spinal shock

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.