In one breath
Posture and movement are integrated at six levels of the CNS, and each level is studied by cutting the neuraxis below it: because the higher centres normally hold the lower ones back, the motor activity that survives a cut is usually exaggerated — the release phenomenon. Cut below the medulla and you have a spinal animal, which passes through shock, then recovery, then failure. In shock everything below the cut is flaccid, areflexic and anaesthetic; in recovery the flexors come back first (paraplegia in flexion) and the extensors much later (paraplegia in extension). Even alone, the cord can still withdraw a limb, give supporting reactions, and — with the right stimulus — generate walking.
Builds on: Movement and organization of the motor system · Stretch reflex · Withdrawal reflex · Leads to: Medullary integration and decerebrate rigidity · Upper vs lower motor neuron lesions
Levels of integration
Posture and movement are regulated at six levels, from the bottom up:
- Spinal cord
- Medulla
- Midbrain
- Cortex
- Basal ganglia
- Cerebellum
- At cord level an afferent input buys you a simple reflex. The higher you go up the neuraxis, the more the same input changes motor behaviour as a whole, and the more complex the response.
- To find out what any one centre contributes, separate it from the centres above it — in experimental animals, by cutting the neuraxis at that level.
Release phenomenon
Cut the neuraxis and the motor activity run by the centres below the cut is usually stepped up, not lost. That accentuation is the release phenomenon, and it lets the final motor output through more freely. Two reasons:
- The lower centre is freed from inhibition by the centres above it.
- Denervation hypersensitivity of the centre below the cut.
Draw it: where each cut is made
Draw the neuraxis as a vertical column and label from the top: cerebral cortex (with basal ganglia tucked beside it), midbrain with its two pairs of colliculi, pons, cerebellum hanging off the back, medulla, then the spinal cord with C5 and the mid-thoracic level marked. Now put in four cuts, each with an arrow and the name of the animal it makes: cortex removed = decorticate; upper border of the midbrain = midbrain animal; between the superior and inferior colliculi (midcollicular) = decerebrate; below the medulla = spinal. Against each cut write the highest reflex that survives it — hopping and placing (cortex), righting (midbrain), antigravity tone (medulla), spinal reflexes (cord).
Postural reflexes
These are reflexes integrated at various CNS levels that, once triggered, produce the motor response the moment needs. They do three jobs:
- hold the body in a balanced posture,
- give movement a steady background to happen against,
- and keep adjusting posture while the movement is going on.
They fall into two classes:
| Class | What it does | Examples |
|---|---|---|
| Phasic (dynamic) | Short-lived, transient movements for an immediate change in posture and quick adjustments | Phasic stretch reflex, righting reflexes, vestibular placing reactions |
| Tonic (static) | Sustained muscle contraction; mainly a stable background for holding a posture, and adjusts posture during movement | Tonic stretch reflexes, tonic neck reflexes, tonic labyrinthine reflexes |
What the cord does on its own
Four motor jobs belong to the spinal cord:
- It holds the circuitry for spinal reflexes — the basic postural reflexes that give an immediate change in output, such as pulling a limb away from something painful.
- It holds circuitry that can change motor neuron output to set muscle tone. Chiefly, altering γ motor neuron discharge changes how sensitive the spindle is to stretch, and that shifts tone. The γ neurons are themselves driven mostly by the descending fibres.
- It holds a pattern generator for locomotion, which on suitable stimulation produces basic movements such as walking.
- The tonic stretch reflex, run in the cord, is essential for holding posture.
The spinal preparation
A spinal animal (usually a cat) is one in which the brain’s influence on the cord has been removed by a section below the medulla.
- Ideally below C5, so that the diaphragm still works and respiration is left intact.
- In practice below the mid-thoracic level, which spares cardiovascular control as well and makes the animal far easier to keep alive.
Three stages follow, in order:
- Stage of shock (stage of flaccidity)
- Stage of recovery (stage of reflex activity)
- Stage of failure
Stage of shock
The moment the cord is cut, spinal shock begins. Sensation and voluntary movement below the lesion are lost at once and for good; on top of that, every spinal reflex response is deeply depressed for a while. This happens in all vertebrates.
How long it lasts
Duration tracks how far motor function has been handed over to the brain (encephalization): the more the brain has taken over, the longer the cord stays silent.
| Animal | Duration of shock |
|---|---|
| Frog | 2–4 minutes |
| Dog, cat | 2–4 hours |
| Monkey | 2–4 days |
| Human | 1–4 weeks |
Mechanism
The exact mechanism is unknown. The best-supported explanation is the sudden loss of the tonic bombardment of the motor neurons by the descending fibres — that is, loss of supraspinal (more exactly, suprasegmental) influence in the acute phase. Three observations support it:
- Areflexia is deeper and longer in species whose cord is more heavily controlled from above.
- If a second cut is made below the first one after recovery, the muscles already affected do not go areflexic again — there is no suprasegmental influence left to lose. So it was the loss of descending influence that caused shock in the first place.
- Recordings show that motor neuron excitability falls after transection.
Features
Below the level of the lesion:
- Flaccid paralysis of all muscles.
- Areflexia: every reflex abolished.
- Anaesthesia: complete loss of all sensation.
At the level of the lesion: cramp-like pain.
Other features
- Bladder and rectum are generally paralysed, though the sphincter vesicae often keeps working or gets going again quickly.
- The penis stays flaccid and erection is impossible.
- Blood pressure: a cut below T1 drops BP as sharply as destroying the vasomotor centre would. The vasoconstrictor fibres leave the cord between T1 and L2, so a cut below L2 barely touches BP.
- With the muscles paralysed the muscle pump stops, so venous return and cardiac output fall steeply and the legs turn blue and cold.
- With the lesion at T6, afferents from the abdominal viscera are cut off, so griping pain and visceral distension are no longer felt.
Shock is not the release phenomenon
The two look like opposites and both follow the same cut. Shock is the early, temporary depression of reflexes; the exaggerated reflexes of the release phenomenon belong to the recovery stage, weeks later. In the viva, give the time course, not just the words.
Stage of recovery
Smooth muscle first
As shock lifts, smooth muscle is the first to work again. The sphincter vesicae recovers very quickly, the detrusor slowly. Paralysed vessels regain tone and BP creeps back to normal.
The first reflexes back
A feeble contraction of the leg flexors to a noxious stimulus is the first reflex response to appear; the adductors also answer a painful stimulus. In some patients the knee jerk is what returns first.
Why recovery happens
Not clearly known. It is probably the segmental influences becoming more effective, through axonal sprouting: entering sensory fibres throw out extra collaterals and spinal interneurons grow extra terminals, and these take over the synaptic space left empty when the cut descending fibres degenerated.
Muscle tone and size
- Skeletal muscle tone returns after 2–3 weeks in man.
- Order of return: flexors of the lower limbs first, then flexors of the upper limbs and trunk. The extensors stay flabby much longer.
- Because flexor tone is the tone that comes back, the body is pulled into a flexed attitude: this is paraplegia in flexion.
- The muscles are paralysed but usually do not waste, because reflex activity keeps working them.
Reflexes that return, one by one
Spontaneous involuntary flexion of the limb occurs, with the small toes separated and lifted. Flexors contract and, by reciprocal inhibition, the extensors let go.
Flexor reflex
- The first reflex to come back, to a noxious stimulus.
- Stroking the outer edge of the sole gives the Babinski sign: the big toe turns up, the other toes fan out, knee and hip flex and the thigh swings outward. The antagonists are inhibited.
- It is a protective withdrawal reflex — it takes the limb off whatever is hurting it.
Mass reflex
Scratching anywhere on the inner thigh or the lower front of the abdominal wall sets off a very widespread response:
- Flexor spasm of the lower limbs with contraction of the anterior abdominal wall.
- Emptying of bladder and bowel, partly just from the rise in abdominal pressure.
- Profuse sweating below the lesion. Sweat fibres reach head and neck from T1–T2 and the arm from T5–T9, so with a lesion at T1 or above the whole body sweats.
It is a late arrival — sometimes several months after the transection.
Coitus reflex
Elicited from the glans penis, or from genital skin nearby:
- the penis swells and stiffens;
- the testis is drawn up (cremaster) and the scrotal skin puckers (dartos);
- hip flexors and thigh abductors contract;
- seminal emission may happen.
Full intercourse, however, is never achieved.
Deep reflexes
- Knee jerk returns 1–5 weeks after the flexor response. The quadriceps contracts well enough but lets go at once, so the limb drops back quickly.
- Ankle jerk returns later, and mild ankle clonus may be found.
Extensor responses
Extensor activity builds up much later: by about six months, tone appears in the extensors and then becomes marked, giving extensor spasm and a body held in extension. This stage is paraplegia in extension. In it:
- Knee and ankle jerks are exaggerated.
- A sudden passive stretch — extending a flexed thigh abruptly, say — throws one or both limbs into reflex extension. Extensors and flexors contract together, turning the limbs into rigid pillars.
- The mass reflex can no longer be obtained.
- The glans still gives the genital response, but now without seminal emission.
Flexion first, extension last
Paraplegia in flexion is the early picture (flexor tone at 2–3 weeks); paraplegia in extension is the late one (about six months). Getting them the wrong way round is the commonest slip on this topic, and note that the mass reflex, which arrives late in the flexion stage, is lost again once extension takes over.
Autonomic reflexes
- The micturition reflex becomes hyperactive. The bladder empties reflexly but never completely. Kept contracted for long enough, its wall hypertrophies and fibroses and its capacity falls: a spastic neurogenic bladder.
- The defecation reflex comes back too, but reflex contraction of the rectum does not empty it fully.
- Blood pressure is normal at rest, but with no baroreceptor feedback it swings widely in different situations.
- Sweating returns and the skin becomes healthy again.
Supporting reactions
Once the spinal reflexes are back their threshold keeps falling: a trivial noxious stimulus can produce a long withdrawal, flexion can repeat itself for a long stretch, and stretch reflexes turn hyperactive. The supporting reactions are the example of this.
- Positive supporting reaction (PSR) — place a finger on the sole of a spinal animal’s foot and then take it away: the limb extends and follows the finger, which is why it is also called the magnet reaction. Receptors are tactile; the afferents are tactile and proprioceptive. The response turns the limb into a rigid pillar that resists gravity, and the other limbs stiffen too and hold the animal up — hence supporting reaction.
- Negative supporting reaction — the PSR does not just fade, it is actively switched off, and that switching off is the negative supporting reaction. The trigger is stretch of the extensor muscles.
The positive supporting reaction is why a spinal cat or dog can be got to stand and even walk — clumsily, and only for about two minutes.
Locomotion generator
That a spinal animal can stand and walk at all means the cord itself holds a walking circuit — its own central pattern generator (CPG).
- There are two spinal CPGs: a cervical one for the upper limbs and a lumbar one for the lower limbs.
- Each is a group of interneurons that drives the motor neurons, producing alternate contraction of flexors and extensors — which is what walking is.
- Injecting glutamate or L-dopa into the cord makes motor neurons fire the rhythmic pattern of locomotion.
- Normally the spinal CPGs are switched on by the mesencephalic locomotion generator (MLG) in the midbrain (see Midbrain integration and righting reflexes). In a spinal animal that drive is cut off, so the CPG has to be stimulated from outside to run.
Stage of failure
In chronic spinal patients, poor nutrition and hygiene and repeated infection or toxaemia finally make reflex activity fail:
- Reflex thresholds rise so reflexes are hard to elicit at all, and the mass reflex disappears.
- Muscles waste and turn flaccid.
- Bedsores form over pressure points and become decubitus ulcers. Protein depletion suppresses immunity, the ulcers heal badly, and septicaemia follows.
- Long immobilization and breakdown of the protein matrix of bone give hypercalcaemia and hypercalciuria, hence urinary stones and repeated urinary infection.
Most such patients used to die of repeated septicaemia and uraemia. Early antibiotics and glucocorticoids, with proper feeding and nursing, now stretch their lives out considerably.
Applied: why nursing decides the outcome
Nearly everything in the stage of failure is preventable, and none of it is neurological: two-hourly turning and pressure care for the bedsores, bladder drainage and fluids for the stones and infection, protein in the diet for healing, and physiotherapy to keep joints moving. The cord lesion is fixed on day one; the stage of failure is not.
Worth knowing, though not in your pages: with a complete lesion at or above T6, a distended bladder or loaded rectum can set off autonomic dysreflexia — a sudden, dangerous rise in blood pressure with a reflex bradycardia, relieved by draining the bladder. It is the same mass-reflex wiring, and it is a medical emergency.
Exam-answer skeleton: "What happens below a complete spinal cord transection? Describe the stages and their features" (long essay)
- Define the spinal animal; where the section is made and why (below C5 for respiration, below mid-thoracic for the circulation). Name the three stages.
- Spinal shock: the immediate permanent losses (sensation, voluntary movement) versus the temporary depression of reflexes. Duration in frog, cat, monkey and man, and encephalization as the reason.
- Mechanism of shock: loss of tonic descending bombardment, with the second-transection evidence.
- Features of shock: flaccidity, areflexia, anaesthesia below the lesion; cramp-like pain at it; bladder, penis, blood pressure (T1, L2), cold blue legs, T6 and visceral sensation.
- Recovery: smooth muscle first, then the flexor reflex; axonal sprouting as the mechanism; tone back at 2–3 weeks in the flexors — paraplegia in flexion.
- The individual reflexes: flexor reflex with the Babinski sign, mass reflex, coitus reflex, deep reflexes, then extensor spasm at about six months — paraplegia in extension. Autonomic reflexes and the spastic neurogenic bladder.
- Supporting reactions (positive, magnet; negative) and the spinal CPGs for locomotion, driven normally by the MLG.
- Stage of failure: raised thresholds, wasting, decubitus ulcers, hypercalciuria and stones, septicaemia — and what good nursing prevents.
Asked in exams
- Spinal shock: Jul 2019, 4 marks
- How the spinal cord and medulla control posture: Aug 2024, 15 marks