This document provides an overview of spinal cord anatomy and clinical assessment of spinal cord lesions. Key points include: - The spinal cord extends from the foramen magnum to L1-L2 and is segmented into 31 pairs of spinal nerves. - Sensory and motor function can be localized based on dermatome and myotome patterns. - Spinal cord blood supply comes from the anterior and posterior spinal arteries. The artery of Adamkiewicz is a critical radicular artery. - Ascending tracts include the spinothalamic, posterior, and spinocerebellar tracts. Descending tracts include the corticospinal, rubrospinal, and reticulosp

1. Presenter: Ephrem Fantu (R3)
Moderators: Dr. Samson Y. MD, Consultant Neurologist &
Dr. Nebiyu B. MD, Consultant Neurologist

2. Relevant Anatomy
 The spinal cord is a thin, tubular extension of the CNS.
 It extends from the level of the cranial border of the atlas (base of skull), to
the lower border of the L1 vertebra.
 During fetal development, the vertebral column grows more rapidly than the
spinal cord.
 At birth, it ends around L3 vertebral body and by 2 years of age reaches the
adult position at the L1-L2.

3. 3
The average length of the cord is 45
cm male and 42- 43 cm in female.
The average length of the spinal
column is 70 cm.
B/c of this, caudal spinal nerves must
travel farther to reach their exit.

4. There are 31 spinal cord segments.
Each segment has dorsal and ventral
roots that join to form a spinal nerve.
Each segment corresponds to a vertebra,
except for C8.
Spinal nerves in the cervical region exit
above their vertebra.
Starting with T1, the spinal nerves exit
below their vertebra.

5.  The external surface of the cord is marked by a ventral median fissure and a
dorsal median sulcus.
 The dorsal roots enter along the dorsolateral sulcus.
5

6. 6
Clinically important dermatomes
C2/3 posterior head & neck
C5anterior shoulder,
C6Thumb
C7index & middle finger
C7/8Ring finger
C8little finger
T1= inner forearm
T2 upper inner arm
T2/T3 axilla
T4/5 Nipple
T10 umbilicus
L1 anterior, inner upper thigh
L2Anterior thigh
L3Knee
L4 medial malleolus
L5 dorsum of foot
S3 anus
Key muscles to be tested:
C5-->Shoulder abduction
C6--> Elbow flexors, Wrist extension
C7Elbow extension & wrist flexion
C8 Finger flexion
T1 Finger abduction
L2 Hip flexion
L3 Knee extension
L4 Ankle dorsiflexion
L5 Big toe extension
S1 Ankle plantar flexor, hip extension
S2 Knee flexion

7. Vasculature of SC
An anterior and posterior arterial
system supply to the spinal cord.
Anterior spinal artery from descending
branches of the vertebral arteries and
supplies the anterior 2/3rd of the cord.
Paired posterior spinal arteries from
PICA and serve the posterior third.

8. 8
The spinal arteries are further fed by
segmental radicular arteries, from:
Vertebral arteries in the cervical region,
Intercostal branches of the aorta in the
midthoracic region,
Great radicular artery (of Adamkiewicz) in
the lower thoracic or lumbar.
This artery enters the cord anywhere b/n
T5 and L1 (mostly b/n T9 - T12).

9.  Posterior spinal artery receives 10 to 16 radicular branches.
 Anterior spinal artery has fewer, but larger radicular arteries, making the
anterior spinal artery distribution more prone to embolic or thrombotic
infarction.
 Upper cervicothoracic region (C1- T2), and lower thoracolumbosacral region
richly vascularized.
 The midthoracic region (T3-T8), poorly vascularized

10. 10
Venous Drainage
Similar distribution to the arteries.
The venous drainage feeds into a
longitudinal anterior and posterior
vein, forming a pial plexus.
Radicular veins drain from the pial
plexus into epidural plexus. (Batson
plexus)
Then drains into intervertebral veins
and also into the external vertebral
venous plexus

11. Cross-sectional Anatomy
11
The spinal cord consists of gray
matter surrounded by white
matter).
The gray matter is divided into
posterior, anterior and lateral
(intermediate) horns.
The horns divide the white matter
into posterior, lateral, and anterior
columns (funiculi).

12. Gray Matter
 Centrally placed and surrounded by white
matter.
 The dorsal horn is the entry point of
sensory information.
 The motor nuclei are contained within the
ventral horn.
 The anterior horn contains alpha and
gamma motor neurons as well as
interneurons that help to fine-tune the
motor output.

13. 13
The anterior horn is organized
somatotopically;
Neurons controlling the axial muscles--->
medially placed,
Neurons serving for the motor control of the
distal limbs are lateral
Neurons controlling the proximal limb
muscles lie in between
Neurons serving extensor muscles are
ventral to those controlling flexors.
The intermediolateral cell
column:
T1 to L3 contains:
Sympathetic nuclei
S2 to S4 contains:
parasympathetic nuclei

14. Laminae
A cross section of the gray matter shows a
number of laminas (layers of nerve cells),
termed Rexed’s laminae.
Laminae I - VI (dorsal horn),
Lamina VII (intermediate zone),
Laminae VIII and IX (ventral horn).
Lamina I: Posteromarginal Nucleus
Lamina II: Substantia Gelatinosa of Rolando
Lamina IV, V, VI: Nucleus Proprius
Lamina III: Part of Nucleus Proprius
Lamina VII: Autonomic and Clarke’s neurons
Lamina VIII: Termination of some descending
fibers.
Lamina IX: Anterior Horn (Motor) Cell
Lamina X: Gray Commissure

15. White Matter
 Ascending Tracts:
 Anterolateral system
 Spinothalamic tracts
 Spinoreticular tract
 Spinomesencephalic
 The posterior columns
 Spinocerebellar tracts

16. Spinothalamic tracts
Smaller-diameter and
unmyelinated axons
They carry information about pain
and temperature, and crude touch
They enter via the dorsal root
entry zone.
They make first synapse in the
gray matter, mainly in the
marginal zone and lamina V.

17.  Axons of the 2nd order sensory neurons cross over in the ventral
commissure to ascend in the anterolateral white matter.
 Decussating fibers take about two to three segments to reach the opposite
side.
 The somatotopic organization is with arms medial and legs lateral.
 Then they enter the pontine tegmentum just lateral to the medial lemniscus
in the pons and midbrain. (spinal lamniscus)

18.  Then enter to ventral posterior lateral nucleus (VPL) of the thalamus.
 Then via the thalamic somatosensory radiations to the primary
somatosensory cortex in the postcentral gyrus.

19. Posterior Column–Medial
Lemniscal Pathway
Large-diameter, myelinated axons
Carrying information about
proprioception, vibration, and fine
touch
Enter via the medial portion of the
dorsal root entry zone.
Many of these axons ascend
ipsilaterally in the posterior columns

20.  Both pathways synapse in the medulla in their respective nuclei.
 2nd order neurons send projections via internal arcuate fibers to the
contralateral medial lemniscus and then to the thalamic VPL nucleus.
 The next major synapse occurs in the VPL of the thalamus.
 The neurons of the VPL then project through the posterior limb of the
internal capsule to the primary somatosensory cortex in the postcentral
gyrus.

21. Descending Tracts
Lateral and medial systems
Lateral motor systems
Lateral corticospinal tract
Rubrospinal tract
Medial motor systems are:
Anterior corticospinal tract,
Vestibulospinal tracts,
Reticulospinal tracts, and
Tectospinal tract.

22. Cortico Spinal Tracts:
Controls the movement of the
extremities and trunk.
It is essential for rapid, dextrous
movements at individual digits or
joints.
Over half of the fibers originate in the primary
motor cortex (A4) of the precentral gyrus.
The remainder from the premotor and
supplementary motor areas (A 6) or parietal
lobe (areas 3, 1, 2, 5, and 7).

23. 23

24. Autonomic Nervous System
 The autonomic fibers are another important descending system.
 Autonomic dysfunction is an important determinant of site, extent, and
severity of spinal cord pathology.
 They travel in the lateral aspect, but without a well-defined tract.
 Many autonomic functions can be affected by spinal cord pathology, but for
clinical evaluation, the most useful symptoms related to bladder control.

25. 25
Sympathetic
Concerned with fight or flight functions.
Polysynaptic fibers from hypothalamus
(PL area) ----> laterally to
intermediolateral horn of T1 to L2/3
(lamina VII).
Then exit to sympathetic ganglia through
ventral root.

26. 26
Parasympathetic
Concerned with rest and digest functions.
Fibers from hypothalamus (AM area) --->
Upper brain stem nuclei and polysynaptic
fibers laterally to intermediolateral horn of
S2, S3 and S4.
Then exit from spinal cord through ventral
root.

27. 27
Bladder control:
Sympathetic fibers (T12-L2)
Parasympathetic fibers (S2-S4)
Somatic motor fibers (S2-S4)
Central nuclei:
Frontal lobe
Periaqueductal gray (PAG)
Pontine micturition center

29. Bowel Control
Like urinary continence, it is controlled by
descending pathways originating mainly in the
medial frontal lobes.
Anal sphincter closure is maintained by:
Internal sphincter (parasympathetics),
External sphincter (pelvic nerves from Onuf’s
nucleus)
Pelvic floor muscles (sacral anterior horn cells).
GI motility depends on parasympathetics (S2 to
S4) for colorectal smooth muscle beyond the
splenic flexure.
Fecal incontinence can
be caused by:
Diffuse cerebral or
medial frontal
lesions,
Spinal cord lesions
Lesions of the sacral
nerve roots or
pudendal nerves.
Acute spinal cord lesions:
Anal sphincter is completely flaccid.
Colorectal smooth muscle is also flaccid, causing constipation. (PS)

30. Sexual Function
The genital organs are innervated by three sets of nerves:
Parasympathetic
Thoracolumbar sympathetic,
Somatic (pudendal nerves).
During sexual arousal, sensation from the genitalia is conveyed by
the pudendal nerve, reaching S2 to S4.
Then, erection occurs through parasympathetic pathways.
Ejaculation occurs through sympathetically mediated contraction of
smooth muscle (seminal vesicles, vas deferens, prostate, bladder
neck), followed by rhythmic reflex contractions of striated muscles
(pelvic floor, urethral sphincter, bulbospongiosus, ischiocavernosus),
(Pudendal)
In spinal cord lesions,
reflex erection and reflex
ejaculation may occur.
Peripheral nerve lesions,
higher-order cortical
lesions, medications,
and psychological
factors can also cause
sexual
dysfunction.

31. Localizing A Cord Lesion
 Important questions:
1. Is the lesion in the spinal cord?
2. Where in the SC (Longitudinal localization)
3. What is the horizontal extent of the lesion?
4. Is the problem intra-medullary or extramedullary?
5. What is the likely cause?

32. Is It SC?
 Suspect spinal cord lesions when :-
 Bilateral motor and sensory signs and symptoms, sparing the head and
neck.
 Cardinal features:
 Paraparesis/ Quadriparesis (bilateral weakness)
 Sensory level, (reduced or absent)
 Bowel/bladder dysfunction

33. Longitudinal Localization
 A horizontally defined level below which sensory, motor, &/or autonomic
function is impaired is the hallmark of spinal cord disease.
 Important clues for longitudinal localization:
 1. Sensory level :
 A definite segmental level below which posterior column or spinothalamic
sensations are diminished or lost
 Posterior column: the sensory level is the same as the perceived level
 STT: the sensory level is 1 or 2 segments below

34.  2. Segmental signs: due to disturbed sensory and motor innervations at the
level.
 Motor: LMNL signs - paresis, fasciculations, atrophy of the muscle group
innervated by the segment with depressed or absent DTR.
 Sensory: a band of altered sensation (hyperalgesia or hyperpathia)
 N.B. Segmental signs can result from root lesions or PN. Thus they are most
useful in the presence of long tract signs.

35.  3. UMNL signs: spastic paralysis below the lesion with exaggerated DTR
and +ve Babinski sign.
 Ipsilateral to the lesion
 4. Radicular Sensory Involvement
 Sensory changes from cord or root involvement often cause pain, esp. if lesion is
extrinsic rather than intrinsic.
 The pain occurs spontaneously/ movement/ percussion.
 5. Vertebral Column Deformity:
 Deformity – such as angulations or scoliosis
 Tenderness on local percussion

36. Cervicomedullary Junction and Upper Cervical Cord
Involves upper cervical cord and extend to the
medulla.
Tetraparesis (often mimicking a central
cord syndrome with arms affected more
than legs) (Around the clock pattern)
Hemiplegia cruciata
Respiratory compromise,
Neck and occipital pain are common
Onion-skin sensory loss over the face

37.  Due to extension of the lesion, long tract
sensory findings, and bladder disturbance, CN
(IX–XII) palsies.
 May compromise CN XI, resulting in
anomalous head position, weakness of the
SCM and trapezius muscle.
 Lower cervical and upper thoracic LMN signs,
due to venous congestion/anterior spinal
artery compression affecting the more caudal
anterior horns.
Causes:
Extramedullary
Meningioma, neurofibroma,
glioma,
Spondylosis,
Chiari malformation, and
trauma;
Intramedullary etiologies
include:
Syringomyelia, MS, and
NMO.

38. Lower Cervical and Upper Thoracic Cord
 Lesions at lower cervical levels produce quadriparesis
 C5-C6: deltoid, biceps, spinati, depressed biceps and brachioradialis
reflexes (elbow flexion and wrist extension)
 C7: triceps, triceps reflex is depressed; (elbow extension)
 C8-T1: wrist and finger flexion, finger flexor reflex is depressed.
 Horner's syndrome (miosis, ptosis and facial hypohidrosis) may occur with a
cervical cord lesion at any level.

39. Thoracic Spinal Cord
 Localizing features are:
 Sensory level on the trunk
 Site of back pain if well localized
 Weakness of lower limbs (spared UL)
 Involvement of bowel and bladder
 Autonomic dysreflexia may occur with lesions
above T6 (splanchnic sympathetic outflow)
 BelowT6 lesions will abolish superficial
abdominal reflexes.
39

40.  T9 –T10 lesions affect the lower abdominal reflex, but upper and middle
abdominal reflexes are spared.
 T10 lesion is characterized by a Beevor's sign:
 With neck flexion at supine, preserved upper abdominal muscles will pull
the umbilicus upward.

41. Lumbosacral Spinal Cord
 L1 lesion affect all muscles of the lower extremities.
 Sensory loss in the lower extremities up to the groins and the back up to a
level above the buttocks.
 L2-L4 level lesions:
 Weakness of thigh flexion and adduction, weakness of knee extension
and loss of knee jerk. (Thigh flexion, Knee extension, ankle dorsiflexion)
 The cremasteric reflex (L2/1) is not elicitable.
 Lesions at L5-S1 result in:
 Weakness of foot and ankle, knee flexion, thigh extension and ankle jerks.

42.  S1-S2 lesions:
 Ankle reflexes without impacting the patellar.
 Sensory loss over the sole, heel, and outer aspect of the foot and ankle.
 The medial aspects of the calf and posterior thigh and the outer aspect of
the “saddle” area are also anesthetic.

43.  Conus Medullaris/ syndrome
 Saddle anesthesia (S3-S5)
 Urinary retention with overflow incontinence
(detrusor areflexia)
 Constipation and impaired erection and ejaculation
 Loss of anal reflexes (S4-S5) and bulbocavernosus
(S2-S4)
 Preserved motor function of LL, Loss of ankle jerks
(S1),
 Paralysis of the pelvic floor muscles (not marked).

44. Cauda Equina Syndromes
Injury of lumbar & sacral roots below L2 vertebra
Early radicular pain – may be unilateral (over
thigh, perineum, legs, back)
Sensory deficits in legs and saddle area,
Flaccid paralysis of lower limbs with areflexia
areflexia
Urinary retention, fecal incontinence with
impotence and loss of anal tone
Tumors, lumbar disc herniation

45. Cross Sectional Localization
 Motor involvement
 Corticospinal tract involvement: UMNL involving one or both sides
 Involvement of autonomic functions
 Sensory loss:
 Posterior column dysfunction:
 Spinothalamic dysfunction:

46. Complete Cord Transection
46
All descending and ascending pathways are affected.
There is often a sensory level, (diminished sensation in
all dermatomes below the level of the lesion).
A flaccid paralysis and associated ‘‘flaccid’’ autonomic
dysfunction may occur acutely below the level of injury.
Over time, spasticity and hyperreflexia ensue, with a
segmental anterior horn syndrome.
Autonomic disturbance also occurs

47. Hemicord Lesions: Brown–Séquard
Syndrome
47
Damage to the CST
Ipsilateral UMN–type weakness.
Damage to the posterior columns
Ipsilateral loss of vibration and joint
position sense.
Interruption of the anterolateral systems
Contralateral loss of pain and
temperature sensation.
Ipsilateral segmental sign (Anterior horn)

48. Central Cord Syndrome
48
In small lesions, the crossing spinothalamic
fibers are affected:
Bilateral loss to pain and T° (in one or more
adjacent dermatomes)
The CST and STT are spared, sensation above
and below the lesion remains intact, leading to a
‘‘suspended’’ sensory level.

49. Posterior Cord Syndrome
49
Impairment in vibration and proprioception, sensory
ataxia with a ‘‘stomping’’ gait.
With larger lesions, lateral CST may be involved,
causing UMN–type weakness.
If the dorsal roots are involved (as in tabes dorsalis),
reflexes are absent.
Cervical involvement may cause Lhermitte sign, due
to aberrant mechanical activation of damaged
posterior columns with neck flexion.

50. Posterolateral Column Syndrome
50
Posterior column and the lateral CST are
involved.
Impairments of vibratory and proprioceptive
sensation and UMN weakness.
Patients develop a spastic and ataxic gait,
Reflexes may be increased, but may also be
depressed due to concomitant involvement
of peripheral nerves.
Autonomic disturbance may occur.

51. Anterior Cord Syndrome
51
Damage to the anterolateral pathways:
Loss of pain and T° below the lesion,
Damage to the anterior horn cells
LMN weakness at the level of the lesion.
With larger lesions, the lateral corticospinal tracts
may also be involved, causing UMN signs.
Autonomic disturbance
Common causes include anterior spinal artery
infarct, trauma, multiple sclerosis.

52. Anterior Horn Syndrome
Selective damage to anterior horn cells causes
a flaccid weakness with atrophy and
fasciculations with reduced reflexes.
No sensory involvement occurs.
Poliovirus is the common example of a disease
causing this syndrome.
Other non polio enteroviruses and flaviviruses
such as WNV and Japanese encephalitis virus
may also affect the anterior horn.

53. Extramedullary Vs Intramedullary
The differentiating features are only relative
and serve as clinical guides.
Intramedullary lesions produce poorly
localized burning pain and spare sensation in
the perineal and sacral areas.
Extramedullary lesions have prominent
radicular pain, and early sacral sensory loss
and spastic weakness in the legs.
Extramedullary lesions (extradural and
intradural).

54. 10/4/2022 54

55. 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.
 Many spinal cord diseases are reversible if recognized and treated at an
early stage; thus, they are among the most critical of neurologic
emergencies.
 Myelopathy still remains a clinical diagnosis.
 Investigations including neuroimaging and laboratory studies provide
supportive evidence

56. HISTORY
 AGE AND SEX
 Young age: Inherited disorders
 Old age: malignancies
 PAIN
 Radicular pain
 Funicular/ central pain
 Vertebral pain
 WEAKNESS OF ARM/LEG
 SENSORY SYMPTOMS
 Numbness, tingling
 Lhermitte's sign
 Uhthoff’s phenomena
56

57.  SPHINCTER
DISTURBANCES
 Early: TM
 Late: Neoplastic, Potts
 No involvement: Degenerative
e.g. HSP, Nutritional e.g.
SACD, lathyrism
 DURATION
 ACUTE: TM/ inflamatory,
Vascular, Trauma
 SUBACUTE (2-6wks)
Neoplastic, Pott’s
 CHRONIC: (>6wk) Neoplastic,
Degenerative
 History of
 Recent Fever, URTI, Vaccination
 Trauma
 Hx of surgery
 Cancer
 Cough, Fever, weight loss, Rx for
TB
 Nutritional history
 Family history
 Bleeding tendency/anticoagulant
use
 HIV
 HTN and DM
57

58. PE
 VITAL SIGNS
 HEENT: Rash, conjunctiva, stiff
neck
 LAP, Gland examinations
 Chest finding
 Abdominal findings: mass,
organomegaly, abdominal bruit
 Skin: vesicles, Rash
 MSK: deformity and tenderness,
Paraspinal mass
 Sphincters
 NS; complete motor , sensory ,
cortical dysfunctions
 Pupillary abnormality
 Visual acuity
 Quadriplegia, Paraplegia
 Beevor’s sign
 Ataxia

59. INVESTIGATIONS
 X-RAY SPINE:
 does not image the spinal
cord.
 Can show abnormalities in the
alignment of the vertebral
bodies
 Collapse or erosion of
vertebrae, herniated disc,
fracture, or dislocation of
vertebra etc.
 Allows for dynamic imaging
 MRI:
 Investigation of choice
 Can visualize nerve roots, lesions in
the spinal cord, and surrounding
bony/soft tissue abnormalities.
 Clinically localize the lesion and
image a focused region.
 Imaging of the entire spine is
appropriate for oncologic
surveillance and for screening for
compressive myelopathy.
59

60.  In standard sequences, as in the
brain, T1-weighted images produce
hyperintense signal for lipid and
blood products.
 T2-weighted images produce
hyperintense signal for CSF, edema,
and gliosis and are particularly
useful for evaluating the spinal cord
parenchyma.
 CT SCAN
 Provides cross-sectional views of
the bones but does not image
the cord or nerves.
 It is used in initial trauma surveys
and in patients with
contraindication to MRI.

61.  CSF examination:
 Inflammatory lesions,
cells and proteins are
increased.
 In malignancy, malignant
cells may be present.
 In MS, monoclonal IgG is
increases
 Others (VDRL, ACE..)
10/4/2022 61
 BLOOD Workup:
 CBC, PM
 ESR is raised in inflammatory cases.
 Serum vitamin B12, methylmalonic
acid,
 Serology for different viruses, syphilis
 Thyroid hormones
 Tumor markers
 Serum AQP- 4- autoantibodies (NMO-
IgG)
 ANA, APS Ab,....

62.  Etiologies of myelopathy include: (non traumatic)
 Inflamatory:- TM, Sarcoidosis, Paraneoplastic, SLE
 Infectious:- Epidural abscess, Viral myelitis, AIDS myelopathy, Syphilis,
TB, Parasite infections,
 Vascular:- Spinal cord infarction, Dural AV fistula, Intramedullary spinal AV
malformation
 Toxic/ Metabolic:- SCD, Cu deficienc, radiation, Lathyrism
 Neoplastic
 Hereditary-degenerative diseases:- ALS, HSP, Friedrich ataxia
10/4/2022 62

63. YES
No

65.  COMPRESSIVE
 Neoplasms
 Epidural abscess
 Epidural hemorrhage
 Cervical spondylosis
 Herniated disk
 Posttraumatic compression by
fractured or displaced vertebra
or hemorrhage
 NON COMPRESSIVE
 TM
 Autoimmune diseases, including
SLE, sarcoidosis
 Spinal cord infarction
 Infections (Primarily Viral)
 Demyelinating diseases, MS, NMO
 Degenerative diseases
 Toxic / Metabolic diseases

66. 1. Neoplastic Spinal Cord Compression
 Primary or metastatic tumors to
the spinal cord.
 Extramedullary
 Extradural
 Intradural
 Intramedullary
66

67. 1.1 EXTRADURAL
 Extradural spinal metastases are the most common type of spinal
metastases.
 Almost any malignant tumor can metastasize with breast, lung, prostate,
kidney, lymphoma, and myloma being particularly frequent.
 Extradural metastatic deposits typically occur in the thoracic spine (60%),
the lumbosacral and cervical (10%), and in multiple spinal regions (30%).
 Manifestation:
 The most common presentation is axial pain (b/c of direct invasion of the
tumor to vertebral body periosteum and surrounding soft tissue)
 Typically worsens with movement, coughing, or sneezing and
characteristically awakens pts at night. (distention of the epidural venous
plexus)

68.  The most dreaded complication is spinal cord compression:
 Weakness
 Sensory loss begins in the toes and usually ascends.
 Vibration and position sense is lost early
 Sphincter disturbance at presentation is less common
 Dx= If an epidural spinal metastasis is suspected, the entire spine should be
imaged with MRI (one-third of patients will have multifocal disease).
68

69. 69
Sagittal T1-weighted (A) and T2-weighted (B) MRI scans through the cervicothoracic
junction reveal an infiltrated and collapsed second thoracic vertebral body with posterior
displacement and compression of the upper thoracic spinal cord. The low-intensity bone

70.  Rx= Treatment is aimed at minimizing or reversing the neurologic
symptoms.
 Glucocorticoids to reduce cord edema,
 Local radiotherapy (initiated as early as possible) to the symptomatic
lesion, and
 Specific therapy for the underlying tumor.
 Glucocorticoids (dexamethasone, 10 mg IV loading) can be administered
before an imaging if there is clinical suspicion of cord compression and
continued at a lower dose (4 mg every 6 h orally) until definitive treatment.
 Indications for surgery
 Worsened cord compression despite radiotherapy
 When max dose of radiotherapy is reached
 Vertebral compression fracture or spinal instability
70

71. 1.2 INTRADURAL TUMORS
 Slow-growing and benign.
 Manifestations:-
 Radicular sensory symptoms followed
by an asymmetric, progressive SC
syndrome.
 Therapy is surgical resection.
 Metastasis can occur when there is high
systemic tumor burden.
 Symptoms are typically multifocal and
can be attributed to one or more of the
following compartments: cerebrum,
cranial nerves and brainstem, or spine.
71

72. 1.3 INTRAMEDULLARY TUMORS
 Uncommon.
 Manifestations:
 They present as central cord or
hemicord syndromes,
 Poorly localized burning pain in the
extremities and sparing of sacral
sensation.
 Often in the cervical region.
 Complete resection of an intramedullary
ependymoma is often possible with
microsurgical techniques.
 Intramedullary spinal cord metastases
are rare and only 0.5% of spinal
metastases.
72

73. 2. Spinal Epidural Abscess
 Most cases are due to S.aureus; GN bacilli, Streptococcus, anaerobes,
and fungi
 TB from an adjacent vertebral, an important cause in the developing
world.
 Risk factors include:
 Immunity (HIV, DM, renal failure, alcoholism, malignancy),
 IV drug abuse,
 Infections of the skin , vertebral osteomyelitis, decubitus ulcers, IE
 LP, epidural anesthesia or surgery.
 Frequently affects the thoracic or lumbar segments (any segment may
be affected)
73

74.  Manifestations:
 Symptoms result from mechanical compression and, in some cases,
ischemia.
 As the abscess expands, further spinal cord damage results from venous
congestion and thrombosis.
 Midline back or neck aching pain, fever, and progressive limb weakness.
 Fever is typically but not invariably present,
 Elevated WBC, ESR, and CRP.
 Blood culture (>50%),
 Aspiration of the abscess at surgery
 LP is required if encephalopathy or other clinical signs raise the question of
associated meningitis
74

75. 75
A. Sagittal T2-weighted free spin-echo MR sequence. A hypointense mass replaces the posterior
elements of C3 and extends epidurally to compress the spinal cord (arrows). B. Sagittal T1-weighted
image after contrast administration reveals a diffuse enhancement of the epidural process (arrows) with
extension into the epidural space

76.  Rx =
 Surgical management remains the treatment of choice unless the
abscess is limited in size and causes few or no neurologic signs.
 Broad-spectrum antibiotics (vancomycin, ceftriaxone, and
metronidazole) should be started empirically and then modified on the
basis of culture results;
 Medication is generally continued for 6–8 weeks.
 If surgery is contraindicated or if there is a fixed paraplegia or
quadriplegia that is unlikely to improve, long-term systemic and oral
antibiotics can be used
 With prompt diagnosis and treatment, up to 2/3rd of patients experience
significant recovery
76

77. SPONDYLITIS (POTTs DISEASE)
 The most common form of skeletal TB , comprises approximately half of
musculoskeletal TB cases.
 Leading cause of paraplegia in Africa and is the most common cause in
childhood, adolescence and in young adults.
 Most commonly affects the lower thoracic and upper lumbar region;
 Infection generally begins with inflammation of the anterior aspect of the
intervertebral joints; typically it spreads behind the anterior ligament to
involve the adjacent vertebral body.
 Once two adjacent vertebrae are involved, infection enters the adjoining
intervertebral disc space.
77

78.  Eventually the avascular disc tissue dies; there is vertebral narrowing and
subsequent vertebral collapse.
 Gibbus deformity, a form of structural kyphosis, distorts spinal canal
anatomy.
 The spinal cord is then at risk of compression
 Manifestations:
 The most common symptom is local pain, which increases in severity over
weeks to months, sometimes in association with muscle spasm and
rigidity.
 In some cases a characteristic erect posture and 'aldermanic' gait may be
observed, in which the patient walks with short deliberate steps to avoid
jarring of the spine.
 Constitutional symptoms such as fever and weight loss (present in less
than 40%) 78

79. Treatement
 Anti TB
 Surgery- Indication;
 Advanced neurological deficits
 Worsening neurological deficits progressing while on appropriate
therapy
 Kyphosis >40 degrees at the time of presentation
 Patients with chest wall cold abscess
Prognosis
Vary, but functional recovery rates as high as 90% have been reported
 Thoracic lesions with severe neurological deficit show the least
improvement whereas lumbar disease has the best outcome.
79

80. 1. Transverse Myelitis (TM)
 Segmental spinal cord injury caused by acute inflammation.
 TM can be:
 Idiopathic ATM
 Demyelinating TM (MS, NMO, ADEM)
 TM associated with infection/ Post infection
 TM associated with Systemic Autoimmune Disease (SLE, APS, RA,
Sjogren’s syndrome, Scleroderma, Ankylosing spondylitis)
 Most cases are idiopathic and presumably result from autoimmune process.
 Usually in the thoracic cord
 Typically the inflammation is bilateral
10/4/2022 80

81.  Manifestations
 Pain and tingling
 Tight banding or girdle-like sensation around the trunk
 Almost all patients develop leg/ arm weakness of varying severity
 Diminished sensation,
 Bowel and bladder dysfunction, reflective of autonomic involvement, also
occur.
10/4/2022 81

82.  Dx=
 It is a clinical diagnosis.
 MRI shows gadolinium-enhancing signal abnormality, usually extending
over one or more cord segments, the cord often appears swollen at these
levels.
 CSF is abnormal in half of patients
○ Elevated protein (usually100 -120)
○ Moderate lymphocytosis (<100 /mm3)
○ Glucose levels are normal.
○ Oligoclonal bands are usually not present in isolated TM, and when
present suggest a higher risk of subsequent MS.
10/4/2022 82

83.  Rx=
 Should be started before investigations have been completed (MRI and
CSF).
 IV steroids are often instituted
 Methylprednisolone 1000 mg/d or dexamethasone (200 mg/d) for 5
consecutive days.
 In some cases, this is followed by an oral prednisone extension as part of a
maintenance therapy regimen (eg, in NMOSD or neurosarcoidosis).
 Plasma exchange:
 Severe myelopathies that progress or fail to improve despite IV
methylprednisolone.
 In some refractory patients, a trial of IVIG (NMOSD)
 Subsequent treatment decisions after acute immunomodulatory therapy depend
on the suspected etiology of the myelopathy.
10/4/2022 83

84. PROGNOSIS
 Most have at least a partial recovery, which usually begins within 1-3 months
 Significant recovery is unlikely if there is no improve by 3rd month
 Rapid onset complete paraplegia & spinal shock are associated with poorer
outcomes
 TM is generally a monophasic illness (75-90%)
10/4/2022 84

85.  A. Myelitis in SLE
 Occurs in 1% of patients with SLE
 May appear as the presenting manifestation of SLE.
 Thought to be due to an arteritis, with resultant ischemic necrosis
 Antiphospholipid antibodies are present in 2/3rd of patients
 CSF is normal or mild lymphocytosis; oligoclonal bands are a variable
finding.
 Rx= Possible responses to glucocorticoids and/or cyclophosphamide
 Recurrence of myelopathy in particular within the 1st year is common
10/4/2022 85

86.  A. Sarcoid myelopathy
 Granulomatous inflammation that affects the spinal cord
 Lesion can be extra or intramedullary
 May present as a slowly progressive or relapsing disorder.
 Dx:
 MRI
 CSF profile consists of a variable lymphocytosis and mildly elevated
protein level; in a minority of cases oligoclonal bands are found
 CXR and CT to assess pulmonary involvement; and mediastinal
lymphadenopathy
 A slit-lamp examination of the eye to search for uveitis;
 Serum or CSF ACE; present in only a minority of cases,
10/4/2022 86

87.  MRI
 Edematous swelling of the
spinal cord that may mimic
tumor;
 Thre is almost always
gadolinium enhancement of
active lesions and in some
cases nodular enhancement of
the adjacent surface of the
cord;
 Lesions may be single or
multiple.
87

88.  Rx=
 Prednisone for 8 to 12 months (60 mg/d for several months, slow taper).
 Some individuals will enter a long-term remission, but clinical relapse is an
indication for preventive therapy.
 Immunosuppressive drugs such as methotrexate, MMF,
cyclophosphamide, azathioprine, and others have been associated with
good
outcomes in uncontrolled studies.
 Infliximab is a monoclonal antibody and appears beneficial in aggressive
or treatment-resistant disease
10/4/2022 88

89. C. Myelitis in Multiple Sclerosis
 Is a chronic demyelinating inflammatory CNS disease.
 MS may present with acute myelitis, particularly in Asian / African
ancestry
 It is among the most common causes of a partial syndrome
 Dx=
 Oligoclonal bands in CSF, suggestive lesions on brain MRI, short-segment
cord lesion located peripherally, history of prior neurologic deficits
 No adequate trials of therapy for MS-associated transverse myelitis.
 IV methylprednisolone followed by oral prednisone (1 mg/kg/ day for several
weeks, then gradual taper) has been used as initial treatment.
10/4/2022 89

90. D. Myelitis in Neuromyelitis Optica (NMO)
 NMO is an immune-mediated demyelinating disorder consisting of a
severe myelopathy that is typically longitudinally extensive.
 NMO is associated with optic neuritis that is often bilateral
 Affected individuals are usually female, and often of Asian ancestry.
 Dx=
 AQP-4 IgG in serum, long-segment lesion in spinal cord located centrally,
history of optic neuritis or brainstem syndrome
10/4/2022 90

91.  Rx=
 Usually treated with rituximab, mycophenolate mofetil, or azathioprine
 AQP-4 positive individuals are at high risk for relapse ( 60% in the first
post attack year), so preventive treatment is recommended.
 In breakthrough attacks switch to another drug or combine
 AQP4-IgG seronegative may undergo a trial of treatment discontinuation
after several years of clinical remission.
10/4/2022 91

92. F. Viral ATM (Viral Myelitis)
 Many viruses have been associated with an acute myelitis that is
infectious in nature rather than postinfectious.
 HZ is the best characterized viral myelitis, but HSV types 1 and 2, EBV,
CMV, and rabies virus are other well-described causes
 HSV-2 causes recurrent sacral cauda equina neuritis in association with
outbreaks of genital herpes mimicking MS.
 Poliomyelitis is the prototypic viral myelitis, but it is more or less restricted
to the gray matter of the cord.
10/4/2022 92

93.  In cases of suspected viral myelitis, start specific therapy pending laboratory
confirmation:
 HZ, HSV, and EBV: IV Acyclovir 10mg/kg/dose for 10–14 days
 CMV: Ganciclovir (5 mg/kg IV bid induction, then daily as maintenance )
 Longer duration in immunocompromised
 With adjuvant steroid
10/4/2022 93

94. G. Schistosomiasis
 Causes myelitis in endemic areas
 Mostly by S. mansoni and occasionally with S. haematobium.
 The lower thoracic region of the spinal cord is most frequently
involved
 The myelopathy is b/c of marked acute inflammatory
response to schistosome eggs being deposited in and
around the spinal cord.
 The time between exposure and onset of the paraplegia is
usually weeks to months and rarely years.
94

95.  Dx=
 Considered in patients with an acute onset paraplegia who is living in or has
come from an endemic area.
 Diagnostic studies include serologic testing and stool studies/ rectal snip,
although histopathologic confirmation is required for definitive diagnosis.
 CSF examination may show lymphocytes and occasionally eosinophils as well as
an elevation in protein.
 MRI demonstrates signal change and swelling within the cord.
 Rx=
 Praziquantel 40mg/kg divided in 3 doses for 1 day, prednisone 60–80 mg/d, taper
over 6 months.
 Surgical debridement may be necessary, in the event of granuloma formation or
if any medullary compression is present.
 10% mortality, 30% remaining permanently paraplegic and 60% showing moderate
to good recovery.
95

96. 2. Spinal Cord Infarction
 Spinal cord infarction accounts about 1% to 2% of all ischemic
strokes and 5% to 8% of all acute myelopathies.
 It can occur at any level; however, mostly in a region of marginal blood flow
 The lower thoracic segment and conus medullaris are most frequently
involved.
 Causes:
 Hypotension or cross-clamping of the aorta
 Surgical procedures and pathologies affecting the aorta (aortic
atherosclerosis, dissecting aortic aneurysm) vertebral artery occlusion
 Cardiogenic emboli, vasculitis
10/4/2022 96

97.  Manifestations:
 Sudden onset but more typically is progressive over minutes or a few
hours, unlike stroke in the cerebral hemispheres.
 Paraplegia or quadriplegia,
 Dissociated sensory loss affecting pain and temperature but sparing
vibration and position, and loss of sphincter control (“anterior cord
syndrome”).
 Sharp midline back pain localized to the area of ischemia is frequent.
 Less common is infarction in the territory of the posterior spinal arteries,
resulting in loss of posterior column function either on one side or bilaterally.
97

98.  Dx= Spinal cord infarction is a clinical
diagnosis; however, imaging can be
useful to confirm the diagnosis and
rule out other possibilities.
 MRI can show longitudinal “pencil-
like” T2 hyperintensities on sagittal
sequences with associated spinal
cord cytotoxic edema.
 Gadolinium enhancement typically
does not occur acutely, and its
presence should evoke suspicion
for other etiologies.
10/4/2022 98

99.  Rx=
 Generally supportive and focused on the underlying pathology and/or
secondary stroke prevention.
 Improve spinal cord perfusion through BP augmentation and reducing
CSF counter pressure through spinal fluid drainage.
 BP augmentation is initiated with volume replacement followed quickly by
vasopressor support that is titrated to symptom improvement or adverse
effects.
 Placement of a lumbar drain can be considered with a goal ICP of 8 to 12
mm Hg.
10/4/2022 99

100. CHRONIC COMPRESSIVE MYELOPATIES
SPONDYLITIS MYELOPATHY
 One of the most common causes of chronic compression and gait difficulty in
the elderly.
 Cervical spondylosis refers to degenerative changes of the spine that can
produce canal stenosis or neural foraminal stenosis.
 Cervical spondylosis results from damage to disks, vertebral joints, and
hypertrophy of spinal ligaments.

101.  Manifestations:
 Symptoms present insidiously, with gait impairment often early (spastic,
scissoring).
 Neck and shoulder pain with stiffness
 Radicular arm pain, most often in a C5 or C6 distribution.
 Later, weakness
 Vibratory sense is diminished in the legs, there is a Romberg sign.
 Lhermitte sign
 Urinary urgency or incontinence occurs in advanced cases.
10/4/2022 101

102.  Dx
 Clinical presentation
 MRI
 AP canal diameter < 10 mm suggests
probable cervical spondylotic
myelopathy, and a diameter > 16 mm
renders it unlikely.
 Multilevel involvement,
102

103.  Rx=
 Cervical soft collar in milder cases with pain control, but the likelihood of
progression is high, estimated at 8% over 1 year.
 Definitive therapy is surgical decompression, with resection of the
protruded disk and bony material.
 Surgical intervention is often warranted in:
 Demonstrable weakness on examination,
 Progression of symptoms,
 Pain refractory to multimodality treatment,
 Concordant spondylotic findings on imaging, and patient fitness for
surgery.
10/4/2022 103

104. SCD (Vitamin B12 Deficiency)
 Deficiency in vitamin B12 leads to degeneration of the dorsal and lateral
columns
 Optic atrophy and other cognitive changes may be prominent in
advanced cases
 Causes:
 Malabsorption due to chronic gastrointestinal disease, gastric surgery,
 Pernicious anemia,
 Drugs such as histamine 2 receptor antagonists and metformin,
 Nitrous oxide abuse, and
 Parasitic infestation ( Diphyllobothrium latum)
10/4/2022 104

105.  Manifestation:
 Symptoms of gait and balance difficulties are common along with distal
sensory loss and paresthesia.
 Loss of vibration and position sensation, and a progressive spastic
weakness.
 Dx=
 CBC may show evidence of a megaloblastic anemia with increased MCV.
 Peripheral blood smears may reveal hypersegmented PMN.
 Low serum cobalamin levels confirms the diagnosis;
 If borderline or normal, measure homocysteine and methylmalonic acid
levels
10/4/2022 105

106.  MRI Findings:
 T2 hyperintensity involving the posterior and
lateral columns, extending over several
segments
 Rx=
 Urgent replacement of vitamin B12.
 1000 mcg/d of cobalamin IM for 2 weeks,
followed by 1000 mcg monthly.
 Treatment is lifelong regardless of parenteral
or oral treatment.
 Some improvement of neurologic symptoms
can occur in the first 6 months following
initiation of therapy.
 Significant improvement, may be delayed and is
often incomplete in patients with severe
symptoms
10/4/2022 106

107. 3. Tabes Dorsalis
 Tabes dorsalis refers to a late (tertiary) manifestation of neurosyphilis
 Occurs decades after primary infection
 It is very rare currently because syphilis is usually treated early.
 The posterior columns are selectively damaged,
 Manifestations:
 Lancinating pains, primarily in the legs or back
 Progressive gait abnormalities. (stomping)
 Patients often fall forward following eye closure ( positive “sink” sign).
 The affected limbs are hypotonic, but not weak.
10/4/2022 107

108.  CSF Findings
 Normal or may show
 A mild lymphocytosis with 10 to 50 cells/microL and
 Protein concentrations of 45 to 75 mg/dL
 VDRL (negative in 25 % of cases).
 Rx=
 Parenteral penicillin G for 10 to 14 days
 Systemic steroids have not been found to be effective in neurosyphilis but
have been used in some myelitis cases for cord edema
 Recovery is often suboptimal, particularly in cases with cord ischemia.
108

109. 4. Retrovirus-Associated Myelopathies
 VACUOLAR MYELOPATHY
 Vacuolar myelopathy is the classic spinal cord pathology associated with
AIDS
 Characterized by vacuolar degeneration of the posterior and lateral tracts
 Presents late in the course of HIV disease.
 It is found in up to half of patients with AIDS at autopsy.
 The thoracic cord is preferentially involved.
 Manifestation:
 Slowly progressive spastic paraparesis with brisk reflexes, bilateral
extensor plantar responses,
 Sensory ataxia with impaired vibration and position sense,
 Occasional bladder incontinence.
10/4/2022 109

110.  Patients may have associated dementia (AIDS dementia complex) (>50%)
 Cobalamin and folate levels are usually normal.
 There may be increased CSF protein content with pleocytosis.
 MRI of the spine is usually normal.
 Rx= antiretroviral therapy can lead to improvement of symptoms.
10/4/2022 110

111. Tropical Myelopathies
1.NEUROLATHYRISM
 Associated with prolonged consumption of chickling pea (Lathyrus sativus)
(amino acid b-N- oxalyl amino-L-alanine)
 Endemic in parts of Bangladesh, India, and Ethiopia.
 Causes an irreversible but non progressive spastic paraplegia associated
with degenerative changes in the spinal cord.
 Pathologic studies have demonstrated a loss of myelinated fibers in the
corticospinal and spinocerebellar tracts.
 On neurologic examination, an upper motor neuron pattern of weakness with
spastic gait
 Sensory loss and autonomic symptoms are not uncommon.
10/4/2022 111

112.  MRI studies are negative.
 Rx is supportive with
measures to reduce
spasticity such as physical
therapy, medication, and
assistive devices.
 Prevention is possible by
proper preparation of the
grass pea and combining it
with other cereals.
10/4/2022 112

113. 2. KONZO
 A distinct form of tropical myeloneuropathy caused by consumption of
poorly processed cassava root that contains cyanide.
 It occurs mainly as epidemics in exclusively cassava growing areas of the
east, central and western Africa.
 Symptom onset is abrupt with initial symptoms of muscle cramps
and leg weakness.
 An UMN pattern of injury is seen resulting in a spastic
paraparesis or quadriparesis.
 The condition is irreversible and non progressive.
 Optic neuropathy occurs in about one-half of the patients.
 Sensory symptoms and autonomic symptoms do not usually
occur.
10/4/2022 113

114.  Dx=
 History of exposure
 measurement of
thiocyanate levels
 MRI is typically negative
114

115. Hematomyelia
 Hemorrhage into the substance of the spinal cord is a rare result of trauma,
intraparenchymal vascular malformation, vasculitis due to polyarteritis
nodosa or SLE, bleeding disorders, or a spinal cord neoplasm.
 Presents as an acute painful transverse myelopathy
 With large lesions, extension into the subarachnoid space results in
subarachnoid hemorrhage.
 Diagnosis is by MRI or CT.
 Therapy is supportive, and surgical intervention is generally not useful
 An exception is hematomyelia due to an underlying vascular malformation,
for which selective spinal angiography may be indicated, followed by surgery
to evacuate the clot and remove the underlying vascular lesion
10/4/2022 115

116. Vascular Malformations of the Cord & Dura
 Comprises ~4% of all mass lesions of the cord and overlying dura, are
treatable causes of progressive myelopathy.
 Vascular malformations of the spinal cord include: AVMs, AVFs, dural AVFs,
epidural vascular malformations, cavernous malformations, and complex
vascular malformations (metameric angiomatosis or Cobb syndrome,
disseminated angiomatosis or Osler–Weber–Rendu syndrome, Klippel–
Trenaunay–Weber, and Parkes Weber syndrome).
 Spinal dural AVFs account for 80% of spinal cord vascular malformations.
 Most common are fistulas located within the dura or posteriorly along the
surface of the cord.
 Most dural AV fistulas are located at or below the midthoracic level, usually
consisting of a direct connection between a radicular feeding artery in the
nerve root sleeve with dural veins.
10/4/2022 116

117.  Spinal cord vascular malformations may present with myelopathy, radiculopathy, or
localized back pain.
 Symptoms may result from hemorrhage, ischemia, venous hypertension, or mass
effect.
 The typical presentation is a middle-aged man with a progressive myelopathy that
worsens slowly or intermittently and may have periods of remission, sometimes
mimicking MS.
 Acute deterioration due to hemorrhage into the spinal cord (hematomyelia) or
subarachnoid space may also occur but is rare.
 In many cases, progression results from local ischemia and edema due to venous
congestion.
 Most patients have incomplete sensory, motor, and bladder disturbances.
 The motor disorder may predominate and produce a mixture of upper and restricted
lower motor neuron signs, simulating amyotrophic lateral sclerosis (ALS).
 Pain over the dorsal spine, dysesthesias, or radicular pain may be present.
 Other symptoms suggestive of AV malformation (AVM) or dural fistula include
intermittent claudication; symptoms that change with posture, exertion, Valsalva
maneuver, or menses; and fever.
117

118.  Spinal bruits are infrequent but may be sought at rest and after exercise in
suspected cases.
 A vascular nevus on the overlying skin may indicate an underlying vascular
malformation as occurs with Klippel-Trenaunay-Weber syndrome.
 MR angiography and CT angiography can detect the draining vessels of
many AVMs.
 Definitive diagnosis requires selective spinal angiography, which defines the
feeding vessels and the extent of the malformation.
 Treatment is tailored to the anatomy and location of the lesion, and generally
consists of microsurgical resection, endovascular embolization of the major
feeding vessels, or a combination of the two approaches.
118

119. 119
abnormally high signal
intensity is noted in the central
aspect of the spinal cord
(arrowheads). Numerous
punctate flow voids indent the
dorsal and ventral spinal cord
(arrow). These represent the
abnormally dilated venous
plexus supplied by a dural
arteriovenous fistula

120. Syringomyelia
 Is a fluid-filled, gliosis-lined cavity within the spinal cord
 Symptoms begin insidiously in adolescence or early adulthood, and may
undergo spontaneous arrest for several years.
 >50% of all cases are associated with Chiari type 1 malformations in which
the cerebellar tonsils protrude through the foramen magnum.
 The pathophysiology of syrinx expansion is controversial, but some
interference with the normal flow of CSF seems likely, perhaps by the Chiari
malformation.
 Acquired cavitations of the cord in areas of necrosis are also termed syrinx
cavities; these follow trauma, myelitis, necrotic spinal cord tumors, and
chronic arachnoiditis due to tuberculosis and other etiologies.
10/4/2022 120

121.  A syrinx can be asymptomatic and discovered incidentally on spinal cord
imaging.
 The presentation is a central cord syndrome consisting of a regional
dissociated sensory loss (loss of pain and temperature sensation) and
areflexic weakness in the upper limbs.
 As the cavity enlarges and compresses the long tracts, spasticity and
weakness of the legs, bladder and bowel dysfunction, and a Horner’s
syndrome appear.
 Some patients develop facial numbness and sensory loss from damage to
the descending tract of the trigeminal nerve (C2 level or above).
 Extension of the syrinx into the medulla, syringobulbia, causes palatal or
vocal cord paralysis, dysarthria, horizontal or vertical nystagmus, episodic
dizziness, and tongue weakness.
121

122. 122
MRI accurately identifies syrinx cavities and their
associated spinal cord enlargement.
MRI scans of the brain and the entire spinal cord
should be obtained to delineate the full longitudinal
extent of the syrinx, assess posterior fossa
structures for the Chiari malformation, and
determine whether hydrocephalus is present.

123.  Treatment of syringomyelia is generally unsatisfactory.
 The Chiari tonsillar herniation may be decompressed, generally by
suboccipital craniectomy, upper cervical laminectomy, and placement of a
dural graft.
 Surgery may stabilize the neurologic deficit, and some patients improve.
 Patients with few symptoms and signs from the syrinx do not require surgery
and are followed by serial clinical and imaging examinations.
123

124. Rehabilitation
 SKIN CARE:
 Change posture every 2-4 hourly to avoid bed sores.
 Daily skin exams;
 Keep skin dry and clean.
 The use of special mattresses, and cushioning of areas where pressure
sores often develop, such as the sacral prominence and heels.
 PAIN
 Despite the loss of sensory function, many patients with spinal cord injury
experience chronic pain sufficient to diminish their quality of life.
 Rx= TCA, anticonvulsants, SSRI, NSAIDs, or Narcotics.
10/4/2022 124

125.  DVT PROPHYLAXIS
 Use of calf-compression devices
 Anticoagulation with LMWH is recommended
○ Prophylaxis up to 3 months post injury or until d/c from rehab;
10/4/2022 125

126.  BLADDER CARE
 Detrusor spasticity is treated with anticholinergic drugs (oxybutynin, 2.5–
5 mg qid) or TCA with anticholinergic properties (imipramine, 25–200
mg/d).
 Failure of the sphincter to relax during bladder emptying (urinary
dyssynergia):
○ α-adrenergic blocking agents (terazosin),
○ Intermittent catheterization, or, if that is not feasible, by use of a condom
catheter in men or a permanent indwelling catheter.
 Surgical options (creation of an artificial bladder by isolating a segment of
intestine that can be catheterized intermittently or can drain continuously
to an external appliance).
126

127.  BOWEL CARE:
 Constipation
 High-fiber diet, increased fluid intake (at least 2 L daily),
 Stimulant or osmotic laxatives ( bisacodyl).
 Digital stimulation of the anal canal serves to manually disimpact
 Abdominal massage may be helpful.
 For refractory cases: colostomy, neuromodulation.
 Fecal incontinence
 Mild and infrequent: loperamide, codeine phosphate.
 Anal plugs or pads may be needed
 Severe cases: surgical intervention
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128.  SPASTICITY
 Stretching exercises to maintain mobility of joints.
 Drug treatment is effective but may result in reduced function, as some
patients depend on spasticity as an aid to stand, or walk.
○ Baclofen 5mg bid is effective
○ Diazepam useful for leg spasms that interrupt sleep (2–4 mg at
bedtime).
○ Tizanidine (2–8 mg tid), an α2 adrenergic agonist
 For non ambulatory patients, the direct muscle inhibitor dantrolene (25–
100mg qid)
 In refractory cases, intrathecal baclofen, botulinum toxin injections, or dorsal
rhizotomy may be required to control spasticity.
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129.  DYSAUTONOMIA:
 A paroxysmal autonomic hyperreflexia may occur following lesions above
the major splanchnic sympathetic outflow at T6.
 Headache, flushing, and diaphoresis above the level of the lesion, as well
as hypertension with bradycardia or tachycardia, are the major symptoms.
 Trigger by a noxious stimulus—bladder or bowel distention, UTI….
 Rx=
 Remove the offending stimuli;
 Ganglionic blocking agents (mecamylamine, 2.5–5 mg) or
 Short-acting antihypertensive drugs
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132. References
 CONTINUUM SPINAL CORD DISORDERS 2018
 Up-to-date 2018
 ADAMS AND VICTOR‘S 11TH ED.
 BRADLEY‘S NEUROLOGY 7TH ED.
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