The document provides information on diseases of the spinal cord. It begins by describing the anatomy of the spinal cord and its white and gray matter. It then discusses different types of compressive and non-compressive myelopathies, including tumors, abscesses, hemorrhages, spondylosis, herniated discs, transverse myelitis, multiple sclerosis, Guillain-Barré syndrome, bacterial and tuberculous meningitis, and leprosy. For each condition, it describes causes, symptoms, imaging findings, diagnostic criteria and complications. Approaches to patients with spinal cord diseases focus on distinguishing compressive from non-compressive etiologies through history, exam and imaging.

1. Disease of the Spinal Cord
Presenter: Dr Sa’ad Saleban(Im resident )
MAY , 18 ,2023

2. Spinal cord
• 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 (18 in.)
• The white matter tracts containing ascending sensory and
descending motor pathways are located peripherally,
whereas nerve cell bodies are clustered in an inner region of
gray matter shaped like a four-leaf clover that surrounds the
central canal (anatomically an extension of the fourth
ventricle).
• The spinal cord has 31 segments, each defined by an exiting
ventral motor root and entering dorsal sensory root.

3. Introduction
 Diseases of the SC are frequently devastating
 The presence of a horizontally defined level below which
sensory, motor, and autonomic function is impaired is a
hallmark of spinal cord disease
 Many spinal cord diseases are reversible if recognized and
treated at an early stage.
most critical of neurologic emergencies
 The first priority is to exclude a treatable compression of the
cord by a mass

4. Approach to the Patient

Compressive myelopathy

Causes warning signs that precede
the dev’t of weakness:
Spinal subluxation and hemorrhage
may not have warning symptoms

Noncompressive myelopathy
produce myelopathy without antecedent
symptoms
Rapidly progressive
Maximum deficit in hrs to days
neck or back pain
 bladder disturbances
 sensory symptoms

5. Compressive Myelopathies
 Epidural, intradural, or intramedullary neoplasm
 Epidural abscess
 Epidural hemorrhage
 Cervical spondylosis
 Herniated disk
 Posttraumatic compression by fractured or displaced
vertebra
hemorrhage

6. Neoplastic, Epidural
 Commonest, due to metastases to the adjacent vertebral column.
 Breast, lung, prostate, kidney, lymphoma, and myeloma commoner origin.
 Involvement:-
 Prostate & Ovarian metastasis involves, the sacral and lumbar vertebrae, b/c spread
through Batson’s plexus, a network of veins along the anterior epidural space.

Thoracic ……….. 60%

Lumbosacral …… 30%
cervical spine ……10%

7. Imaging
Infiltrated & collapsed T2 vertebral body with posterior displacement and compression of
the upper thoracic spinal cord.
The low-intensity bone marrow signal in A signifies replacement by tumor.
T2
T1

8. Tuberculosis
Spondylitis (Pott's disease):-
 anterior intervertebral joints……. spreads behind the anterior
ligament to involve the adjacent vertebral body.
 the avascular disc tissue dies; there is vertebral narrowing and
subsequent vertebral collapse
 local pain, which increases in severity over weeks to months
 Bone necrosis and collapse of a lower thoracic or upper lumbar
vertebra resulting in a characteristic angulated kyphotic
deformity called GIBUS
 Paraparesis .

9. 
A gibbous deformity has occurred as a consequence of collapse of the 8th, 9th, and
10th thoracic vertebral bodies with sparing of the posterior vertebral elements.
The paravertebral abscess is extensive projecting laterally and anteriorly (arrows).

Bony debris is present in the abscess.

10. NONCOMPRESSIVE MYELOPATHIES
 The most frequent causes of non compressive acute transverse
myelopathy are:-
 spinal cord infarction
 systemic inflammatory disorders
 Demyelinating diseases, including MS; NMO
 Post infectious or idiopathic TM, immune condition related to
acute and infectious (primarily viral) causes.
 After spinal cord compression is excluded, LP and a search for
underlying systemic disease is important.

11. Transverse myelitis
INTRODUCTION
Acute transverse myelitis (TM) is a rare, acquired neuro-immune
spinal cord disorder that can present with the rapid onset of
weakness, sensory alterations, and bowel or bladder dysfunction.
TM can occur as an independent entity, usually as a postinfectious
complication, but TM also exists on a continuum of neuro-
inflammatory disorders that includes acute disseminated
encephalomyelitis, multiple sclerosis, myelin oligodendrocyte
glycoprotein antibody disease (MOGAD) ,
neuromyelitis optica spectrum disorder (NMOSD), and acute flaccid
myelitis (AFM)

12. Etiology
Immunopathogenesis
Traditionally the majority of TM cases were thought to be
characterized by perivascular infiltration by monocytes and
lymphocytes in the lesion , Axonal degeneration was also
reported .
Pathologic heterogeneity and the involvement of both gray
and white matter suggest that TM is not a pure
demyelinating disorder but rather a mixed inflammatory
disorder that affects neurons, axons, and oligodendrocytes
and myelin.

13. Inflammatory & Immune Myelopathies
 Includes:-
 25% cases of myelitis , no underlying cause can be identified.
 Some will later manifest additional symptoms of an immune-
mediated disease.
 Recurrent episodes of myelitis are usually due to one of the
immune-mediated diseases or to infection with HSV-2.

Demyelinating conditions MS, NMO

Post infectious myelitis
Sarcoidosis and systemic autoimmune disease

14. MULTIPLE SCLEROSIS
 May Present with acute myelitis, particularly in individuals of Asian/ African ancestry.
 In Caucasians, rarely cause a transverse myelopathy (i.e., attacks of bilateral sensory
disturbances, unilateral or bilateral weakness, and bladder or bowel symptoms), but it
is among the most common causes of a partial cord syndrome.
MRI
 Mild swelling of the cord
 Diffuse or multifocal “shoddy” areas of abnormal
signal on T2-weighted sequences.
CE, disruption of BBB associated with inflammation.
Demonstrates a fusiform high-signal-intensity lesion in the mid thoracic SC
T2WI fast spin echo

15. Guillain-Barré syndrome
INTRODUCTION
The acute immune-mediated polyneuropathies are classified under
the eponym Guillain-Barré syndrome (GBS) ,
GBS is one of the most common causes of acute, acquired
weakness and is often provoked by a preceding infection. GBS may
be complicated in some cases by respiratory failure or autonomic
dysfunction.
PATHOGENESIS
The acute polyneuropathy of GBS is often triggered when an
immune response to an antecedent infection or other event cross-
reacts with shared epitopes on peripheral nerve (molecular
mimicry) All myelinated nerves (motor, sensory, cranial,
sympathetic) can be affected.
 Infection with C. jejuni is the most common antecedent in GBS
and a leading cause of acute gastroenteritis

16. CLINICAL FEATURES
The typical clinical features of GBS include a progressive and
symmetric muscle weakness and absent or depressed deep tendon
reflexes. Patients may also have sensory symptoms and
dysautonomia.
GBS symptoms typically progress over a period of two weeks. By
four weeks after onset, more than 90 percent of patients have
reached the nadir of the disease.
Common variant forms include.
 Acute inflammatory demyelinating polyneuropathy
 Acute motor axonal neuropathy (AMAN)
 Acute motor and sensory axonal neuropathy (AMSAN)
 Miller Fisher syndrome (MFS)
 Bickerstaff brainstem encephalitis (BBE)

17. DIAGNOSTIC
The clinical diagnosis of GBS is supported by results of diagnostic
testing such as cerebrospinal fluid (CSF) and Electrodiagnostic
studies consist of nerve conduction studies (NCS) and
electromyography (EMG) and are performed in most patients to
support the diagnosis of GBS as well as to provide prognostic
information .
Diagnostic criteria — Diagnostic criteria for GBS
Required features include:
Progressive weakness of the arms and/or legs, ranging from
minimal weakness of the legs to total paralysis of all four limbs,
and including the trunk, bulbar and facial muscles, and external
ophthalmoplegia.
Areflexia or decreased deep tendon reflexes in weak limbs.

18. Bacterial meningitis
Meningitis is an inflammatory disease of the
leptomeninges, the tissues surrounding the brain
and spinal cord, and is characterized by an
abnormal number of white blood cells (WBCs) in
the cerebrospinal fluid (CSF) in the majority of
patients .
The meninges consist of three parts:
the pia, arachnoid, and dura maters. Bacterial
meningitis reflects infection of the arachnoid mater
and the CSF in both the subarachnoid space and
the cerebral ventricles

19. Etiology
Bacterial meningitis can be community acquired or health care
associated.
●The major causes of community-acquired bacterial meningitis
in adults in developed countries are Streptococcus
pneumoniae, Neisseria meningitidis.
●The major causes of health care-associated ventriculitis and
meningitis are different (usually staphylococci and aerobic
gram-negative bacilli) and occur more commonly after
neurosurgical procedures (eg, post-craniotomy,
ventriculoperitoneal shunts, lumbar shunts, external
ventricular drains or following head trauma such as basilar
skull fracture with or without clinical evidence of leak of
cerebrospinal fluid

20. CLINICAL FEATURES
 The classic triad of acute bacterial meningitis, consists of fever,
nuchal rigidity, and a change in mental status, usually of sudden
onset , Older patients (age >60 years) more commonly present
with the triad than younger patients .
The most common clinical features include.
severe headache , fever greater than 38°C , stiff neck, a Glasgow
Coma scale <14 and nausea .
almost all patients (95 percent) presented with at least two of four
symptoms (ie, headache, fever, stiff neck, and altered mental status) .
The absence of all of these findings essentially excludes the presence
of bacterial meningitis

21. DIAGNOSTIC
Cerebrospinal fluid analysis
CSF should be sent for:
•Cell count and differential
•Glucose concentration
•Protein concentration
•Gram stain and bacterial culture
•Other appropriate tests (eg, rapid tests, polymerase chain
reaction .

22. Tuberculous meningitis
Forms of central nervous system (CNS) infection
due to Mycobacterium tuberculosis include
meningitis, tuberculoma, and spinal arachnoiditis.
Tuberculous meningitis develops most commonly
as a complication of progressive primary infection
in infants and young children, and from chronic
reactivation bacillemia in adults with immune
deficiency caused by aging, alcoholism,
malnutrition, malignancy, human
immunodeficiency virus (HIV) infection

23. Signs and symptom
Typical presentation — Patients with tuberculous meningitis
commonly present with headache, fever, vomiting, and altered
sensorium; these symptoms are also frequently observed with
bacterial meningitis.
Features that may help distinguish tuberculous meningitis from
bacterial meningitis include:
●Subacute presentation; the time between the one to three
weeks in 57 percent.
 Presence of neurologic symptoms.
 Presence of cranial nerve palsies (most frequently involving
cranial nerve II and VI)

24. DIAGNOSIS
The diagnosis may be definitively established in the setting
of cerebrospinal fluid (CSF) with positive smear for acid-fast
bacilli (AFB), CSF culture positive for M. tuberculosis, or CSF
with positive nucleic acid amplification test (NAAT)
However, definitive diagnosis can be challenging, given
suboptimal sensitivity and specificity of diagnostic tests .
A presumptive diagnosis of tuberculous meningitis may be
made in the setting of relevant clinical and epidemiologic
factors and typical CSF findings (lymphocytic pleocytosis,
elevated protein concentration, and low glucose
concentration).

25. Complications
Complications of tuberculous meningitis include.
 Stroke
 Seizures
 Hydrocephalus
 Hyponatremia
 Vision loss
 Transverse myelitis

26. Leprosy (Hansen’s disease)
• Chronic granulomatous infection by M. leprae
• Worldwide disease but mainly in the
developing world
• Affects the skin, and nerves
• Clinical features depend on the patients CMI
to the bacilli
• Complications of leprosy due to: nerve
damage, bacillary infiltration and immunologic
reactions

27. Epidemiology and transmission
• 4 million people worldwide
• 750,000 new cases annually
• 70% in India
• Bacilli discharged from the nose of patients
with lepromatous leprosy
• Close household exposure necessary for
acquiring the disease
• Infection occurs through the nose, then
hematogenous spread  skin/nerve
involvement.

28. Pathogenesis
• M.leprae infects skin macrophages and schwann
cells
• If CMI is good: paucibacillary but if absent
multibacillary leprosy
• Immunological reactions can also occur
• HIV-Leprosy: not an obvious shift to lepromatous
leprosy
• The nine-banded armadillo (Dasypus
novemcinctus) remains the only well-documented
zoonotic reservoir

30. Classification of leprosy

31. Clinical features

32. Leonine facies

33. Lepromatous leprosy

35. Tuberculoid leprosy (TT/PB

36. 36
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