250
SECTION III
Central & Peripheral Neurophysiology
locomotor region, and, of course, this is only possible in pa-
tients with incomplete spinal cord transection. Interestingly,
the generators can also be turned on in experimental animals
by administration of the norepinephrine precursor L-dopa
(levodopa) after complete section of the spinal cord. Progress
is being made in teaching humans with SCI to take a few steps
by placing them, with support, on a treadmill.
BASAL GANGLIA
ANATOMIC CONSIDERATIONS
The term
basal ganglia
(or
basal nuclei
) is generally applied
to five interactive structures on each side of the brain (Figure
16–9). These are the
caudate nucleus, putamen,
and
globus
pallidus
(three large nuclear masses underlying the cortical
mantle), the
subthalamic nucleus,
and
substantia nigra.
The
globus pallidus is divided into external and internal segments
(GPe and GPi). The substantia nigra is divided into a
pars
compacta
and a
pars reticulata.
The caudate nucleus and
putamen are commonly called the
striatum;
the putamen and
globus pallidus are sometimes called the
lenticular nucleus.
The main inputs to the basal ganglia terminate in the stria-
tum (Figure 16–10). They include the excitatory
corticostri-
ate pathway
from M1 and premotor cortex. There is also a
projection from intralaminar nuclei of the thalamus to the
striatum
(thalamostriatal pathway).
The connections between the parts of the basal ganglia
include a dopaminergic nigrostriatal projection from the sub-
stantia nigra pars compacta to the striatum and a correspond-
ing GABAergic projection from the striatum to substantia
nigra pars reticulata. The striatum projects to both GPe and
GPi. GPe projects to the subthalamic nucleus, which in turn
projects to both GPe and GPi.
The principal output from the basal ganglia is from GPi via
the
thalamic fasciculus
to the ventral lateral, ventral anterior,
and centromedian nuclei of the thalamus. From the thalamic
nuclei, fibers project to the prefrontal and premotor cortex.
The substantia nigra also projects to the thalamus. These con-
nections, along with the probable synaptic transmitters
involved, are summarized in Figure 16–10.CLINICAL BOX 16–3
Spinal Cord Injury
It has been estimated that
the worldwide annual incidence
of sustaining
spinal cord injury (SCI)
is between 10 and 83
per million of the population. Leading causes are vehicle ac-
cidents, violence, and sports injuries. The mean age of pa-
tients who sustain an SCI is 33 years old, and men outnum-
ber women with a nearly 4 to 1 ratio. Approximately 52% of
SCI cases result in quadriplegia and about 42% lead to para-
plegia. In quadriplegic humans, the threshold of the with-
drawal reflex is very low; even minor noxious stimuli may
cause not only prolonged withdrawal of one extremity but
marked flexion–extension patterns in the other three limbs.
Stretch reflexes are also hyperactive. Afferent stimuli irradi-
ate from one reflex center to another after SCI. When even a
relatively minor noxious stimulus is applied to the skin, it
may activate autonomic neurons and produce evacuation of
the bladder and rectum, sweating, pallor, and blood pres-
sure swings in addition to the withdrawal response. This dis-
tressing
mass reflex
can sometimes be used to give para-
plegic patients a degree of bladder and bowel control. They
can be trained to initiate urination and defecation by strok-
ing or pinching their thighs, thus producing an intentional
mass reflex. If the cord section is incomplete, the flexor
spasms initiated by noxious stimuli can be associated with
bursts of pain that are particularly bothersome. They can be
treated with considerable success with baclofen, a GABA
B
receptor agonist that crosses the blood–brain barrier and fa-
cilitates inhibition.Treatment of SCI patients presents complex problems. Ad-
ministration of large doses of
glucocorticoids
has been shown
to foster recovery and minimize loss of function after SCI. They
need to be given soon after the injury and then discontinued
because of the well-established deleterious effects of long-
term steroid treatment. Their immediate value is likely due to
reduction of the inflammatory response in the damaged tissue.
Due to immobilization, SCI patients develop a negative nitro-
gen balance and catabolize large amounts of body protein.
Their body weight compresses the circulation to the skin over
bony prominences, causing
decubitus ulcers
to form. The ul-
cers heal poorly and are prone to infection because of body
protein depletion. The tissues that are broken down include
the protein matrix of bone and this, plus the immobilization,
cause Ca
2+
to be released in large amounts, leading to
hyper-
calcemia, hypercalciuria,
and formation of
calcium stones
in
the urinary tract. The combination of stones and bladder paral-
ysis cause urinary stasis, which predisposes to
urinary tract in-
fection,
the most common complication of SCI. The search
continues for ways to get axons of neurons in the spinal cord to
regenerate. Administration of
neurotrophins
shows some
promise in experimental animals, and so does implantation of
embryonic stem cells
at the site of injury. Another possibility
being explored is bypassing the site of SCI with
brain–com-
puter interface devices.
However, these novel approaches are
a long way from routine clinical use.