by:
spinal cord tumors
 injuries such as falls
 gunshot injury
 ischaemia
infectious or inflammatory diseases such as tuberculosis or multiple
sclerosis.
Brown-Séquard syndrome
• The primary characteristic is the dissociation of function between conscious
proprioception, pain and temperature sensations.
• Loss of conscious proprioception and two-point discrimination occurs below
the level of the lesion on the ipsilateral side
• loss of pain and temperature sensation occurs one or two segments below
the level of the lesion on the contralateral side as well as bilaterally.
• There is also an upper motor neuron paralysis below the level of the lesion
on the ipsilateral side and a lower motor neuron paralysis at the level of the
lesion on the ipsilateral side.
• This kind of incomplete transection may occur by fracture dislocation of
vertebrae, tumor, or missile wounds.
 Tracts involved in BSS
1. Dorsal column transection
• results in ipsilateral loss of tactile discrimination, proprioception, and vibration
sensation below the lesion.
2. Lateral spinothalamic tract transection
• results in contralateral loss of pain and temperature sensation, starting one segment
below the lesion.
3. Ventral spinothalamic tract transection
• results in contralateral loss of crude touch sensation starting three or four segments
below the lesion.
4. Dorsal spinocerebellar tract transection
• results in ipsilateral leg dystaxia.
• Damage of dorsal column below
the level of sensory decussation
• Dorsal column crosses at the level
of the brain stem, the lesion
below it will produce ipsilateral
symptoms
• Ipsilateral; loss of joint position
sense, tactile discrimination,
touch and vibratory sensation at
the level below the level of injury
ANTERIOR LATERAL SENSORY PATHWAY

(Ventral white commissure)

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DORSAL COLUMN-MEDIAL LEMNISCAL PATHWAY

(Lemniscus fibres)

(Internal arcute )

07/09/2024 27
• Damage to corticospinal tract below
the level of pyramidal decussation
• Corticospinal tract crosses at the
level the brain stem, the lesion below
will produce ipsilateral symptoms
• Ipsilateral upper motor lesions below
the level of injury
• Damage of lower motor neurons at
the level of injury
• Ipsilateral lower motor neuron
lesions at the level of injury
Complete transection of the spinal cord

• results in the following conditions:

1. Exitus lethalis between C1 and C3
2. Quadriplegia between C4 and C5
3. Paraplegia below T1
4. Spastic paralysis of all voluntary movements below the lesion
5. Complete anesthesia below the lesion
6. Urinary and fecal incontinence, although reflex emptying may occur
7. Anhidrosis and loss of vasomotor tone
8. Paralysis of volitional and automatic breathing if the transection is above C5
(the phrenic nucleus is found at C3–C5)
Ventral (anterior) spinal artery occlusion

• causes infarction of the ventral two-

thirds of the spinal cord.
• usually spares the dorsal columns and
dorsal horns.
• results in paralysis of voluntary and
automatic respiration in cervical segments;
• it also results in bilateral Horner
syndrome.
• results in loss of voluntary bladder and
bowel control, with preservation of reflex
emptying.
• results in anhidrosis and loss of
vasomotor tone.
• 1. Ventral horn destruction
• • results in complete flaccid paralysis and areflexia at the level of the lesion.
• 2. Corticospinal tract transection
• • results in a spastic paresis below the lesion.
• 3. Spinothalamic tract transection
• • results in loss of pain and temperature sensations, starting one segment
below the lesion.
• 4. Dorsal spinocerebellar tract and ventral spinocerebellar tract transection
• • results in cerebellar incoordination, which is masked by LMN and UMN
paralysis.
Conus medullaris

• include neurologic deficits and signs that are

most always bilateral.
1. Conus medullaris 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.
• causes perianogenital 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.
Cauda equina syndrome

• classically involves spinal roots L3

to Co.
• produces neurologic deficits similar
to those seen in conus or epiconus
lesions.
• results in signs that frequently
predominate on one side.
• may result from intervertebral disk
herniation.
• commonly results in severe
spontaneous radicular pain.
Filum terminale (tethered cord) syndrome

• results from a thickened, shortened filum terminale that adheres to

the sacrum and causes traction on the conus medullaris.
• results in sphincter dysfunction, gait disorders, and deformities of the
feet.
Subacute combined degeneration (vitamin
B12 neuropathy)
• This disease results from a deficiency of enzymes necessary for
vitamin B12 absorption.
• Deficiency of vitamin B12 results in pernicious anemia as well as
degenerative changes in the dorsal and lateral funiculi of the spinal
cord.
• These patients have defects in both sensory and motor function.
• The symptoms of sensory loss include tingling and the loss of senses
of vibration and position.
• motor function includes upper motor neuron dysfunction.
• This may include a weakness of the lower limbs and an ataxic gait.
Friedreich hereditary ataxia
• is the most common hereditary ataxia with autosomal recessive
inheritance.
• results in spinal cord pathology and spinal cord symptoms that are
similar to subacute combined degeneration with dorsal column,
spinocerebellar, and corticospinal tract involvement.
• cerebellar involvement (Purkinje cells and dentate nucleus) is
frequent with progressive ataxia.
• commonly leads to cardiomyopathy, pes cavus, and kyphoscoliosis.
 Syringomyelia
• is a central cavitation of the cervical spinal cord of unknown
etiology.
• results in destruction of the ventral white commissure and
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 lumbricals and 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 extension into the lateral funiculus
(interruption of descending autonomic pathways), resulting in
Horner syndrome.
Multiple sclerosis
• is the most common form of demyelinating disease.
• has asymmetric lesions and may affect all tracts of the
spinal cord white matter.
Spinal cord lesions occur most frequently in the cervical
segments.
Exact cause is not known yet.
• Most theories suggest that MS is an immunogenetic viral
disease (with Epstein Barr virus).
• Risk factors are:
 Age ( most of the time between 20-40 yrs).
 Sex (women have more chance).
 Family history (genetic susceptibility).
 Certain infections ( like Epsteinbarr virus).
clinical patterns MS
• The 4 clinical patterns (types) have been identified:-
• 1. Relapsing – remitting MS (most common initial pattern): Episodes of
acute worsening with recovery and a stable course between relapses.
• 2. Primary progressive MS: Gradual, nearly continuous neurologic
deterioration from onset of manifestations.
• 3. Secondary progressive MS: Gradual neurologic deterioration with or
without superimposed acute relapses in a client who previously had
relapsing remiting MS.
• 4. Progressive relapsing MS: Gradual neurologic deterioration from the
onset of manifestations but with sub-sequent superimposed relapses.
• The other symptoms are:-
• Cerebellar sign: – Nystagmus – Ataxia – Dysarthria – dysphagia
• Motor: – weakness or paralysis of limbs , trunk or head – Diplopia –
Scanning speech – Spasticity of muscles that are chronically affected.
• Sensory: – Numbness , tingling and other parasthesias – Patchy
blindness (scotomas) – Blurred vision – Vertigo, tinnitus, decreased
hearing, chronic neuropathic pain – Radicular (nerve root) pain in
lower thoracic abdominal region. – Lhermitte’ s sign is a transient
sensory symptom described as an electric shock radiating down the
spine or into limbs with flexion of neck.
• Emotional problems: – Fatigue (associated with energy needs) –
Depression – Deconditioning – Medication side effects.
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 pulposus through the defective
annulus fibrosus into the vertebral canal.
• 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, but several may be involved at the L5–S1 interspace (cauda equina).
• 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, and spastic leg
weakness with dystaxia; sensory disorders are frequent.
Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease)
• Amyotrophic lateral sclerosis (ALS) is a progressive degenerative disease
in which the corticospinal tracts (upper motor neuron) and ventral horn
cells (lower motor neuron) degenerate, often beginning with the lower
limbs and later involving the upper limbs.
• Degeneration of the ventral horn cells in the cervical spinal cord results
in weakness and ultimately in loss of control in muscles of the hand,
trunk, and lower limbs.
• Involuntary twitching of muscle fascicles (fasciculations) occurs in these
muscles.
• Bladder and bowel functions are also impaired due to the loss of
descending autonomic pathways. The cause of this disease is not
known.
Tabes Dorsalis
• This syndrome represents late consequences of syphilitic infection of the
nervous system and is also referred to as tertiary syphilis or neurosyphilis.
• In this syndrome, the large diameter central processes of the dorsal root
ganglion neurons (primary afferent sensors) degenerate, especially in the
lower thoracic and lumbosacral segments.
• Therefore, the fibers in the fasciculus gracilis degenerate, and there is a loss
of vibration sensation, two-point discrimination, and conscious
proprioception.
• The loss of conscious proprioception results in ataxia (uncoordinated
muscular movements) because the patient is now deprived of the
conscious sensory feedback of signals that detect the position of the lower
limbs at any given point in time.
Lesions of the Dorsal Root

• Section of three consecutive dorsal roots causes abolition of all

sensory function in a particular dermatome (anesthesia of the
dermatome);
• section of one dorsal root does not cause much sensory loss because
of overlap between dermatomes that are associated with intact
dorsal roots and those that are damaged.
• With muscle tone also dependent on segmental reflexes, interruption
of the afferent limb of these reflexes caused by the section of a dorsal
root results in loss of muscle tone innervated by the affected
segment.
END!