The document discusses various spinal cord syndromes classified as either complete or incomplete cord syndromes. It provides details on complete cord transection which results in paralysis, loss of sensation, and autonomic dysfunction below the level of injury. Brown-Sequard syndrome and central cord syndrome are discussed as examples of incomplete cord syndromes characterized by mixed upper and lower motor neuron findings on one or both sides of the body. The document also covers syndromes involving specific regions of the spinal cord including conus medullaris, cauda equina, and anterior spinal artery syndromes.
5. COMPLETE CORD TRANSECTION
• All ascending tracts from
below and descending tracts
from above are interrupted.
• Affects motor, sensory and
autonomic functions.
6. COMPLETE CORD TRANSECTION
SENSORY:
ď‚— All sensations are affected.
ď‚— Pin prick test is very valuable.
ď‚— Sensory level is usually 2 segments below the level of
lesion.
ď‚— Segmental paraesthesia occur at the level of lesion.
7. COMPLETE CORD TRANSECTION
MOTOR:
ď‚— Paraplegia due to corticospinal tract involvement.
ď‚— First spinal shock-followed by hypertonic hyperreflexic
paraplegia.
ď‚— Loss of abdominal and cremastric reflexes.
ď‚— At the level of lesion LMN signs occur.
8. COMPLETE CORD TRANSECTION
AUTONOMIC:
ď‚— Urinary retention and constipation.
ď‚— Anhidrosis, trophic skin changes, vasomotor instability
below the level of lesion.
ď‚— Sexual dysfunction can occur.
10. BROWN SEQUARD SYNDROME
= Hemi-section of the spinal cord
ď‚— Caused by extramedullary lesions
ď‚— Usually caused by penetrating trauma or tumour.
11.
12. BROWN SEQUARD SYNDROME
SENSORY:
ď‚— Ipsilateral loss of proprioception due to posterior
column involvement.
ď‚— Contralateral loss of pain and temperature due to
involvement of lateral spinothalamic tract.
13. BROWN SEQUARD SYNDROME
MOTOR:
ď‚— Ipsilateral spastic weakness due to descending
corticospinal tract involvement
ď‚— LMN signs at the level of lesion.
16. CENTRAL CORD SYNDROME
ď‚— Commonest cause is Syringomyelia.
ď‚— Other causes:
â—¦ Hyperextension injuries of neck
â—¦ Intramedullary tumours
â—¦ Trauma
â—¦ Associated with Arnold Chiari type 1 and 2, Dandy walker
malformation
17. CENTRAL CORD SYNDROME
SENSORY:
ď‚— Pain and temperature are affected.
ď‚— Touch and proprioception are preserved.
ď‚— Dissociative anaesthesia.
ď‚— Shawl like (= Cape like) distribution of sensory loss.
MOTOR:
ď‚— Upper limb weakness > Lower limb
18. SYRINGOMYELIA
OTHER FEATURES :
 Horner’s syndrome
ď‚— Kyphoscoliosis
ď‚— Sacral sparing
ď‚— Neuropathic arthropathy of shoulder and elbow
joint
ď‚— Prognosis is fair.
19.
20. POSTERIOR CORD SYNDROME
ď‚— Commonest causes include diabetes mellitus &
neurosyphilis.
ď‚— Usually occurs 10 to 20 yrs after disease onset.
21. POSTERIOR CORD SYNDROME
SENSORY :
ď‚— Impaired position and vibration sense in LL
ď‚— Tactile and postural hallucinations can occur.
ď‚— Numbness or paresthesia are frequent complaints..
ď‚— Sensory ataxia.
ď‚— Positive rhomberg sign.
ď‚— Positive sink sign
ď‚— Positive lhermittes sign.
22. POSTERIOR CORD SYNDROME
SENSORY (contd):
 Abadie’s sign (of tabes dorsalis) positive
ď‚— Urinary incontinence
ď‚— Absent knee and ankle jerk (Areflexia, Hypotonia)
 Charcot’s joint
ď‚— Miotic and irregular pupil not reacting to light
ď‚— Argyl Robertson Pupil
24. POSTERIO LATERAL COLUMN DISEASE
FEATURES :
ď‚— Paresthesia in feet
ď‚— Loss of proprioception and vibration in legs
ď‚— Sensory ataxia
ď‚— Positive Rhomberg sign
ď‚— Bladder atony
ď‚— Corticospinal tract involvement:
â—¦ Spasticity
â—¦ Hyperreflexia
â—¦ Bilateral Babinski sign - Positive
25. POSTERIO LATERAL COLUMN DISEASE
ď‚— AIDS:
â—¦ Associated dementia and spastic bladder is present
ď‚— HTLV associated myelopathy:
â—¦ Slowly progressive paraparesis
â—¦ Increase in CSF IgG with antibodies to HTLV 1
26. ANTERIOR CORD SYNDROME
ď‚— Due to acute disc herniation or ischemia from anterior
spinal artery occlusion.
ď‚— Usually caused by hyperflexion injuries
ď‚— Area supplied by anterior spinal artery is affected
27. ANTERIOR CORD SYNDROME
ď‚— Sudden onset of paralysis
(quadriparesis/paraparesis)
below the level of lesion.
ď‚— Pain and temperature loss.
ď‚— Dorsal column is
preserved.
ď‚— Prognosis is poor.
30. ANTERIOR SPINAL ARTERY SYNDROME
ď‚— Commonest of the vascular syndromes of the cord.
ď‚— Spinal cord infarction usually occurs in T1 to T4 segment & L1.
ď‚— Occurs due to aortic dissection, atherosclerosis of aorta, SLE,
AIDS, AV malformation
ď‚— Rarely due to dissection of the anterior spinal artery or systemic
arteritis. Syphilitic arteritis is now rare.
ď‚— Conus medullaris is frequently involved.
ď‚— Neck pain of sudden onset is a common feature.
 Also called as “Beck’s syndrome”.
31. ANTERIOR SPINAL ARTERY SYNDROME
SENSORY :
ď‚— Loss of pain and temperature.
ď‚— Preservation of position and vibration.
MOTOR :
ď‚— Sudden onset flaccid and areflexic paraplegia.
AUTONOMIC :
ď‚— Urinary incontinence +
32. POSTERIOR SPINAL ARTERY
SYNDROME
ď‚— UNCOMMON
ď‚— Loss of proprioception and vibratory sense.
ď‚— Pain and temperature is preserved.
ď‚— Absence of motor deficit.
33. ANTERIOR HORN CELL SYNDROMES
ď‚— CAUSED BY SPINAL MUSCULAR ATROPHY
â—¦ Spinal muscular atrophy (SMA) is an autosomal recessive
disorder that causes decreased survival of the anterior horn
cells – motor neurons – that innervate voluntary muscles,
resulting in progressive muscle atrophy and weakness.
â—¦ Types I to IV
â—¦ Eponyms: Werdnig-Hoffman disease, Kugelberg-Welander
disease, SMA, Anterior horn cell disease
34. ANTERIOR HORN CELL SYNDROMES
MOTOR :
ď‚— Weakness, atrophy and fasciculations.
ď‚— Hypotonia, depressed reflexes.
ď‚— Muscles of trunk and extremities are affected.
ď‚— Sensory system is not affected.
35. ANTERIOR HORN CELL & PYRAMIDAL
TRACT SYNDROME
ď‚— Occurs in amytrophic lateral sclerosis (ALS).
â—¦ Also called Lou Gehrig's disease.
â—¦ A form of Motor Neuron Disease caused by the degeneration of
upper and lower neurons, located in the ventral horn of
the spinal cord and the cortical neurons that provide
their efferent input.
ď‚— Affects the anterior horn cells and corticospinal tract.
ď‚— Both LMN and UMN signs occur.
36. ANTERIOR HORN CELL & PYRAMIDAL
TRACT SYNDROME
MOTOR :
ď‚— Ant horn cell related:
â—¦ Paresis, Atrophy and Fasciculations.
ď‚— Corticospinal tract related:
â—¦ Paresis, Spasticity and Extensor plantar response.
37. ANTERIOR HORN CELL & PYRAMIDAL
TRACT SYNDROME
ď‚— It is usually unilateral with muscle weakness +
ď‚— Reflexes are often exaggerated.
ď‚— Bulbar and pseudo bulbar involvement occurs.
ď‚— Sensory system is not affected.
ď‚— Superficial reflex - Abdominal reflex is preserved.
39. CONUS MEDULLARIS SYNDROME
ď‚— CM: Lies opposite to vertebral bodies of T12 and L1.
ď‚— Contributes to 25% of spinal cord injuries.
ď‚— Caused by flexion distraction injuries and burst
fractures.
ď‚— Both UMN and LMN deficits occur.
ď‚— Development of neurogenic bladder.
40. CAUDA EQUINA SYNDROME
ď‚— CE: Begins at L2 disk space
distal to conus medullaris.
ď‚— CE syndrome occurs due to:
â—¦ Acute disk herniation
â—¦ Epidural haematoma
â—¦ Tumour
41. CAUDA EQUINA SYNDROME
MOTOR :
ď‚— Flaccid lower extremities.
ď‚— Knee and ankle jerk absent.
SENSORY :
ď‚— Asymmetrical sensory loss
ď‚— Saddle anaesthesia
ď‚— Loss of sensation around perineum, anus, genitals.
43. DDx: CONUS vs CAUDA
FEATURE CONUS MEDULARIS CAUDA EQUINA
PRESENTATION Sudden & Bilateral Gradual & Unilateral
REFLEXES Knee present, Ankle – Knee & Ankle –
(If the epiconus is
involved, patellar reflex Bulbocavernosus reflex
maybe absent but is absent in low CE
bulbocavernosus is (sacral) lesions
spared)
RADICULAR PAIN Less severe More severe
LOW BACK ACHE More Less
Ref: http://www.emedicine.com/neuro/topic667.htm
44. FEATURE CONUS MEDULARIS CAUDA EQUINA
SENSORY Numbness tends to be Numbness tends to be more
SYMPTOMS more localized to localized to saddle area;
perianal area; asymmetrical, maybe
symmetrical and unilateral; no sensory
bilateral; sensory dissociation; loss of sensation
dissociation occurs. in specific dermatomes in lower
extremities with numbness and
Sensory loss of pin paresthesia; possible numbness
prick & temperature in pubic area, including glans
sensations (Tactile penis or clitoris.
sensation is spared.)
Ref: http://www.emedicine.com/neuro/topic667.htm
45. FEATURE CONUS MEDULARIS CAUDA EQUINA
MOTOR Typically symmetric, Asymmetric areflexic paraplegia
SYMPTOMS distal paresis of lower that is more marked;
limbs that is less fasciculations rare;
atrophy more common .
marked; fasciculations
may be present.
IMPOTENCE Frequent Less frequent; ED is common
erectile dysfunction that includes
inability to have erection, inability
to maintain erection, lack of
sensation in pubic area (including
glans penis or clitoris), and inability
to ejaculate.
Ref: http://www.emedicine.com/neuro/topic667.htm
46. FEATURE CONUS MEDULARIS CAUDA EQUINA
SPHINCTER Urinary retention and Urinary retention
DYSFUNCTION atonic anal sphincter
cause overflow urinary Tends to present late in
incontinence and fecal course of disease
incontinence
Tend to present early
in course of disease.
EMG Mostly normal lower Multiple root level
extremity with external involvement; sphincters may
anal sphincter invlmnt also be involved.
OUTCOME Less favourable More Favourable
Ref: http://www.emedicine.com/neuro/topic667.htm
 SMA is traditionally classified by age of onset and severity, however some experts classify by functional levels (non-sitters, sitters, and walkers) as which correlate better with clinical care needs than the traditional classification. [Wang: 2007] Clinical characteristics often overlap between types.Type I SMA (Werdnig-Hoffman ) presents near birth; these children never learn to sit or walk and have severe respiratory and swallowing problems, including difficulty handling oral secretions, and a significantly shortened life span. Risk of death in infancy is high, and most survivors are ventilator dependent by two years of age. Other features include poor head control, a bell-shaped chest, weak cry and cough, tongue atrophy and fasciculation, and paradoxical breathing.Type II SMA presents later in the first year of life or up to about two years of age. These children usually learn to sit. They often have respiratory and swallowing problems, including difficulty gaining weight due to bulbar muscle weakness, weak cough and night-time hypoventilation. Swallowing problems and difficulties opening the jaw widely have been shown to contribute to malnutrition in children with SMA II. [Messina: 2008] A tremor may be noted in these children. Joint contractures and scoliosis develop over time in nearly all affected children, and warranting proactive intervention.Type III SMA (Kugelberg-Welander) presents later in childhood or adolescence and these children usually sit and walk (although some may lose this ability over time) and have fewer problems with respiratory function and swallowing. Scoliosis and contractures as well as joint pain are often noted in older children.Infants with type 0 SMA present before birth, with decreased fetal movement noted around 30 weeks of age. They are hypotonic at birth with swallowing and breathing problems and, in some infants, arthrogryposis.Type IV SMA presents in adults.
ALS is often called Lou Gehrig's disease in North America, after the New York Yankees baseball player who was diagnosed with the disease in 1939. The disorder is characterized by rapidly progressiveweakness, muscle atrophy and fasciculations, spasticity, dysarthria, dysphagia, and respiratory compromise. Sensory function generally is spared, as is autonomic and oculomotor activity. ALS is a progressive,[1] fatal, neurodegenerative disease with most affected patients dying of respiratory compromise and pneumonia after 2 to 3 years; although some perish within a year from the onset of symptoms, and occasional individuals have a more indolent course and survive for many years.[2]