CHAPTER 16
Control of Posture & Movement 249SPINAL SHOCK
In all vertebrates, transection of the spinal cord is followed by a
period of
spinal shock
during which all spinal reflex responses
are profoundly depressed. Subsequently, reflex responses re-
turn and become hyperactive. The duration of spinal shock is
proportionate to the degree of encephalization of motor func-
tion in the various species. In frogs and rats it lasts for minutes;
in dogs and cats it lasts for 1 to 2 h; in monkeys it lasts for days;
and in humans it usually lasts for a minimum of 2 wk.
The cause of spinal shock is uncertain. Cessation of tonic bom-
bardment of spinal neurons by excitatory impulses in descending
pathways undoubtedly plays a role, but the subsequent return of
reflexes and their eventual hyperactivity also have to be
explained. The recovery of reflex excitability may be due to the
development of denervation hypersensitivity to the mediators
released by the remaining spinal excitatory endings. Another
possibility for which there is some evidence is the sprouting of
collaterals from existing neurons, with the formation of addi-
tional excitatory endings on interneurons and motor neurons.
The first reflex response to appear as spinal shock wears off
in humans is often a slight contraction of the leg flexors and
adductors in response to a noxious stimulus. In some patients,
the knee jerk reflex recovers first. The interval between cord
transection and the return of reflex activity is about 2 weeks in
the absence of any complications, but if complications are
present it is much longer. It is not known why infection, mal-
nutrition, and other complications of SCI inhibit spinal reflex
activity. Once the spinal reflexes begin to reappear after spinal
shock, their threshold steadily drops.LOCOMOTION GENERATOR
Circuits intrinsic to the spinal cord can produce walking
movements when stimulated in a suitable fashion even after
spinal cord transection in cats and dogs. There are two
loco-
motor pattern generators
in the spinal cord: one in the cervi-
cal region and one in the lumbar region. However, this does
not mean that spinal animals or humans can walk without
stimulation; the pattern generator has to be turned on by tonic
discharge of a discrete area in the midbrain, the mesencephalicCLINICAL BOX 16–2
Uncal Herniation
Space-occupying lesions from large tumors, hemorrhages,
strokes, or abscesses in the cerebral hemisphere can drive
the uncus of the temporal lobe over the edge of the cere-
bellar tentorium, compressing the ipsilateral cranial nerve
III
(uncal herniation).
Before the herniation these patients
experience a decreased level of consciousness, lethargy,
poorly reactive pupils, deviation of the eye to a “down and
out” position, hyperactive reflexes, and a bilateral Babinski
sign (due to compression of the ipsilateral corticospinal
tract). After the brain herniates, the patients are decere-
brate and comatose, have fixed and dilated pupils, and eye
movements are absent. Once damage extends to the mid-
brain, a
Cheyne–Stokes respiratory pattern
develops,
characterized by a pattern of waxing-and-waning depth of
respiration with interposed periods of apnea. Eventually,
medullary function is lost, breathing ceases, and recovery is
unlikely. Hemispheric masses closer to the midline com-
press the thalamic reticular formation and can cause coma
before eye findings develop
(central herniation).
As the
mass enlarges, midbrain function is affected, the pupils di-
late, and a decerebrate posture ensues. With progressive
herniation, pontine vestibular and then medullary respira-
tory functions are lost.FIGURE 16–8
Decerebrate and decorticate postures. A)
Damage to lower midbrain and upper pons causes decerebrate posturing in which
lower extremities are extended with toes pointed inward and upper extremities extended with fingers flexed and forearms pronate. Neck and head
are extended.
B)
Damage to upper midbrain may cause decorticate posturing in which upper limbs are flexed, lower limbs are extended with toes
pointed slightly inward, and head is extended.
(Modified from Kandel ER, Schwartz JH, Jessell TM [editors]:
Principles of Neural Science,
4th ed. McGraw-Hill, 2000.)
B Upper midbrain damageA Upper pontine damage