AN4002 L7 spinal cord

What is the embryological origin of the spinal cord?

The spinal cord develops from the neural tube, which arises from specialised dorsal ectoderm.

What is the difference between primary and secondary neurulation?

Primary neurulation forms most of the neural tube by folding and fusion of neural ectoderm, while secondary neurulation forms the caudal-most neural tube from tail bud cells.

What do neural crest cells contribute to in spinal cord development?

They form the dorsal root ganglia, which contain the cell bodies of sensory neurons.

What do the ventricular, mantle and marginal layers of the neural tube become?

The ventricular layer becomes the central canal lining, the mantle layer becomes grey matter, and the marginal layer becomes white matter.

What is the developmental significance of the alar and basal plates?

The alar plate forms the dorsal sensory region of the spinal cord, while the basal plate forms the ventral motor region.

What are the main functions of the adult spinal cord?

It conducts sensory information to the brain, conducts motor commands from the brain, and integrates spinal reflexes.

What is found in the white matter of the spinal cord?

Ascending sensory tracts and descending motor tracts.

What is found in the grey matter of the spinal cord?

Neuronal cell bodies, interneurons, and local circuits involved in reflex integration.

How is a spinal nerve formed?

A spinal nerve is formed by the union of a dorsal sensory root and an anterior motor root, making it a mixed nerve.

Where does the human spinal cord end?

It ends around the level of L1, with the conus medullaris and cauda equina below.

What is a somatic reflex arc?

A neural circuit involving a receptor, sensory neuron, interneuron, motor neuron and effector muscle that allows rapid involuntary responses.

What are central pattern generators (CPGs)?

They are spinal/brainstem neural circuits that generate rhythmic motor patterns such as stepping or respiration without needing continuous rhythmic input.

Why are CPGs important in spinal cord injury research?

They may help explain how locomotor function can be partly restored using rehabilitation and electrical stimulation.

What causes spina bifida?

Spina bifida is caused by failed neural tube closure during development.

What is myelomeningocele?

It is a severe open form of spina bifida in which spinal tissue protrudes and is exposed, leading to damage.

How does lesion level affect outcome in spina bifida?

Higher lesions generally produce more severe motor and bowel/bladder dysfunction, while lower lesions may allow better mobility.

What maternal factors increase the risk of neural tube defects?

Folate deficiency, obesity, and some drugs such as valproate and carbamazepine.

How does folic acid help prevent neural tube defects?

Maternal folic acid supplementation can reduce the risk of neural tube defects by up to 80%.

What is the difference between complete and incomplete spinal cord injury?

Complete injury causes total loss of sensory and motor function below the lesion, while incomplete injury preserves some function.

What are the main mechanical causes of primary spinal cord injury?

Hyperflexion, hyperextension, rotation, and axial compression.

Why is spinal cord damage often central rather than peripheral in compression injuries?

Compression produces greatest deformation centrally, causing haemorrhage, and grey matter is more vascular and vulnerable than white matter.

What is secondary injury in spinal cord trauma?

It is the delayed worsening of damage after the initial trauma due to cell death, ischaemia, free radicals, axon die-back, inflammation, and scar formation.

Why does the adult spinal cord regenerate poorly?

Because of cell loss, demyelination, inhibitory myelin molecules, and a non-permissive scar rich in molecules such as CSPGs and Nogo-A.

What are some important inhibitory molecules that block spinal cord regeneration?

CSPGs, KSPGs, tenascin, Semaphorin-3A, Ephrin-B2, Slit proteins, Nogo-A and MAG.

What is the ASIA scale used for?

It is used to classify the severity of spinal cord injury from complete injury (A) to normal function (E).

What factors determine prognosis after spinal cord injury?

The spinal level of injury, whether the injury is complete or incomplete, the type of injury, and the extent of secondary damage.

What are common complications of spinal cord injury?

Bladder and bowel dysfunction, infections, pressure sores, pneumonia, spasticity, and autonomic dysreflexia.

What is the aim of conventional acute spinal cord injury treatment?

To stabilise the spine, reduce further damage, assess function, and surgically relieve compression if necessary.

Why is even small functional recovery important in spinal cord injury?

Because regaining limited movement, sensation, or bladder/bowel control can greatly improve independence and quality of life.

What kinds of therapies are being explored for spinal cord repair?

Stem cells, scaffolds, peripheral nerve grafts, growth factors, inhibitors of scar/myelin molecules, electrical stimulation, and rehabilitation.

How may electrical stimulation help spinal cord repair?

It may enhance axon growth, reduce die-back, activate regeneration-associated genes, improve spared pathway function, and help re-engage CPGs.

Why is a combinatorial approach likely needed for spinal cord repair?

Because successful repair requires neuroprotection, axon regrowth, overcoming inhibitory barriers, reconnecting circuits, remyelination, and rehabilitation.