Spinal Cord Syndromes

Dr.W.A.P.R.S. Weerarathna

Registrar-Ward 10/02

THJ

Objectives…

• Basic spinal cord Anatomy

• Types of spinal cord lesions

• Main spinal cord syndromes-Eight!

• Common clinical presentation

• Basic Neuroimaging-MRI/CT appearances

• Other spinal cord lesions

• Summary

Spinal cord Anatomy31 pairs of spinal cord segments,45 cm

Ventral-motor & Dorsal-sensory functions

Combined –mixed spinal nerves neuroforamina

Foramen magnum lower margin of L1

Vert. & SC segments –not nessasarily the same( SC is shorter than the vert.)

Blood supp-1 ant.spinal artery& 2 post.spinalarteries (vertebral)

Ant.2/3 & dorsal columns respectively.

Spinal cord lesions• Intra medullary vs extramedullary lesions

• Complete vs incomplete lesions

Intramedullary Extramedullary

Root pain rare Root pain common

Corticospinal signs-late early

LMN signs- several segments

localized

Dissociated sen.loss +/- BSS if lateral cord compression

CSF changes-minimally altered/NL

Early & marked

May have sacral sparing

• Incomplete:– Sensory, motor or both functions are partially

present below the neurologic level of injury

– Some degree of recovery

• Complete:

– Absence of sensory and motor function below the level of injury

– Loss of function to lowest sacral segment

– Minimal chance of functional motor recovery

Important SC syndromes (8)

1) Complete cord transection syndrome

2) Brown-Sequard syndrome

3) Central cord syndrome (syringomyelia)

4) Posterior column syndrome (tabes dorsalis)

5) Posterolateral cord syndrome (SACDC)

6) Combined AHC-pyramidal tract syndrome (ALS)

7) AHC syndrome

8) Anterior spinal artery artery occlusion

Others important condisions

• Conus medullaris syndrome(L2)

• Cauda equina syndrome is not a SC syndrome!(represent spinal roots, rather than SC.)-usually lesions below L2 level.

• Friedreich’s ataxia-spino cerebellardegeneration.

• 1-complete cord transection•

• Causes- trauma, h’age,epiduralabscess,metastasis,MS ,post vaccinial syn.ect

• Results in

1. Spinal shock

2. Spastic paralysis(hypertonic,hyperfeflexic)

3. Loss of all sensory modalities bilaterally

4. Autonomic disturbances

• Spinal shock-

1. Complete loss of voluntary movements, sensations below the level of lesion

2. Loss of all reflexes in isolated cord segments

3.Duratin varies-1-6 weeks commonly

• Spastic paralysis

1. Follows the period of spinal shock

2. Initially positive Babinski sign ,later-increased tone & deep tendon reflexes

3. Disuse muscle atrophy

• Loss of superficial reflexes(abdominal, cremasteric) below the level

• Loss of all sensations bilaterally below the lesion

1. Loss of propioception, vibration,tactilediscrimination, pain,temp, light touch, viseralsensibility

2. Complete lesion-no recovery

• Autonomic disturbances

1. Bowel/bladder dysfunction-urinary retention/constipation

2. Initial retention due to loss of vol.control

3. Flaccid neuropathic bladder with overflow incontinence with recovery……

• Spastic neuropathic bladder with autonomic bladder

5.few-’’ mass reflex’’ bowel/bladder empty on a segmental autonomic basis reflexly.

6. Vasomotor instability-Cutaneous BV below do not respond to cold/hot stimuli

7.Anhydrosis-Honer’s syndrome may occur in some.

8.Sexual dysfunction

• Transection of SC above C5- not survive due to involvement of phrenic nerve nuclei-res.paralysis

• Below C5-quadriplagic/between Cx & L-S segments-paraplagic.

• 2. BSS

• Motor changes-

1. UMN signs below the hemisection on I/L side

2. LMN signs at the level on I/L side

• Sensory changes-

1. Pain/temp loss on C/L side –upper level of sen. Loss is few segments below the leasion.(?)

2. Vib. & propi, loss on I/L side

3. There may be band of sensory loss on the I/L side at level of the leasion.

• Causes-

1. MS

2. Angioma

3. Glioma

4. Trauma

5. Myelitis

6. Post radiation myelopathy

3.Central cord leasion-syryngomyelia

Others-hyperextention injuries,trauma,intramedtumors

• Expanding central canal in the SC –more in Cervical cord,symetrical leasions

• STTsalways affected- fibers cross through syrinx

• CSTs spares until syrinx very large

• DCs always spared

• nerve roots at sequential levels affected

• Clinical triod-

1. Loss of pain/temp. over neck, shoulders & arms-’’cape distribution’’

2. Amyotrophy-weakness,atrophy ,areflexia of hands/arms

• 3.UMNL in lower limbs

• Other features horner’s syndrome(syrinxaffecting sym. Nerves & C8/T1

• Charcot’s joints-long standing ,loss of pain sensation

• Associated kypphoscoliosis.

• Syringobulbia syrinx in brain stem/extention-facial dissociated sensory loss,bulbar palsy,nystagmus & cebellar ataxia

• 4.Posterior column syndrome-Tabesdorsalis(neuro syphilis) & also DM

• CNS infection of syphilis after 3-18 years

• DCs & dorsal roots degenerate

• DCs loss of vibration & propioception ,+veRomberg’s sign(&+ve Hermitte’s sign)

• CSTs not affected. if involved =‘’TABUPARESIS’’

• STTs spared.

• Others neuropathic joint destruction <10% (charcot’s joints) trophic ulcers,

• Argyll Robertson pupils 90% (ARP),optic atrophy(rare),opthalmolagia.

• Autonomic degeneration-neuropathic bladder(incontinance),constipation

• 5.Posterolateral cord syndrome-SACDC

• Others-HIV,HTLV,CERVICAL SPONDYLOSIS

• Due to Vit.B12 deficiency

• DCs symmetrically degenarate,loss of vibration & propioception over feet,+veRhomberg’s sign, Ataxic gait

• CSTs symetrical UMN signs in LLs(spastic paraparesis),extensor planters, absent AJ, possible brisk KJ

• STTs spared or involved as part of PN(less common & mild)

• Others optic atrophy with centrocecalscotomata,dementia,autoimmunedisease(pernicious anemia)

• Causes of extesor planters &absent KJ

• D- DM(uncommon)

• M-MND,metachromatic leucodystrophy

• A- Adrenoleucodystrophy

• S- SACDC,SYPHILIS

• T-Tabuparesis

• Cauda equina syndrome

• 6.Combined AHC –pyramida tract syndrome-(ALS)

• typical form of MND, AD inheritance, mutation in SOD1

• Mixed UMN & LMN degeneration with cerebral motor pathways & brain stem nuclei

• Muscle wasting or weakness with preserved or brisk reflexes, sphincter involvement is very late if at all.

• Progressive bulbar involvement(20%) sialorrhoea, dysarthria,dysphagia

• Cognition generally spared, 15% FTD

• Sensory-NOT affected, superficial reflexes-preserved

• ANS-intact

• 7.Anterior horn cell syndrome (AHC)

• CAUSED BY SPINAL MUSCULAR ATROPHY.

• MOTOR

• weakness ,atrophy and fasciculations.

• Hypotonia, depressed reflexes.

• Muscles of trunk and extremities are affected.

• Sensory system is not affected.

• 8.Anterior spinal artery occlusion/syndrome

• MOTOR-Flaccid and areflexic paraplegia• SENSORY-• Loss of pain and temperature.• Preservation of position and vibration.• AUTONOMIC-• urinary incontinence.• Spinal cord infarction usually occurs in T1 to

T4 segment. and L1 • Occurs due to syphilitic arteritis ,aortic

dissection, atherosclerosis of aorta, SLE & AIDS,AVM

• Posterior spinal artery occlusion/syndrome-

• Uncommon.

• Loss of proprioception and vibratory sense.

• Pain and temperature is preserved.

• Absence of motor deficit.