Spinal shock occurs after sudden spinal cord injury and is characterized by loss of motor and sensory function below the injury, along with loss of reflexes. It represents a lack of descending facilitation from the brain after damage to upper motor neurons. Spinal shock is thought to be caused by hyperpolarization of neurons below the injury due to loss of supraspinal input. It resolves over time in four phases as reflexes return gradually from the feet upwards over days to months.

1. SPINAL SHOCK
Dr. P S S V HARITHA
M.D general medicine
Neurology I year resident
Date: 5-8-22

2.  Whyte in 1750 - loss of sensation accompanied by motor
paralysis with gradual recovery of reflexes
 The term “spinal shock” - 1840 by Hall
 Bastian in 1890 - complete severance of the spinal cord
resulting in a total loss of motor and sensory function below
the level of the lesion, as well as permanent extinction of
tendon reflexes and muscle tone despite the reflex arc
remains intact.
 Sherrington replaced the term “permanent” with a
“temporary” extinction of the reflexes below the level of the
lesion.

3. Spinal shock occurs mainly in sudden onset of spinal
cord lesion
 traumatic,
 infectious, or
 vascular varieties
rarely seen in slowly progressive lesions such as
tumors of the spinal cord, spondylotic myelopathy,
or multiple sclerosis

4.  Spinal shock - represents a lack of descending
facilitation after upper motor neuron lesions.
 difficult to clinically distinguish between upper and
lower motor neuron lesions after spinal cord injury
due to spinal shock.
 more pronounced in severe spinal cord injury and
at higher neurological levels of injury.

5.  It has been hypothesized that the loss of
supraspinal input leading to hyperpolarization of
neurons is responsible for this physiological
change.
 There have been additional observations that an
upward spread of reflex depression, the Schiff-
Sherrington phenomenon, is not uncommon

6.  The severity of the injury correlates - severity of spinal
shock.
 An injury alters reflexes that occur closest to the insult
first, with those more distal from the transection
presenting later.
 high-level cervical injuries - retention of sacral reflexes,
such as a preserved bulbocavernosus and anal wink.
 The observation that a proximal-to-distal spread of reflex
depression occurs on the order of minutes suggests a
physiological explanation for these changes

7. NEUROPHYSIOLOGICAL MECHANISMS
 Spinal shock can be mediated by synaptic changes
in spinal cord segments below the level of injury,
such as
 by enhancement of presynaptic inhibition and
 high concentration of glycine as a major inhibitory
neurotransmitter, as well as by
 hyperpolarization of spinal motoneurons
 Sherrington’s hypothesis - most explainable
mechanisms - sudden withdrawal of facilitatory
influences of the descending pathways leads to a
disruption of synaptic transmission and
interneuronal conduction.

8. NEUROCHEMICAL MECHANISM
 three to four fold increase of glycine, an inhibitory
amino acid neurotransmitter, in absence or
depression of reflexes during spinal shock
 associated with flaccidity following spinal cord injury
or spinal shock

9.  It is important to delineate blood pressure drops
from circulatory shocks from those of spinal shock
(Table 63.3).
 As there is loss of sympathetic tone, there is
pooling of blood in the venous system and a loss of
sympathetic tone in the cardiovascular system.
 On the one hand, circulatory shock requires
volume replacement, and on the other hand, spinal
shock requires vasopressors. As

11.  As spinal shock resolves, muscle spindle reflexes
return in a caudal-to-cranial direction, except at the
level of injury.
 Over time, a spastic syndrome results

12.  There is no uniform consensus on what constitutes
the cessation of spinal shock.
 Most references define the end of spinal shock with
a return of certain reflexes.
 However, not all reflexes are uniformly depressed in
each patient; reflexic changes are individualized.
 The resolution of spinal shock occurs over a period
of days to months, so
 there is a slow transition from spinal shock to
spasticity that occurs on a continuum

13. TRANSITION IN FOUR PHASES

14. THE FIRST PHASE (0 TO 24 HOURS)
 characterized by areflexia or hyporeflexia.
 the first pathological reflex to appear - the delayed
plantar reflex,
 followed by a series of cutaneous reflexes such as the
bulbocavernosus, abdominal wall, and cremasteric
reflex.
 Impaired sympathetic control - bradyarrhythmias,
atrioventricular conduction block, and hypotension.
 Motor neuron hyperpolarization explains the
changes that occur

15. PHASE 2 (DAY 1 - DAY 3 )
 Cutaneous reflexes - prominent
 deep tendon reflexes remain mute.
 elderly individuals and children - recovery of deep
tendon reflexes during this time.
 The Babinski sign may become apparent in the elderly as
well.
 Denervation supersensitivity and receptor
upregulation

16. PHASE 3 (4 DAYS - 1 MONTH)
 Deep tendon reflexes usually recuperate by day 30.
 The recovery of the Babinski response closely parallels
the return of the ankle jerk reflex.
 There is also diminution of the delayed plantar reflex.
 Autonomic changes such as bradyarrhythmias and
hypotension begin to subside.
 Axon-supported Synapse Growth.

17. PHASE 4 (1 TO 12 MONTHS)
 hyperactive reflexes
 Vasovagal hypotension and bradycardia generally
resolve in 3–6 weeks, but orthostatic hypotension may
take 10–12 weeks before it disappears.
 Episodes of malignant hypertension or autonomic
dysreflexia (AD) begin to appear during this time period.
 Soma-supported synapse growth accounts for these
findings.