Seminar on

SPINAL CORD
DISORDER
PRESENTER DR GADISA DEJENE (R1)
MODERATOR DR DEJENE (NEUROLOGIST)

1
 INTRODUCTION

• Diseases of the spinal cord are frequently devastating.

– They produce quadriplegia, paraplegia, and sensory deficits

far beyond the damage they would inflict elsewhere in the
nervous system because the spinal cord contains, in a small
cross-sectional area, almost the entire motor output and
sensory input of the trunk and limbs.

• Many spinal cord diseases are reversible if recognized

and treated at an early stage;
– Thus, they are among the most critical of neurologic
emergencies.

2
• Cord lesions can lead to motor, sensory, or sphincter
disturbances or to some combination of these deficits.
• Pathologies that affect the spinal cord are diverse.
• In addition to trauma, common etiologies of
myelopathy include:
– Autoimmune
– Infectious
– Neoplastic
– Vascular, and
– Hereditary-degenerative diseases

3
 Spinal Cord Anatomy

• The spinal cord is a thin, tubular extension of the

central nervous system contained within the bony
spinal canal.
– It originates at the medulla and continues caudally to the
conus medullaris at the lumbar level; its fibrous extension,
the filum terminale, terminates at the coccyx.
– The adult spinal cord is 46 cm long, oval in shape, and
enlarged in the cervical and lumbar regions, where neurons
that innervate the upper and lower extremities,
respectively, are located.
4
5
6
Spinal Cord Levels Relative to the Vertebral Bodies

SPINAL CORD CORRESPONDING VERTEBRAL

LEVEL BODY
Upper Cervical Same as cord level
Lower Cervical 1 level higher
Upper Thoracic 2 levels higher
Lower Thoracic 2 to 3 levels higher

Lumbar T10-T12
Sacral T12-L1

7
8
9
10
 Determining the Level of the Lesion

• The presence of a horizontally defined level

below which sensory, motor, and autonomic
function is impaired is a hallmark of spinal
cord disease.
– This sensory level is sought by asking the patient
to identify a pinprick or cold stimulus applied to
the proximal legs and lower trunk and successively
moved up toward the neck on each side.
11
• Sensory loss below this level is the result of
damage to the spinothalamic tract on the opposite
side one to two segments higher in the case of a
unilateral spinal cord lesion, and at the level of a
bilateral lesion.
– The discrepancy in the level of a unilateral lesion is the
result of the course of the second-order sensory fibers,
which originate in the dorsal horn, and ascend for one
or two levels as they cross anterior to the central canal
to join the opposite spinothalamic tract.
12
• Lesions that transect the descending corticospinal
and other motor tracts cause paraplegia or
quadriplegia with heightened deep tendon
reflexes, Babinski signs, and eventual spasticity
(the upper motor neuron syndrome).

• Transverse damage to the cord also produces

autonomic disturbances consisting of absent
sweating below the implicated cord level and
bladder, bowel, and sexual dysfunction.
13
 Cervical Cord

• Upper cervical cord lesions produce quadriplegia and

weakness of the diaphragm. Lesions
• At C4-C5 produce quadriplegia
• At C5-C6, there is loss of power and reflexes in the biceps
• At C7 weakness affects finger and wrist extensors and triceps;
and
• At C8, finger and wrist flexion are impaired
• Horner's syndrome (miosis, ptosis, and facial
hypohidrosis) may accompany a cervical cord lesion
at any level.
14
 Thoracic Cord
• Lesions here are localized by the sensory level on
the trunk and by the site of midline back pain that
may accompany the syndrome.
– Useful markers for localization are the nipples (T4)
and umbilicus (T10).
• Leg weakness and disturbances of bladder and bowel
function accompany the paralysis.
• Lesions at T9-T10 paralyze the lower—but not the upper—
abdominal muscles, resulting in upward movement of the
umbilicus when the abdominal wall contracts (Beevor's
sign).

15
 Lumbar Cord
• Lesions at the L2-L4 spinal cord levels paralyze
flexion and adduction of the thigh,weaken leg
extension at the knee, and abolish the
patellar reflex.
• Lesions at L5-S1 paralyze only movements of
the foot and ankle, flexion at the knee, and
extension of the thigh, and abolish the ankle
jerks (S1).

16
 Sacral Cord/Conus Medullaris
• The conus medullaris is the tapered caudal
termination of the spinal cord, comprising the
lower sacral and single coccygeal segments.
– The distinctive conus syndrome consists of bilateral
saddle anesthesia (S3-S5), prominent bladder and
bowel dysfunction (urinary retention and
incontinence with lax anal tone), and impotence.
– The bulbocavernosus (S2-S4) and anal (S4-S5) reflexes
are absent.
– Muscle strength is largely preserved.
17
• By contrast, lesions of the cauda equina, the nerve
roots derived from the lower cord, are characterized
by
– Low back and radicular pain
– Asymmetric leg weakness and sensory loss
– Variable areflexia in the lower extremities, and
– Relative sparing of bowel and bladder function
• Mass lesions in the lower spinal canal often produce a
mixed clinical picture with elements of both cauda
equina and conus medullaris syndromes.
18
 Foramen Magnum Syndrome
• Lesions in this area interrupt decussating pyramidal
tract fibers destined for the legs, which cross caudal to
those of the arms, resulting in weakness of the legs
(crural paresis).
• Compressive lesions near the foramen magnum may
produce
– Weakness of the ipsilateral shoulder and arm followed by
weakness of the ipsilateral leg, then the contralateral leg,
and finally the contralateral arm, an "around-the-clock"
pattern that may begin in any of the four limbs.
• There is typically suboccipital pain spreading to the
neck and shoulders.
19
 Total Cord Transection Syndrome

•  Pathologies that affect all functions of the spinal cord.

 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.

20
Causes of a Cord Segmental Syndrome include :

 Acute Myelopathies

1. Traumatic injury and

2. Spinal cord hemorrhage.

 Subacute Myelopathies

1. Epidural or Intramedullary abscess,

2. Tumors, and
3. Transverse Myelitis .
21
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.

22
Transverse injuries above C3

 Involve cessation of respiration

 And are often fatal if acute.

 Cervical cord lesions that spare the Phrenic Nerve ,

 But impair Intercostal Nerve function,

 Can produce respiratory insufficiency.

23
Lesions above L2 cord level will cause :

 Impotence and
 Spastic paralysis of bladder.

 There is loss of Voluntary Control of the bladder,

 Which will empty automatically by reflex action.

24
 2 . 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.

25
Location of lesion in Dorsal Cord Syndrome

26
1 . Dorsal column symptoms include :

 Gait ataxia and

 Paresthesias.

2 . Corticospinal tract dysfunction produces weakness that,

 If Acute, is accompanied by Muscle Flaccidity and Hypo-reflexia

and,
 If Chronic, by Muscle Hypertonia and Hyper-reflexia.

 Extensor Plantar Responses and Urinary Incontinence may be

present.
27
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, and
8. Atlantoaxial Subluxation.

28
 3 . 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 :
1. The corticospinal tracts,
2. The spinothalamic tracts, and
3. Descending autonomic tracts to the sacral centers for
bladder control

29
Location of lesion in Ventral Cord Syndrome

30
1 . Corticospinal tract involvements produce :
 Weakness and
 Reflex changes

2 . Spinothalamic Tract deficit produces :

 Bilateral loss of Pain and Temperature sensation.
 Tactile, Position, and Vibratory sensation are normal.

 Urinary incontinence is usually present.

31
The causes of a Ventral Cord Syndrome include :

1. Spinal Cord Infarction,

2. Intervertebral Disc Herniation, and

3. Radiation Myelopathy.

32
 4 . Brown-sequard (Hemi-cord) Syndrome 

•  A Lateral Hemisection Syndrome, also known as the

Brown–Sequard syndrome, involves :

1. The dorsal column,

2. Corticospinal tract, and

3. Spinothalamic tract Unilaterally.

33
Location of lesion in Brown-Sequard syndrome

34
This produces :
 Weakness, loss of Vibration, and Proprioception ,
 Ipsilateral to the lesion
 And loss of Pain and Temperature,
 On the opposite side.
 The unilateral involvement of descending autonomic
fibers
 Does not produce bladder symptoms.

35
While there are many causes of this syndrome:
 The most common causes are :
1. Knife or Bullet injuries and
2. Demyelination.
 Rarer causes include :
1. Spinal cord tumors,
2. Disc herniation,
3. Infarction, and
4. Infections.
36
 5 . 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.
37
Location of lesion in Central Cord Syndrome

38
 Dermatomes above and below the level of the lesion
have ,

 Normal Pain and Temperature sensation,

 Creating the so-called "Suspended Sensory Level."

 Vibration and Proprioception are often spared.

39
As a central lesion enlarges, it may encroach on the :

 Medial aspect or the corticospinal tracts or ,

 On the anterior horn gray matter,

 Producing weakness in the analgesic areas.

40
Fibers mediating the deep tendon reflexes,

 Are interrupted as they pass from the dorsal to the

ventral horn,

 Thus causing tendon reflex loss in the analgesic areas.

 There are usually no bladder symptoms.

41
The classic causes of a Central Cord Syndrome are :

 Slow-growing Lesions such as :

1. Syringomyelia or
2. Intramedullary Tumor.

 However, central cord syndrome is most frequently the

result of :

 A hyperextension injury in individuals with long-standing

Cervical Spondylosis.
42
This form of central cord syndrome is characterized by :

1. Disproportionately greater motor impairment in upper

compared with lower extremities,

2. Bladder dysfunction, and

3. A variable degree of sensory loss below the level of

injury.

43
 6 . Pure Motor Syndrome 

•  A pure motor syndrome produces :

 Weakness without sensory loss or bladder involvement.

This may involve only :

 The Upper Motor Neurons,

 Producing hyperreflexia and extensor plantar responses,

OR
44
 Lower Motor Neuron bilaterally,

 Producing Muscle Atrophy and Fasciculations.

 Other disorders involve both the upper and lower

motor neurons ,

 And produce mixed signs.

45
The causes of a Pure Motor Syndrome include :

 Chronic Myelopathies such as :

1. HTLV-I myelopathy,
2. Hereditary spastic paraplegia,
3. Primary lateral sclerosis,
4. Amyotrophic lateral sclerosis,
5. Progressive muscular atrophy,
6. Post-polio syndrome, and
7. Electric shock-induced myelopathy.
46
 7 . Conus Medullaris Syndrome 

• Lesions at vertebral level L2,

 Often affect the conus medullaris.

1. There is early and prominent sphincter dysfunction

2. With flaccid paralysis of the bladder and rectum,

3. Impotence, and

4. Saddle (S3-S5) anesthesia.

47
Leg muscle weakness may be mild,

 If the lesion is very restricted and ,

 Spares both the lumbar cord and the adjacent spinal and
lumbar nerve roots.

Causes include :

1. Disc herniation,
2. Spinal fracture, and
3. Tumors
48
 8 . Cauda Equina Syndrome 

• Though not a spinal cord syndrome,

 Cauda equina syndrome is considered here because,

 Its location within the spinal canal subjects it to many of

the same disease processes that cause myelopathy.

49
The syndrome is caused by :

 The loss of functions of two or more of the 18 nerve

roots constituting the cauda equina.

 Deficits usually affect both legs,

 But are often asymmetric.

50
Symptoms include:

1 . 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.

51
2 . Weakness of plantar flexion of the feet,

 With loss of ankle jerks occurs with mid cauda equina

lesions,
 Involving S1, S2 roots.

 Involvement of progressively higher levels leads to

corresponding weakness in other muscles.

52
3 . Bladder and rectal sphincter paralysis usually reflect

 Involvement of S3-S5 nerve roots.

4 . Sensory loss of all sensory modalities occurs,

 In the dermatomal distribution of the affected nerve

roots.

53
Many etiologies can cause a Cauda Equina Syndrome :

1. Intervertebral disc herniation,

2. Epidural abscess,
3. Epidural tumor,
4. Intradural extramedullary tumor,
5. Lumbar spine spondylosis, and
6. A number of inflammatory conditions including :
 Spinal arachnoiditis,
 Chronic inflammatory demyelinating polyneuropathy, and
 Sarcoidosis
54
 Intramedullary and Extramedullary
Syndromes

• It is useful to differentiate
– Intramedullary processes, arising within the substance
of the cord, from
– Extramedullary ones that compress the spinal cord or
its vascular supply
• The differentiating features are only relative and
serve as clinical guides.

55
 Classification of spinal cord disorder

I-Acute and Subacute Spinal Cord Diseases

• Compressive
• Non compressive
II-Chronic spinal chord diseases

10/01/20 56
 Compressive
Myelopathies
Acute and Subacute Spinal Cord
Diseases

10/01/20 57
 1.TUMOURS
A.Extradural tumors

• Most neoplasms are epidural

– resulting from metastases

• Most frequent
– breast, lung, prostate, kidney, lymphoma, and
multiple myeloma

10/01/20 58
• The thoracic cord is most commonly involved
– except prostate and ovarian cancer→ sacral and
lumbar vertebrae

• Retroperitoneal neoplasms (especially lymphomas or

sarcomas)
– enter the spinal canal through the intervertebral
foramina
– produce radicular pain and other signs of root
involvement prior to cord compression.

10/01/20 59
 Clinical feature
Pain
• usually the initial symptom
• aching and localized / sharp and radiating
• worsens with movement, coughing, or sneezing and
at night waking the patient from sleep
• Rarely, pain is mild or absent

10/01/20 60
 MRI

• Excellent anatomic resolution of the

extent of spinal tumors

• Distinguishes malignant lesions from

infectious ones
– Tumors are usually hypointense
relative to a normal bone marrow
– Don't cross disk space unlike
infections
10/01/20 61
• The whole length of the spine should be
imaged when epidural malignancy is
suspected

– 40% of patients have asymptomatic

epidural disease elsewhere

• Plain radiographs of the spine and

radionuclide bone scans
– miss 15–20% of metastatic vertebral lesions
– fail to detect paravertebral masses

10/01/20 62
 MRI

10/01/20 63
 Treatment
• STEROIDS to reduce cord edema
– dexamethasone 1omg initially then 4mg QID
– Continued at a lower dose until radiotherapy is
completed
• LOCAL RADIOTHERAPY to the symptomatic lesion
– as early as possible
– as effective as surgery, even for radioresistant
metastases
– new weakness is prevented
– some recovery of motor function in half of treated
patients
– Fixed motor deficits established for >12 hrs do not
usually improve
10/01/20 64
• SURGERY
– laminectomy or vertebral body resection
– should be considered when
• signs of cord compression worsen despite
radiotherapy
• vertebral compression fracture or spinal
instability contributes to cord compression

• Specific therapy for the underlying tumor type

10/01/20 65
 B Intradural tumors

 Slow-growing and benign

 Therapy is by surgical resection
1. Meningiomas
 Can arise from the meninges anywhere along
the spinal canal
 Usually located
 posterior to the thoracic cord
 near the foramen magnum

10/01/20 66
2. Neurofibromas
 Benign tumors of the nerve sheath
 arise near the posterior root
 Symptoms usually begin with radicular sensory
symptoms
 asymmetric, progressive spinal cord syndrome
3. chordoma
4. lipoma
5. dermoid, or
6. sarcoma

10/01/20 67
 MRI of a thoracic meningioma
intense and uniform enhancement of a well-circumscribed extramedullary
mass

10/01/20 68
 C. Intramedullary tumors
 Primary intramedullary tumors are rare
 Secondary tumors are common in advanced
metastatic disease
 present as central cord or hemicord syndromes,
often in the cervical region
 there may be poorly localized burning pain in the
extremities and sparing of sacral sensation

10/01/20 69
 Intramedullary tumor
1.Ependymomas
2.Hemangioblastomas
3.low-grade astrocytomas
 Ependymomas :Complete resection
 Astrocytoma (slowly growing lesions) :
Debulking
 Adjunctive radiotherapy and chemotherapy
is uncertain
10/01/20 70
 MRI of an intramedullary astrocytoma. Sagittal T1-weighted

10/01/20 71
 2-Spinal Epidural Abscess
 Triad of midline dorsal pain, fever, and progressive
limb weakness
Risk factors include
1. impaired immune status (diabetes mellitus, renal
failure, alcoholism, malignancy)
2. intravenous drug abuse
3. infections of the skin , viscera, bone and other
tissues
Aching pain is almost always present
– either over the spine or in a radicular pattern
The duration of pain prior to presentation is generally <2
weeks
– may be several months or longer
10/01/20 72
• Further spinal cord damage results from venous
congestion and thrombosis

• Once weakness and other signs of myelopathy

appear, progression may be rapid and
irreversible

• Elevated white blood cell count and

sedimentation rate

• A more chronic sterile granulomatous form of

abscess is also known, usually after treatment of
an acute epidural infection.
10/01/20 73
• 2/3rd :hematogenous spread of bacteria from
1. the skin
2. soft tissue (pharyngeal or dental abscesses)
3. deep viscera (bacterial endocarditis)

• 1/3rd : direct extension of a local infection

1. vertebral osteomyelitis
2. decubitus ulcers
3. lumbar puncture
4. epidural anesthesia
5. Spinal surgery
10/01/20 74
 Etiology
 Staphylococcus aureus inluding MRSA
 TUBERCULOSIS in assocition with pott disease
(tuberculous spinal osteomyelitis )
 Gram-negative bacilli
 Streptococcus
 Anaerobes
 Fungi
Diagnosis
 MRI scans
 Blood Culture
 LP

10/01/20 75
 MRI of a spinal epidural abscess due to tuberculosis

Sagittal T2-weighted Sagittal T1-weighted

10/01/20 76
 Treatment
 Decompressive laminectomy with debridement
 treatment of choice unless the abscess is
1. limited in size and causes few or no neurologic signs.
2. If surgery is contraindicated or
3. if there is a fixed paraplegia or quadriplegia : long-
term administration of systemic and oral antibiotics
 may improve or reverse paralysis in evolution
 unlikely to improve deficits of more than several
days duration
 Anti Tb for tuberculous epidural abscess

10/01/20 77
 3-Spinal Epidural Hematoma
 Acute focal or radicular pain followed by spinal cord
disorder
 Predisposing conditions
 Therapeutic anticoagulation
 Trauma
 Tumor
 blood dyscrasia
 lumbar puncture

Diagnosis MRI and CT confirm the clinical suspicion

Treatment
 Prompt reversal of any underlying clotting disorder
 Surgical decompression

10/01/20 78
 4-Hematomyelia
• Hemorrhage into the substance of the spinal cord
• Result from
– Trauma
– Intraparenchymal vascular malformation
– Vasculitis (polyarteritis nodosa, SLE)
– Bleeding disorders
– a spinal cord neoplasm
• Acute painful transverse myelopathy
• Extension into the subarachnoid space may occur,
resulting in subarachnoid hemorrhage

10/01/20 79
 Hematomyelia
Diagnosis is by MRI or CT
THERAPY

• Supportive
• surgical
intervention not
useful except in
underlying vascular
malformation

10/01/20 80 80
 Noncompressive Myelopathies
After spinal cord compression is excluded the following
should be considered
1. Spinal cord infarction
2. Myelitis
– infectious (primarily viral)
– Postinfectious/ post vaccinal
– systemic inflammatory disorders
– SLE and sarcoidosis
3. Demyelinating diseases
– multiple sclerosis and neuromyelitis optica
10/01/20 81
 1-Spinal Cord Infarction
A- With systemic hypotension
• cord infarction occurs at the level of greatest
ischemic risk
– Usually T3-T4
– Boundary zones between the anterior and
posterior spinal artery territories
• rapidly progressive syndrome over hours of
weakness and spasticity
– little sensory change

10/01/20 82
83
84
 Anterior spinal artery
 Produces "anterior cord syndrome
 Sharp midline or radiating back pain localized to
the area of ischemia
 paraplegia or quadriplegia
 loss of sphincter control
 dissociated sensory loss
 usually progressive over minutes or a few hours
 unlike stroke in the cerebral hemispheres

10/01/20 85
  Areflexia due to spinal shock is often present initially with
time, hyperreflexia and spasticity appear

 A few patients have vertigo at the onset

 Rarely, infarction is preceded by transient spinal ischemic

attacks

 Many patients regain a substantial degree of motor

function, mainly in the first month but extending over a
year

Posterior spinal arteries

 not common

10/01/20 86
 Diagnosis
• MRI
– Usually detects the abnormality
– May fail to demonstrate limited infarctions of the cord,
especially in the first day
– In the chronic stages, the infarcted region collapses and
has an attenuated signal on MRI
• Treatment
– presumed thromboembolism, acute anticoagulation is
probably not indicated, with the exception of the unusual
transient ischemic attack or incomplete infarction with a
stuttering or progressive course
– ?CSF drainage

10/01/20 87
 2. Inflammatory and Immune Myelopathies
(Myelitis)
• Includes Demyelinating conditions:
• MS, NMO, and postinfectious myelitis, as well
as sarcoidosis and systemic autoimmune
disease.
• In approximately one-quarter of cases of
myelitis, no underlying cause can be identified.
• Recurrent episodes of myelitis

10/01/20 88
 1.Acute Infectious Myelitis
• EBV, CMV, rabies virus,
• Often difficult to Poliomyelitis
distinguish from • Bacterial and mycobacterial
postinfectious myelitis
• Herpes zoster – less common
– most are essentially
– best characterized abscesses
• HSV types 1 and 2 – Almost any pathogenic
– recurrent sacral species
 Parasitic myelitis
myelitis in – Schistosomiasis
association with
– Toxoplasmosis cause a
outbreaks of genital focal myelopathy in HIV
herpes. pts

10/01/20 89
 Treatment
• Herpes zoster, HSV, and EBV intravenous
acyclovir (10 mg/kg q8h) or oral valacyclovir
(2 g tid) for 10–14 days.

• CMV with ganciclovir (5 mg/kg IV bid) plus

foscarnet (60 mg/kg IV tid) or cidofovir (5
mg/kg per week for 2 weeks).

10/01/20 90
 2.Post infectious /post vaccinal

 The characteristic features of these diseases are

(1)their temporal relationship to certain viral infections
or vaccinations
(2)the delayed development of neurologic signs over
the period of a few days
(3)a monophasic temporal course, i.e., a single attack
of several weeks' duration with variable degrees of
recovery and no recurrence.

10/01/20 91
 Pathogenesis
 Immunologic in nature more or less confined
to spinal cord myelin
 Often begins upon recovery from an AFI or in
the subsequent days or weeks
 infectious agent cannot be isolated
 If it also affects the brain it is called acute
disseminated encephalomyelitis (ADEM)

10/01/20 92
 Organisms
• Bacterial
 Mycoplasma
• Viral
 Epstein-Barr virus
 cytomegalovirus
 Influenza
 Measles
 Varicella
 Rubeola
 mumps
10/01/20 93
 Diagnosis
• CSF
– lymphocytes and other mononuclear cells :10 -100/mm3
– Some times normal
– slightly raised protein and normal glucose content
• MRI
– slight T2 signal abnormalities
– minimal gadolinium enhancement extending over 2 or 3
spinal segments
– the cord may be swollen in these regions
– several patients with mild and partial myelitis may have
normal MRI studies

10/01/20 94
 Treatment
• Once symptoms begin, it is not clear if any treatment is of
consistent value

• ?high doses of corticosteroids :no evidence that this

alters the course of the illness

• ?plasma exchange or intravenous immune globulin

• Usually the myelitic disease improves, sometimes to a

surprising degree

10/01/20 95
 3.Multiple Sclerosis
• MS may present with acute myelitis, particularly
in individuals of Asian or African ancestry.
• It is among the most common causes of a partial
cord syndrome.
• rarely cause a transverse myelopathy
• MRI findings typically consist of mild swelling of
the cord and diffuse or multifocal “shoddy” areas
of abnormal signal on T2-weighted sequences.

10/01/20 96
• Treatment of acute episodes of MS-associated
myelitis consists of intravenous
methylprednisolone (500 mg qd for 3 days)
followed by oral prednisone (1 mg/kg/d for
several weeks,then gradual taper).
• A course of plasma exchange may be indicated
for severe cases if glucocorticoids are ineffective.

10/01/20 97
 Tabes Dorsalis
• Post. Column

• Now rare

• Occurs 18-25 yrs after initial lesion.

• presentation :
-Lightning pain (sudden and severe)
-Ataxia
-Sensory loss and paresthesia
-Visceral crisis(abdominal pain and diarrhea)
-Rectal crisis(tenesmus)
-Charcot jt
-Associated ARP and optic atrophy

10/01/20 98
 Systemic Inflammatory Disorders
• SLE
• Sjögren's syndrome
• mixed connective tissue disease
• vasculitis
• sarcoid myelopathy

10/01/20 99
 3-Demyelinating Myelopathies

10/01/20 100
 Acute Demyelinating Myelitis of MS

• the clinical manifestations of MS tend to evolve more slowly, over a period of 1 to 3 weeks or
even longer.
• antecedent infections is not often seen
• Only the occurrence of subsequent attacks or additional lesions revealed by MRI or evoked
potentials indicates that the basic illness is one of chronic recurrent demyelination
• numbness that spreads over one or both sides of the body from the sacral segments to the
feet, anterior thighs, and up over the trunk
• asymmetric weakness and then paralysis of the legs
• When this process becomes complete, the bladder is also affected
• The sensorimotor disturbance may extend to involve the arms
• a sensory level can be demonstrated on the upper parts of the trunk.
• relatively painless and without fever, and the patient usually improves, with variable residual
signs

10/01/20 101
• The CSF often normal
– may show a mild lymphocytosis, as in the postinfectious variety
– Oligoclonal bands may be absent with the first attack

Treatment
• Corticosteroids
– may lead to a regression of symptoms, sometimes with relapse when the medication is discontinued
(after 1 to 2 weeks)
– No apparent response in some
– a proportion of cases have even continued to worsen on steroids
• Plasma exchange and intravenous immune globulin
– particularly in those with an explosive onset

10/01/20 102
 II-Chronic Myelopathies
1-Spondylitic Myelopathy
 most common cause of gait difficulty in the elderly
 involve the lower and midcervical vertebrae
 Neck and shoulder pain with stiffness are early symptoms
 Radicular arm pain, most often in a C5/C6 distribution
 Compression of the cervical cord
 fewer than one-third of cases
 produces a slowly progressive spastic paraparesis, at times
asymmetric
 accompanied by paresthesias in the feet and hands
 Vibratory sense is diminished in the legs
 positive Romberg sign

10/01/20 103
 • occasionally there is a sensory level for vibration on the
upper thorax
• coughing or straining produces leg weakness or radiating
arm or shoulder pain
• Dermatomal sensory loss in the arms, atrophy of intrinsic
hand muscles,
• increased deep-tendon reflexes in the legs, and extensor
plantar responses
– the biceps is most often affected (C5-C6)
• Urinary urgency or incontinence occurs in advanced cases

10/01/20 104
10/01/20 105
 Diagnosis
• MRI or myelography
– Treatment
• A cervical collar in milder cases
• surgical decompression : definitive therapy
– Posterior laminectomy
– resection of the protruded disc and bony material

10/01/20 106
 2-Syringomyelia
• Developmental cavitary expansion of the cervical cord
• prone to enlarge and produce progressive myelopathy
• Symptoms
– begin insidiously in adolescence or early adulthood
– progress irregularly
– may undergo spontaneous arrest for several years
– Many young patients acquire a cervical-thoracic scoliosis
• More than half of all cases are associated with Chiari type 1
malformations
– cerebellar tonsils protrude through the foramen magnum and into the
cervical spinal canal
• syrinx cavities
– Acquired cavitations of the cord in areas of necrosis
– trauma, myelitis, necrotic spinal cord tumors, and chronic
arachnoiditis due to tuberculosis and other etiologies

10/01/20 107
 Classification
Type I. Syringomyelia with obstruction of the foramen magnum and dilatation of the central
canal (developmental type)
A. With type I Chiari malformation
B. With other obstructive lesions of the foramen magnum
Type II. Syringomyelia without obstruction of the foramen magnum (developmental type)
Type III. Syringomyelia with other diseases of the spinal cord (acquired types)
A. Spinal cord tumors (usually Intramedullary)
B. Traumatic myelopathy
C. Spinal arachnoiditis and pachymeningitis
D. Secondary myelomalacia from cord compression (tumor, spondylosis), infarction,
hematomyelia
Type IV. Pure hydromyelia (developmental dilatation of the central canal), with or without
hydrocephalus

10/01/20 108
10/01/20 109
10/01/20 110
 3-Subacute Combined Degeneration

 Subacute paresthesias in the hands and feet

 A progressive spastic and ataxic weakness
 Loss of vibration and position sensation

 Loss of reflexes due to an associated peripheral neuropathy in a

patient who also has Babinski signs, is an important diagnostic clue
 Optic atrophy and irritability or other mental changes in advanced
cases
 Myelopathy is diffuse rather than focal
 signs are generally symmetric
 predominant involvement of the posterior and lateral tracts

 Romberg's sign

10/01/20 111
• DX confirmed by the finding of
1. macrocytic red blood cells
2. serum B12 concentration
3. elevated serum levels of homocysteine and methylmalonic
acid
4. positive Schilling test
• Treatment
– vitamin B12, beginning with 1000 µg IM
– repeated at regular intervals or by subsequent oral
treatment

10/01/20 112
10/01/20 113
10/01/20 114
 Vascular Malformations of the Cord and Dura
 uncommon
 middle-aged men
 located posteriorly along the surface of the cord or within
the dura
 Pain over the dorsal spine, dysesthesias, or radicular pain
 intermittent claudication
 Spinal bruits are infrequent
 should be sought at rest and after exercise in
suspected cases
 progressive myelopathy that worsens slowly or
intermittently
 A saltatory progression is most common and is the result
of local ischemia and edema from venous congestion.

10/01/20 115
10/01/20 116
10/01/20 117
 Tropical Spastic Paraparesis

 Caused by Human T-Cell Lymphotropic Virus Type I

 cytotoxic
 The posterior columns and corticospinal tracts are the main sites of
disease,
 most evident in the thoracic cord
 slowly progressive paraparesis with increased tendon reflexes and
Babinski signs
 most patients are unable to walk within 10 years of onset
 disorder of sphincteric control is usually an early feature
 but symmetric paresthesias, reduced vibratory and position senses,
and ataxia follow over several months or years
 often lack a well-defined sensory level
 upper extremities usually spared (except for lively tendon reflexes)

10/01/20 118
• CSF contains
– small numbers of lymphocytes of the T type (10 to 50/mm3),
– normal concentrations of protein and glucose
– an increased content of immunoglobulin (Ig) G with antibodies to
HTLV-I
– diagnosis is confirmed by the detection in the serum of the antibodies
to the virus
• MRI :
– Thinness of the spinal cord
– subcortical cerebral white matter lesions may be seen as well
• no effective treatment
– symptomatic therapy for spasticity and bladder symptoms

10/01/20 119
 Vacuolar Myelopathy with AIDS
• 20 of 89 successive cases of AIDS on whom a postmortem
examination was performed had it
• The white matter of the spinal cord is vacuolated, most
severely in thoracic segments
– posterior and lateral columns are affected
• the lesions in the spinal cord resemble those of subacute
combined degeneration
– levels of vitamin B12 and folic acid have been normal
• symptoms and signs obscured by
– a neuropathy or
– one or more of the cerebral disorders that complicate AIDS

10/01/20 120
• Hemi- or quadriparesis, often asymmetrical
– Develop over a period of weeks
• sensory and sphincteric disorder
• A sensory ataxia has also been a common early feature

CSF
– a small number of lymphocytes,
– a slight elevation of protein
– occasionally bizarre giant cells
• Similar vacuolar lesions may be seen in the brain in some cases
• antiretroviral drugs have little effect on the myelopathy
• symptomatic treatment of spasticity

10/01/20 121
 Familial Spastic Paraplegia
• onset may be as early as the first year of life or as late as middle
adulthood
• imperceptibly progressive spasticity and weakness in the legs,
• usually symmetrical
• Sensory symptoms and signs are absent or mild
• sphincter disturbances may be present
• IN some families additional neurologic signs are prominent, including
– nystagmus, ataxia, or optic atrophy
• Only symptomatic therapies for the spasticity are currently available

10/01/20 122
• konzo

10/01/20 123
10/01/20 124
 MANAGEMENT
• Management of SC problems must be
cautious and fast because reversal of
paraparesis is TIME-LOCKED .
• Paraplegia beyond a certain interval may
remain complete, with no prospect of future
ambulation or bladder bowel control.
• So again expedited evaluation and act is
required

10/01/20 125
• Unacceptable delay in diagnosis ,refferal,and
investigation shouldn’t occur.
• If traumatic or other they should immediately
be transferred to institutions providing the
service.
• Specific diagnosis needs specific treatment.

10/01/20 126
 • Postoperative care, rehabilitation are very
important aspects of managing patients
with spinal cord lesions.

10/01/20 127
 THANKS!

10/01/20 128