Syringomyelia and Hydromyelia

Slide 1 · Syringomyelia and Hydromyelia

Cavity anatomy • spinal cord injury • clinicopathologic localization

Pathology lecture

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes: Distinguish cavity types

Cavity anatomy

Tissue injury

Clinical localization

Differentiate expansion of the central canal from an intramedullary syrinx.

Explain how cavity location predicts tissue injury and a sensory phenotype.

Connect Chiari malformation, tumor, and trauma with cavitation and clinical assessment.

Slide 3 · Clinical starting point: Selective sensory loss

Apply the anatomy to the vignette

An adult reports reduced ability to perceive pinprick and temperature in both upper limbs.

Preserved vibration would suggest relatively spared posterior-column pathways.

The anatomical question: Which central spinal cord fibers are vulnerable?

Illustrative teaching case — no individual patient data.

Slide 4 · Two anatomical categories; One central location

Feature

Hydromyelia

Syringomyelia

Defining cavity

Expanded central canal

Intramedullary syrinx

Lining

Ependyma-lined

Not defined by ependymal lining

Location

Canal-centered

Inner spinal cord

Slide 5 · Spinal cord cross-sectional orientation

Posterior (dorsal) structures are shown above and anterior (ventral) structures below.

Gray matter occupies a central butterfly-shaped region.

White matter surrounds the gray matter and contains long ascending and descending tracts.

Dorsal

Ventral

Gray matter

Central canal

Schematic cross-section

Slide 6 · Central canal: An epithelial boundary

The central canal lies within central spinal cord tissue.

Ependymal cells line the normal canal; Hydromyelia expands this pre-existing lumen.

A cavity in adjacent tissue is not defined as hydromyelia merely because it is centrally located.

Dorsal

Ventral

Gray matter

Expanded canal

Schematic cross-section

Slide 7 · Anterior white commissure: Crossing fibers

Second-order nociceptive and thermal fibers cross near the central canal.

The crossing occurs in the anterior white commissure before ascent contralaterally.

A central expanding lesion can interrupt decussation on both sides.

Dorsal

Ventral

Gray matter

Crossing fibers

Schematic cross-section

Slide 8 · Pain and temperature: Circuit logic

Dorsal horn

Anterior crossing

Anterolateral ascent

Primary afferents enter the spinal cord and synapse in dorsal-horn circuitry.

Second-order fibers cross toward the opposite anterolateral system.

A commissural lesion preferentially impairs segmental pain and temperature perception.

Slide 9 · Posterior-column function offers a contrast

Vibration and joint position largely ascend in posterior columns.

Posterior columns are anatomically separated from the anterior commissural crossing.

Their relative preservation helps explain dissociated sensory loss in an early central lesion.

Dorsal

Ventral

Gray matter

Posterior columns

Schematic cross-section

Slide 10 · Hydromyelia: Expansion of a canal

The definition requires enlargement of the ependyma-lined central canal.

Its shape follows the original central-canal compartment rather than a free intraparenchymal cleft.

Clinical consequences depend on whether expansion damages surrounding neural tissue.

Dorsal

Ventral

Gray matter

Expanded canal

Schematic cross-section

Slide 11 · Syringomyelia: A cavitary cord lesion

A syrinx is a fluid-containing cleft or cavity in the inner cord.

The cavity may disrupt both central gray matter and neighboring white matter.

Its anatomical extent determines which pathways and segments are affected.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 12 · Hydromyelia versus syringomyelia: Core distinctions

Dimension

Hydromyelia

Syringomyelia

Principal space

Central-canal lumen

Inner spinal cord cavity

Key tissue relation

Expanded ependymal lining

Parenchymal cleft

Possible overlap

Both may coexist within a complex lesion

Both may coexist within a complex lesion

Slide 13 · Syringobulbia: Extension beyond the cord

Spinal syrinx

Cranial extension

Brainstem involvement

A spinal syrinx can extend cranially into the brainstem.

The name syringobulbia indicates brainstem involvement.

New bulbar findings require anatomical reassessment rather than attributing all deficits to a cervical cord lesion.

Slide 14 · Cavity shape is a diagnostic clue—not a mechanism

Question

Morphologic answer

Etiologic question

Where?

Central canal or cord parenchyma

What altered CSF dynamics?

How far?

Segmental / longitudinal extent

What associated condition exists?

What damage?

Gray / white matter injury

What process caused it?

Slide 15 · Three major associations

Chiari malformation

Intraspinal tumor

Spinal trauma

Chiari malformation links hindbrain position to spinal CSF-flow disturbance.

Intraspinal tumors may coexist with a syrinx.

Syringomyelia can also occur following traumatic spinal injury.

Slide 16 · Chiari I: Low-lying cerebellar tonsils

Cerebellar tonsils extend downward through the foramen magnum region.

The anomaly may be clinically silent.

Symptoms may result from impaired CSF flow, medullary compression, or associated hydromyelia/syringomyelia.

Posterior fossa

Foramen magnum

Cervical canal

Low tonsillar tissue

Slide 17 · Foramen magnum: A CSF-flow bottleneck

Foramen magnum crowding

Abnormal CSF dynamics

Associated syrinx

CSF normally moves between cranial and spinal subarachnoid spaces.

Low-lying tonsillar tissue may narrow the available pathway.

Altered flow and pressure transmission are implicated in formation or enlargement of an associated syrinx.

Slide 18 · Chiari I and the syrinx are related—not identical

Structure

Chiari I

Syrinx

Site

Craniovertebral junction

Spinal cord

Defining feature

Low tonsils

Intramedullary cavity

Study question

Foramen magnum anatomy

Cavity location and extent

Slide 19 · Chiari II: A broader developmental malformation

The posterior fossa is small, with a misshapen midline cerebellum.

The vermis extends below the foramen magnum; Medullary displacement may also occur.

Hydromyelia/syringomyelia is one possible associated change.

Posterior fossa

Foramen magnum

Cervical canal

Downward vermis

Slide 20 · Chiari II: Linked anomalies matter

Anatomic compartment

Associated finding

Posterior fossa

Small, misshapen cerebellum

Ventricular system

Hydrocephalus ± aqueductal stenosis

Spine

Lumbar myelomeningocele; sometimes a syrinx

Slide 21 · Chiari I versus II: Prevent category errors

Comparison

Chiari I

Chiari II

Posterior fossa

Low cerebellar tonsils

Small; distorted midline cerebellum

Key associations

CSF obstruction / syrinx

Hydrocephalus; myelomeningocele

Cavitation

Possible

Possible

Slide 22 · Intraspinal tumors: Examine the whole cord

Tumor-associated process

Disturbed local anatomy

Syrinx may coexist

An intraspinal tumor as an association of syringomyelia.

A cavity must not distract from a coexisting mass or abnormal tissue enhancement.

MRI assessment should describe both the intramedullary fluid cavity and the possible underlying lesion.

Slide 23 · Post-traumatic syringomyelia

Prior spinal injury

Subsequent cavitation

New or progressive deficits

Spinal injury can precede syrinx formation.

A delayed neurological deterioration in an injured segment deserves evaluation.

Assessment must compare new symptoms with the patient’s pre-existing neurological baseline.

Slide 24 · Inflammation and arachnoid scarring

Meningeal inflammation

Scarring / flow disturbance

Possible syrinx

NINDS includes meningitis and arachnoiditis among acquired associations.

Scar-related CSF-flow obstruction is one plausible pathway to cavitation.

These acquired causes are additional clinical context, not specified in the short Robbins excerpt.

Slide 25 · Idiopathic syringomyelia requires careful labeling

Label

What it means

What it does not mean

Idiopathic

No known cause identified

Proof of a unique mechanism

Post-traumatic

History supports acquired association

Every deficit is due to syrinx

Chiari-related

Coexisting relevant malformation

A fixed symptom pattern

Slide 26 · Pathogenesis: A mechanistic model

Altered CSF movement

Altered pressure / fluid transport

Cord cavitation

Disturbance in normal CSF flow is implicated in several forms of syringomyelia.

Abnormal pressure transmission may contribute to intramedullary fluid accumulation.

No single fluid-dynamics model explains every case; Mechanisms remain debated.

Slide 27 · Mechanism should not be confused with proof

Established observation

Interpretation requiring caution

Syrinx coexists with Chiari

Exact fluid transport pathway

Syrinx may follow trauma

Uniform mechanism in every patient

Flow can be abnormal

Same intervention for every cavity

Slide 28 · Morphology: Cavitation damages the cord

Expansion produces a space where functional neural tissue has been displaced or destroyed.

Both gray and white matter may be involved around a syrinx.

Cavity size alone is not a substitute for assessing tissue injury.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 29 · Gray matter injury: Local segmental effects

Central gray matter is anatomically close to the canal and commissural region.

Its disruption can produce segmental neurological deficits.

Anterior-horn injury, when present, may cause lower motor-neuron weakness at affected levels.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 30 · White matter injury: Tract involvement

Longitudinal tracts surround central gray matter.

Extension of a cavity into white matter can disrupt ascending or descending pathways.

Examination may become more complex as tract damage spreads beyond the initial commissural region.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 31 · Dense reactive gliosis surrounds the lesion

Destruction bordered by dense reactive gliosis.

Gliosis is the CNS cellular response to chronic tissue injury.

This microscopic reaction occurs across the listed associated conditions and is not etiologically specific.

Dorsal

Ventral

Gray matter

Gliotic rim

Schematic cross-section

Slide 32 · A lesion can destroy and compress simultaneously

Cavity formation

Parenchymal destruction / distortion

Functional deficit

A cavity removes parenchymal continuity at its center.

Adjacent viable axons may be compressed or distorted as it enlarges.

The pattern of dysfunction reflects which fibers are injured, not simply the presence of fluid.

Slide 33 · Histologic interpretation: What is supportable?

Expect cavitation and adjacent gray/white matter damage.

Dense reactive gliosis is the documented rim response.

The supplied source does not provide a stained photomicrograph; The adjacent diagram is explanatory, not histologic evidence.

Dorsal

Ventral

Gray matter

Gliotic rim

Schematic cross-section

Slide 34 · Morphology does not pinpoint the cause

Microscopy / morphology

Necessary clinical context

Fluid cavity

Cord and hindbrain imaging

Neural tissue loss

Segmental neurologic findings

Reactive gliosis

Tumor, trauma, Chiari, inflammation history

Slide 35 · Cross-section: Cavity location changes injury

A small central lesion first threatens short crossing fibers.

A larger cavity can reach anterior horns and adjacent long tracts.

No precise symptom threshold can be inferred from a schematic cavity diameter.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 36 · Longitudinal extent matters independently

Spinal cavities may extend across multiple vertebral levels.

A longer lesion potentially involves additional segmental sensory and motor structures.

Sagittal MRI helps determine the craniocaudal extent; Axial images show local compartment involvement.

Longitudinal cavity

Simplified schematic — not MRI

Slide 37 · Why pain and temperature are affected first

The anterior white commissure is close to the central canal.

Decussating nociceptive and thermal fibers traverse this central vulnerable zone.

Bilateral injury to crossing fibers creates a characteristic segmental sensory pattern.

Dorsal

Ventral

Gray matter

Crossing fibers

Schematic cross-section

Slide 38 · Segmental rather than whole-body loss

Cervical cord levels

Segmental crossing injury

Upper-limb sensory deficit

Crossing fibers correspond to particular spinal levels.

A syrinx may interrupt pain/temperature pathways at those involved levels.

The deficit should be mapped by dermatome rather than assumed to include every segment below the lesion.

Slide 39 · Dissociated sensory loss: Modality matters

Sensory modality

Early central lesion: expected pattern

Pinprick / thermal

Impaired at involved segments

Vibration / position

Often relatively preserved

Light touch

May be variably preserved; examine directly

Slide 40 · Cape-like involvement: Useful but not universal

Cervical syringomyelia can produce sensory loss across shoulders and upper limbs.

A cape-like distribution is a classic pattern of central cord segment involvement.

Other cavity locations or extents create different sensory maps; Avoid requiring the classic pattern.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 41 · Clinical deficits follow anatomical spread

Crossing fibers

Anterior horn cells

Long tracts

Commissural fibers: Pain and temperature impairment.

Anterior horn: Weakness, wasting, and segmental lower motor-neuron signs.

Long tracts: Additional sensory or motor dysfunction as the cavity extends.

Slide 42 · Anterior-horn involvement and the hand

At affected cervical enlargements, anterior-horn damage can impair upper-limb motor units.

Weakness and muscle atrophy reflect motor-neuron injury rather than loss of sensation alone.

Strength, atrophy, reflexes, and sensory modalities should be documented separately.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 43 · Later motor findings require tract localization

Affected structure

Examination emphasis

Anterior horn

Atrophy, segmental weakness, reduced reflexes

Corticospinal tract

Long-tract motor signs below involved levels

Commissural fibers

Pain and temperature loss at involved segments

Slide 44 · Clinical presentation can be heterogeneous

Location

Extent

Tissue injured

Symptoms may include pain, abnormal sensation, stiffness, or weakness.

Distribution and progression depend on the syrinx location, size, and extent.

Absence of the textbook sensory pattern does not exclude a cavity.

Slide 45 · Age at presentation is a pattern, not a rule

Teaching point

Clinical qualification

Classic onset

Second or third decade in Robbins

Acquired syrinx

May appear later following an insult

Interpretation

Age supports context, not diagnosis

Slide 46 · Bulbar extension changes the examination

Cranial extension

Brainstem structures

Bulbar / cranial-nerve assessment

Syringobulbia denotes extension into the brainstem.

Cranial nerve and bulbar functional findings warrant attention when brainstem extension is suspected.

Image the relevant region rather than assuming every deficit is confined to the spinal cord.

Slide 47 · Bedside examination: Use multiple modalities

Assessment domain

Anatomic question

Pain / thermal

Crossing anterolateral fibers?

Vibration / position

Posterior columns spared?

Strength / reflexes

Gray matter or motor tract injury?

Slide 48 · Clinical localization precedes imaging interpretation

Neurologic examination

Cord localization

Imaging confirmation

A bilateral segmental dissociated deficit points toward central cord structures.

Motor and cranial-nerve signs refine the suspected level and extent.

Localization should guide—but not substitute for—appropriate MRI review.

Slide 49 · MRI: The main test for detecting a syrinx

MRI visualizes a fluid-filled cavity within spinal cord parenchyma.

Axial images define relationships to the central canal and gray/white matter.

Sagittal images demonstrate the length of the cavity and possible cranial extension.

Sagittal concept

Axial concept

Simplified schematic — not MRI

Slide 50 · Axial MRI: Location is the first question

Determine whether a fluid space is canal-centered or forms a larger intramedullary cleft.

Describe cord expansion and remaining surrounding tissue.

The adjacent drawing is a structural schematic, not a clinical MRI.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 51 · Sagittal MRI: Assess longitudinal extension

Record the cranial and caudal limits of any visible cavity.

Assess whether the cord and the cervicomedullary junction are involved.

Relate the demonstrated extent to neurological levels examined at the bedside.

Longitudinal cavity

Simplified schematic — not MRI

Slide 52 · Imaging must search for an associated lesion

Syrinx found

Search for associated cause

Correlate with examination

Examine the craniocervical junction for Chiari-type abnormalities.

Review the spinal cord for a tumor or other obstructive cause.

Relevant history of injury, infection, or arachnoiditis shapes the differential.

Slide 53 · Contrast-enhanced MRI: Answer a specific question

Imaging question

Potential value

Is there a mass?

Assess solid or enhancing components

Is there inflammation?

Evaluate surrounding abnormalities

What is cavity extent?

Use multiplanar MRI anatomy

Slide 54 · Diagnostic differential: Test competing explanations

Possibility

Discriminator to investigate

Chiari-associated

Craniovertebral junction anatomy

Tumor-associated

Intramedullary mass / enhancement

Trauma-associated

Prior injury and interval change

Inflammation-associated

Meningeal history and imaging

Slide 55 · Management depends on symptoms and cause

Clinical course

Etiologic assessment

Individualized management

An asymptomatic, stable cavity may be monitored clinically and radiologically.

Progressive deficits or an enlarging symptomatic syrinx prompt specialist evaluation.

Treating the associated cause may be more important than simply draining fluid.

Slide 56 · Chiari-associated syrinx: Restore CSF passage

Craniocervical narrowing

Decompression when indicated

CSF flow and syrinx follow-up

Surgical management may create more room at the craniocervical junction.

The aim is to improve CSF movement and reduce further cord injury.

Anatomical decompression and symptoms need follow-up; Improvement is not guaranteed.

Slide 57 · Tumor- or scar-associated cavities: Address cause

Identify obstruction

Manage causal lesion

Reassess cavity and function

Identify whether an associated mass or obstructive scar is treatable.

Intervention must be individualized to the actual underlying process.

Cavity drainage alone may not correct a persistent flow obstruction.

Slide 58 · Shunting a syrinx is not a universal first step

Option

Conceptual role

Observation

Stable or asymptomatic lesions

Etiologic surgery

Correct CSF obstruction / associated lesion

Direct drainage

Selected cavities when indicated

Slide 59 · Case: Sensory loss with low-lying tonsils

Apply the anatomy to the vignette

A young adult has progressive loss of pinprick and temperature over the shoulders and hands.

MRI demonstrates an intramedullary fluid cavity and low-lying cerebellar tonsils.

Which two distinct anatomical abnormalities must the diagnosis report?

Educational vignette; Fictional, not source-derived patient data.

Slide 60 · Case reasoning: Correlate two sites

Finding

Anatomic interpretation

Dissociated upper-limb sensory loss

Anterior commissural dysfunction

Intramedullary cavity

Syringomyelia

Low-lying tonsils

Associated Chiari I morphology

Slide 61 · Case: A new deficit after remote trauma

Apply the anatomy to the vignette

A person with a prior spinal cord injury develops a new level of sensory impairment years later.

Imaging reveals a cavity at or near the injured cord region.

The question is whether newly progressive cavitation is contributing to the clinical change.

Educational vignette; Fictional, not an observed patient.

Slide 62 · Case reasoning: Avoid anchoring on old injury

Compare baseline

Localize new deficit

Assess cavity and cause

Record the pre-existing motor and sensory examination before attributing new abnormalities.

Determine cavity extent and consider associated tethering or CSF-flow obstruction.

Post-traumatic syringomyelia belongs in the evaluation of delayed neurological change.

Slide 63 · Knowledge check: Identify the defining feature

Apply the anatomy to the vignette

Which observation uniquely supports hydromyelia rather than a generic central syrinx?

A. Dense gliosis surrounding an intramedullary cavity

B. Enlargement of an ependyma-lined central-canal lumen

C. Loss of pain and temperature over the upper limbs

Correct answer: B. Both conditions can injure neural tissue; Lining and compartment establish the defining difference.

Slide 64 · Knowledge check: Localize dissociated loss

Pain and temperature are lost over selected upper-limb segments, whereas joint-position sense is retained.

Which short crossing pathway lies near the central canal?

Explain why sparing of posterior columns produces a modality dissociation.

Dorsal

Ventral

Gray matter

Crossing fibers

Schematic cross-section

Slide 65 · Integrated pathological reasoning

Anatomy

Neurologic phenotype

Etiology and course

Begin with cavity anatomy: Central canal or intramedullary cleft.

Link tissue injury to local segmental fibers and adjacent long tracts.

Investigate causes separately: Chiari, tumor, prior trauma, and other acquired conditions.

Slide 66 · Final synthesis: Anatomy predicts the phenotype

Hydromyelia is an expanded ependyma-lined canal; Syringomyelia is an inner-cord fluid cavity.

Cavitation causes gray/white matter destruction with reactive gliosis.

Anterior commissural injury explains selective segmental pain and temperature loss.

Dorsal

Ventral

Gray matter

Syrinx cavity

Schematic cross-section

Slide 67 · Final synthesis: Morphology is not etiology

Define cavity

Investigate cause

Plan follow-up / treatment

A syrinx should trigger evaluation for Chiari malformation, tumor, trauma, and relevant acquired conditions.

MRI defines cavity morphology and associated abnormalities.

Treatment depends on symptoms, progression, and the underlying cause.

Slide 68 · Selected references

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. 2026. Chapter 28, p. 1135.

NINDS. Syringomyelia. Current NIH clinical overview (accessed 12 October 2026).

NCBI Bookshelf. Anterior White Commissure; Syringomyelia. Neuroanatomic and clinical context.

Heiss JD. CSF Hydrodynamics in Chiari I Malformation and Syringomyelia. Neurosurg Clin N Am. 2023.