spinal cord disorders and paralegia

1. Spinal cord disorders
Mohamed rizk khodair
Lecturer of neurology
October 6 university
Mohamedrizk.med@o6u.edu.eg

2. Myelopathy: It is an injury to the spinal cord due to severe
compression that may result from trauma, congenital stenosis,
degenerative disease, or disc herniation.
Myelitis: is an inflammation of the spinal cord. This inflammation
can cause the myelin and axon to be damaged resulting in
symptoms such as paralysis and sensory loss.
Radiculopathy: is an injury or damage to nerve roots in the area
where they leave the spine. This condition can affect anyone and
can be the result disc degeneration, disc herniation or other trauma.
Myelopathy vs Radiculopathy
Myelopathy refers to a condition known as spinal cord
compression, while radiculopathy occurs when a nerve root (but
not the cord itself) becomes compressed. The latter is more
commonly known as a pinched nerve root.

5. Internal Divisions of the Spinal Cord
A cross section of the spinal cord shows an H shaped central grey matter surrounded by a peripheral white matter.

7. The following structures are useful in clinical localization of spinal cord
disorders:
1. Descending tracts (motor function):
Lateral corticospinal (pyramidal) tract.
2. Ascending tracts (sensory function):
a) Dorsal (posterior) column (kinesthesia and discriminative touch)
b) Lateral spinothalamic tract (pain and temperature)
3. Neuronal populations:
a) Anterior horn cells (somatic motor function}.
b) Intermediolateral cell column (autonomic sympathetic function).
c) Sacral autonomic neurons (autonomic parasympathetic function).

8. Spinal Cord Tracts
Dorsal (Posterior) columns
Ascending tracts (sensory:
fine touch,
proprioception)
Fasciculus gracilis Lower extremity
Fasciculus cuneatus Upper extremity
Lateral columns
Descending tracts Lateral corticospinal Motor: skeletal muscle
Rubrospinal Motor: cerebellum to skeletal muscle
Ascending tracts
Spinothalamic (anterolateral) Sensory: pain and temperature
Posterior (dorsal) spinocerebellar Sensory: proprioception to cerebellum
Anterior (ventral) spinocerebellar Sensory: proprioception to cerebellum
Ventral (Anterior) columns
Descending tracts
Anterior corticospinal Motor: skeletal muscle
Vestibulospinal Sensory: vestibular, balance to motor
neurons
Reticulospinal Sensory: pain, autonomic to motor
neurons
Tectospinal Sensory: visual to cervical motor neurons

9. Localization of spinal cord disorders
Spinal cord level Corresponding vertebral body
Cervical Same as cord level (C1 to C4)
Lower cervical 1 Level higher (C5-T6)
Upper thoracic 2 Level higher (T3 to T6)
Lower thoracic 2 to 3 level higher (T7 to T9)
Lumbar T10-T12
Sacral T12-L1

10. Useful markers of sensory level
Useful markers of sensory level
T4  Nipple
T10  Umbilicus
T12  Pubic Symphysis
Lesion At T9-T10 (Beevor’s Sign)

12. Paraplegia
Paraplegia is paralysis or weakness (paraparesis) of both lower limbs.
- Pyramidal (U.M.N) lesion resulting in spastic paraplegia.
- Lower motor neuron (L.M.N.) lesion resulting in flaccid paraplegia.
Spastic paraplegia
It is paralysis or weakness of both lower limbs due to bilateral pyramidal tract lesion, most commonly in the
spinal cord (spinal paraplegia and less commonly in the in the brain stem or the cerebral parasagittal region
(cerebral paraplegia).
Spinal paraplegia may be:
- Focal: paraplegia with level
- Systemic: paraplegia without level
- Disseminated: paraplegia without level

13. Causes of spinal paraplegia
1) Focal causes:
a. Compression
1. Vertebral:
- Traumatic: fracture of vertebra
- Degenerative: spondylosis, disc prolapse, kyphoscoliosis
- Pott’s disease.
- Neoplastic diseases: primary as osteosarcoma & hemangioma or Metastatic from 1ry carcinoma of thyroid, breast, kidney, stomach & prostate.
2.Meningeal (extramedullary):
- Extradural: leukemic deposits
- Dural: meningioma
- Intradural: neurofibroma, cystic arachnoiditis
3. Cord (intramedullary):
Syringomyelia, Glioma or Ependymoma of cord
b. Inflammatory:
Transverse myelitis – Myelomeningitis – Myeloradiculitis
C, Vascular:
Anterior spinal artery occlusion.

14. • 2) Systemic causes:
• A systemic disease in neurology is a disease which affects one or more systems
selectively and is usual bilateral and symmetrical. When a systemic disease affects the
pyramidal tracts either alone or with other tracts, paraplegia will result.
• Heridofamilial: Hereditary spastic paraplegia, Hereditary ataxia: Friedreich’s ataxia.
• Symptomatic: pellagra lateral sclerosis, Subacute combined degeneration.
• Idiopathic: motor neuron disease.
•
• 3) Disseminated causes:
• A disseminated disease in neurology is a multifocal disease of the same nature:
• Multiple sclerosis (MS) & Acute disseminated encephalomyelitis (ADEM).

15. Causes of cerebral paraplegia
A. Causes in the parasagittal region: (area of cortical presentation of LL)
1.Traumatic: depressed fracture of the vault of the skull &Subdural hematoma.
2.Vascular: superior sagittal sinus thrombosis.
3.Inflammatory: encephalitis, meningoencephalitis.
4.Neoplastic: parasagittal meningioma.
5.Degenerative: cerebral palsy.
B. Causes in the Brain stem:
Syringobulbia & Midline brainstem tumors.
 these lesions arise in the midline and involve the innermost pyramidal fibers
which are those of the lower limbs.

16. Clinical picture of focal paraplegia
A. At the level of the lesion:
1. Vertebral manifestations: only if the cause is vertebral
- Localized pain or tenderness.
- Localized deformity or swelling.
2. Radicular manifestation: only present in extramedullary cause.
a) Posterior root affection:
- Early pain in the back referred to distribution of affected root and described as girdle pain; it is exaggerated by
coughing, sneezing & straining.
-Later there is hypoesthesia or anesthesia in dermatome supplied the affected root.
b) Anterior root affection:
- Localized L.M.N weakness in the muscles supplied by the affected root.
N.B. As the lesion in paraplegia is below cervical segments (which supply the muscle of the arm), the L.M.N affection at
the level of the lesion is not clinically evident; this is due to difficulty in eliciting wasting and difficulty of testing for tone
and deep reflexes in the trunk and abdominal muscles. If the lesion involves the cervical segments there is quadriplegia
with evident of LMNL in the upper limb.

17. B. Below the level of the lesion (Cord manifestation):
1.Motor manifestations: they depend on whether the cause of lesions is acute or gradual.
a) If the cause is acute:
(Inflammatory, Vascular, Or Traumatic).
The paraplegia passes by 2 stages:
 Stage of flaccidity due to neuronal shock:
Immediately following the lesion there is sudden paralysis of lower limbs associated with complete loss of
tone and absence of reflexes (flaccid paralysis), this stage lasts from 2 to 6 weeks.
 Stage of spasticity due to recovery from the neuronal shock:
On recovery from the shock stage, the picture of U.M.N.L. will be established including hypertonia,
hyperreflexia, positive Babinski sign & may be clonus.
b) If the cause is gradual (e.g., neoplastic):

18.  The shock stage is absent and there will be gradual progressive weakness of the lower limbs with hypertonia
and hyperreflexia:
1.The weakness affects the distal group of muscles more than the proximal group
and the flexor muscles more than the extensors.
2.The hypertonia and hyperreflexia affect the extensor group of muscles
(antigravity) more than the flexor group (progravity), the paraplegia in this stage
is described as (paraplegia in extension).
3.With further progression of the lesion the extrapyramidal fibers in the cord will be
affected, the hypertonia and hyperreflexia will be more in flexor group of muscles
than in the extensors. In this stage the paraplegia is described as (paraplegia in
flexion).
4.This last stage might be associated with the mass reflex where there is
spontaneous urination, defecation and sweating on scratching the skin over medial
side of the thigh associated with reflex erection and ejaculation on squeezing the
glans penis.

19. N.B.: Pierre Marie Foix test is done by firm passive planter flexing of the toes and foot. This will result in spontaneous “withdrawal reflex” i.e.,
spontaneous flexion of the hip, knee, and dorsiflexion of the ankle if the paraplegia is passing from extension to flexion.
Paraplegia In Extension Paraplegia In Flexion
Cause Pyramidal lesion Pyramidal and extrapyramidal
Hypertonia More in extensors More in flexors
Position Of L.L. Extended Flexed
Deep Reflexes Exaggerated Less exaggerated
Clonus Present Absent
Mass Reflex Absent May be present
Bladder Precipitancy Automatic bladder

20. 2. Sensory manifestations:
A) If the cause of the lesion is extramedullary, encroachment on the ascending tracts at the site of lesion results in a
sensory level below which all types of sensations are diminished. There is early loss of sensation in the saddle area (S
3,4,5), as the sacral fibers lie in the outermost part of spinothalamic tracts in the cord.
B) If the cause of the lesion is intramedullary, there will be jacket sensory loss (hyposthetic area with normal sensations
above and below it). The sensory loss of a dissociated nature i.e., pain and temperature sensations are lost but touch and
deep sensations are preserved; this is due to the interruption of crossing fibers carrying pain and temperature by the midline
lesion, while touch and deep sensation fibers ascend in the posterior column without decussation.
The sensations over the saddle area are preserved (sacral spare), as the sacral fibers lie far from the midline lesion.

22. 3. sphincter manifestations:
a) In acute lesions retention of urine in
the shock stage followed by precipitancy
of micturition
b) In gradual lesions: precipitancy of
micturition which may terminate in
automatic bladder when complete
transection of the cord occurs.
These changes start late in the
extramedullary lesions and early in
intramedullary lesions as the pyramidal
fibers controlling the bladder center lie
medially in the cord.

23. Features Extramedullary Intramedullary
Radicular pain Early and common Rare
Sensory deficit No dissociation of
sensation
Dissociation of sensation
common
Sacral sensation Lost early Sacral spare
UMN involvement Early and prominent Less pronounced
LMN Segmental Marked with widespread
atrophy, fasciculations seen
Reflexes Brisk early feature Less brisk late feature
Autonomic
involvement
Late early
Trophic changes Usually not marked common
Vertebral tenderness May be sensitive to local
pressure
No bony tenderness
Changes in CSF Frequent rare

24. Clinical Localization
 Higher Cervical Cord Lesion:
- Sensory loss over occipital (C2).
- Involvement of spinal accessory nerve.
- Wasting of small muscles of hands.
- Quadriplegia with diaphragm weakness.
- Sensory loss of upper portion of face along with loss of corneal reflex due to involvement of spinal nucleus of
5th cranial nerve.
 Lower Cervical Cord:
- C5-C6  weakness in deltoid, supraspinatus, loss of power and reflexes in the biceps.
- C7  weakness is found in triceps, finger, and wrist extensors (radial nerve).
- C8  in finger and wrist flexion are impaired (ulnar nerve).
- Horner’s syndrome occurs lesion at any level.

25.  Thoracic Cord Lesion:
- Sensory level on trunk
- Site of midline back pain
- Paraparesis / paraplegia of lower limb
- Beevor’s sign positive
- Bladder bowel involvement
Lumbar cord lesions:
L2 - L4:
- Weakness of flexion and adduction of thigh
- Weakness leg extension at knee loss patellar reflex
- Exaggerated ankle jerk
L5 - S1:
- Paralyze movement of foot and ankle
- Weakness of flexion at knee
- Weakness of extension of the thigh
- Loss of ankle jerks (L5, S1)

26. Segmental Syndromes
Pathologies that affect all functions of the spinal cord at one or more levels produce a segmental syndrome.
Loss of function may be total or incomplete.

27. Total Cord Transection Syndrome
Results from the cessation of function in all ascending and descending spinal cord pathways and results in the
loss of all types of sensation and loss of movement below the level of the lesion
Acute transection can cause spinal shock, with a flaccid paralysis, urinary retention, and diminished tendon
reflexes.
this is usually temporary, and increased tone, spasticity, and hyperreflexia will usually supervene in days or
weeks after the event.
Causes of a cord segmental syndrome include:
1. Acute myelopathies, such as traumatic injury and spinal cord hemorrhage.
2. Epidural or intramedullary abscess, tumors, and transverse myelitis may have a more subacute presentation

28. Dorsal (Posterior) Cord Syndrome
Dorsal cord syndrome results from the bilateral involvement of the dorsal
columns, the corticospinal tracts, and descending central autonomic tracts
to bladder control centers in the sacral cord.
Dorsal column symptoms include gait ataxia and paresthesias.
Corticospinal tract dysfunction produces weakness that, if acute, is
accompanied by muscle flaccidity and hyporeflexia and, if chronic, by
muscle hypertonia and hyperreflexia.
Causes of a dorsal cord syndrome include:
1. Multiple sclerosis (more typically the primary progressive form).
2. Tabes dorsalis.
3. Friedreich ataxia,
4. Subacute combined degeneration
5. Vascular malformations
6. Epidural and intradural extramedullary tumors.
7. Cervical spondylotic myelopathy

29. Ventral (Anterior) Cord Syndrome
Ventral cord or anterior spinal artery syndrome
usually includes tracts in the anterior two-
thirds of the spinal cord, which include the
corticospinal tracts, the spinothalamic tracts,
and descending autonomic tracts to the sacral
centers for bladder control.
Extensive bilateral motor, superficial and
autonomic functions loss below the level of
lesion. Deep sensations are normal.

30. Brown-Sequard (Hemi-Cord) Syndrome
A lateral hemi section syndrome, also known as the Brown–
Sequard syndrome, involves the dorsal column, corticospinal
tract, and spinothalamic tract unilaterally.
At the level of the lesion:
 Motor: Ipsilateral LMN
 Sensory: Ipsilateral loss of deep and superficial sensation.
Below level of lesion:
 Motor: Ipsilateral UMN
 Sensory: Ipsilateral loss of deep sensation and contralateral
loss of superficial sensation.
While there are many causes of this syndrome, knife or bullet
injuries and demyelination are the most common.

32. Central cord syndromes
The central cord syndrome is characterized by
loss of pain and temperature sensation in the
distribution of one or several adjacent
dermatomes at the site of the spinal cord lesion
caused by the disruption of crossing
spinothalamic fibers in the ventral commissure.
Dermatomes above and below the level of the
lesion have normal pain and temperature
sensation, creating the so-called "jacket sensory
loss." Vibration and proprioception are often
spared.
Bladder & bowel are involvement early.
The classic causes of a central cord syndrome
are slow-growing lesions such as syringomyelia or
intramedullary tumor. However, central cord
syndrome is most frequently the result of a
hyperextension injury in individuals with long-
standing cervical spondylosis.

33. Conus Medullaris Syndrome
• Lesions at vertebral level L2 often affect the conus medullaris.
• There is early and prominent sphincter dysfunction with flaccid paralysis of the bladder and rectum, impotence, and
saddle (S3-S5) anesthesia.
• Preserved motor function of lower limbs including ankle jerk.
• Causes include disc herniation, spinal fracture, and tumors.

34. Cauda Equina Syndrome
Deficits usually affect both legs but are often asymmetric.
Symptoms include:
 Low back pain accompanied by pain radiating into one or both legs.
 Radicular pain reflects involvement of dorsal nerve roots and may have localizing value.
 Weakness of plantar flexion of the feet with loss of ankle jerks occurs with mid cauda equina lesions, involving S1, S2
roots.
 Relative sparing of Bladder and rectal sphincter function.
 Sensory loss of all sensory modalities occurs in the dermatomal distribution of the affected nerve roots.
Many etiologies can cause a cauda equina syndrome including:
1. Intervertebral disc herniation.
2. Epidural abscess & tumor.
3. Intradural extramedullary tumor.
4. Lumbar spine spondylosis.
5. Spinal arachnoiditis.
6. Chronic inflammatory demyelinating polyneuropathy.
7. Sarcoidosis.

35. Conus medullaris syndrome Cauda equina syndrome
Vertebral level L1-L2 L2-sacrum
Spinal level Sacral cord segment and roots Lumbosacral nerve roots
Presentation Sudden and bilateral Gradual and unilateral
Radicular pain Less severe More severe
Low back pain More Less
Motor strength Symmetrical, less marked hyperreflexia distal paresis of
LL, fasciculation
More marked asymmetric areflexic paraplegia, atrophy
more common
Reflexes Ankle jerks affected Both knee and ankle jerks affected
Sensory Localized numbness to perianal area, symmetrical and
bilateral
Localized numbness at saddle area, asymmetrical and
unilateral
Sphincter dysfunction Early urinary and fecal incontinence Tend to present late
Impotence Frequent Less frequent

37. Pattern of sensory loss