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Chapter 9- The Spinal Cord

Terms in this set (67)

Rachischisis
occurs when the neural folds do not join at the midline and the undifferentiated neuroectoderm remains exposed
Rachischisis Totalis
(or holorachischisis), the entire spinal cord remains open
Rachischisis Partialis
(or merorachischisis) is the situation in which the spinal cord is partially closed and partially flayed open
A failure of the anterior neuropore to close resulting in a failure of the skull and the underlying brain to properly develop:
while commonly called anencephaly (meaning without brain) the term meroanencephaly (meaning without part of brain) is actually more accurate since the brainstem may be fairly intact but the forebrain and cerebellum are largely absent
Not compatible with life
Rachischisis and meroanencephaly, in most cases (particularly the latter) are
If the neural tube develops normally, but the surrounding vertebrae doesn't form properly, it will result in:
1) Spina bifida occulta characterized by partially missing vertebral arches; the area of the defect may be indicated by a patch of dark hairs
2) Spina bifida cystica is seen as enlargements that may contain only meninges and CSF (meningocele) or meninges, CSF, and portions of the spinal cord (meningomyelocele)
Sensory information is brought to the spinal cord by
neuronal processes whose cell bodies reside in the posterior root ganglia
The central processes of these neurons penetrate the spinal cord, and the peripheral processes pass outward in the spinal nerves to innervate body structures
Sensory input originates from:
1) Body surface (GSA)
2) Deep structures such as muscles, tendons, and joints (GSA)
3) Internal organs (GVA)
Exteroceptive fibers arise from:
1) Receptors that are sensitive to mechanical, thermal, or chemical stimuli that may cause tissue damage
2) Receptors sensitive to discriminative touch or vibratory stimuli
GSA fibers are further classified as either
exteroceptive or proprioceptive
Fibers carrying information from receptors sensitive to mechanical, thermal, or chemical stimuli (Aδ and C) are
slow conducters (0.5 to 30 m/s) and unmyelinated, or lightly myelinated, and they enter the cord via the lateral division of the posterior root; these fibers may ascend or descend (or both) in the posterolateral tract (tract of Lissauer) before entering the posterior horn to terminate primarily in laminae I to V
Fibers carrying information from receptors sensitive to discriminative touch or vibratory stimuli (Aβ) are
rapidly conducing (30 to 70 m/s) and heavily myelinated, and they enter the cord through the medial division of the posterior root
After entering the posterior funiculus, exteroceptive fibers
may give rise to ascending or descending collaterals
Proprioceptive fibers originate
from receptors located in muscles, tendons, or joints that are sensitive to stretch or pressure; some vibratory sense is also conveyed by these fibers
The central processes of these proprioceptive fibers
(and of the heavily myelinated exteroceptive fibers) may directly enter, and ascend in, the posterior columns, or they may branch into the spinal gray to synapse in relay nuclei (such as posterior nucleus of Clarke) or on cells in the anterior horn that participate in spinal reflexes
The spinal nerve also conveys sensory information from
thoracic, abdominal, and pelvic viscera; this interoceptive input originates primarily from receptors that are sensitive to nociceptive stimuli and is conveyed via GVA fibers
GVA fibers travel through
the splanchnic nerves and traverse the sympathetic chain and white communicating ramus to enter the spinal nerve;
there central processes enter the lateral division of the posterior root and terminate in laminae I and V to VII.
These GVA fibers are also lightly myelinated and slowly conduction (1 to 20 m/s)
The phenomenon of deafferentation pain occurs when
the anatomic pathways for pain perception, that being intact nerve rootlets, tracts and nerves themselves, are partially or entirely disrupted
The Condition of deafferentation pain may develop following:
1) Amputation (traumatic or otherwise)
2) Peripheral nerve injury
3) Lesions of central tract resulting in hemiplegia, quadriplegia or paraplegia
4) Damage to the posterior rootlets at the rootlet-cord interface
Deafferentation pain may be perceived as:
1) Dull and aching
2) Pins-and-needles (sharp pain)
3) Searing
4) Burning sensations
The mechanism for deafferentated pain is likely due to
a combination of an increased sensitivity of the central (disconnected/damaged) neurons, plasticity changes in the damaged cell groups, and a decrease in central inhibition at the lesion site
Avulsion of the posterior rootlets,
commonly seen in accidents involving motorcycles, is the forceful separation (avulsion, a pulling or tearing out) of the posterior roots from the spinal cord, more often in the brachial plexus
One treatment for the avulsion of the posterior rootlets is
the DREZ (dorsal root entry zone) or PREZ (posterior root entry zone) procedure in which a small electrode is placed into the posterior horn at the entry zone and radiofrequency lesions are made at the levels of the avulsed roots
Significant, or total, relief from pain is seen in 80% to 90% of these patients
Complications of dorsal root entry zone or posterior root entry zone procedures may include
deficits related to the laterally adjacent corticospinal tract with weakness of the upper and/or lower extremity on the same side, or the medially adjacent cuneate fasciculus with loss of proprioceptive and vibratory sensation on the ipsilateral upper extremity
Some patients will describe the proprioceptive problem as a buzzing sensation on the upper extremity on the side of the procedure
Myasthenia gravis,
a neurologic disease characterized by moderate to profound muscle weakness, is closely correlated with the presence of circulating antibodies directed against nicotinic receptor sites on the postsynaptic membrane
o The result is a blockage of transmission at the neuromuscular junction
A characteristic of Myasthenia gravis is
muscle fatigability; as the day progresses muscle fatigue becomes progressively worse
Myastehnia gravis is frequently seen in
patients between 20 and 40 years of age, although younger patients may exhibit symptoms
There are three characteristics of myasthenia gravis:
1) Muscle weakness may wax and wane over periods of minutes or hours, one day, or several days or weeks
2) Muscles controlling eye movement are frequently involved first (40% of patients) resulting in diplopia and ptosis, and are ultimately involved in about 85% of patients; muscles of the pharynx or larynx, face, and extremities may eventually be involved, but almost always in concert with ocular muscles; these patients exhibit dysarthria and dysphagia
3) Weakness responds to the administration of drugs that enhance cholinergic transmission
Afferent fibers in spinal nerves may synapse on
tract cells that relay information to higher levels of the neuraxis, or they may terminate on motor neurons or interneurons, both of which may participate in reflex circuits
Reflexes require an
afferent fiber, interneurons and/or motor neurons, and a target tissue, usually skeletal muscle
Reflexes may be relatively simple and confined to a single cord level (intrasegmental) or complex, involving multiple cord segments (intersegmental)
Certain disease or central nervous system lesions can affect spinal reflexes, resulting in
reflexes that are greatly exaggerated (hyperreflexia), diminished (hyporeflexia), or absent (areflexia)
Numerous reflexes are part of the standard neurologic examination and spinal reflexes are valuable measurers of the viability of the spinal nerve and of the spinal cord
Muscle Stretch Reflex
o Sometimes called tendon reflex or deep tendon reflex, muscle stretch reflex test the integrity of afferent and efferent fibers of the spinal nerve
o This reflex may be elicited by tapping any large tendon (such as the triceps or Achilles); a common example is the knee-jerk or quadriceps stretch reflex
How the Muscle Stretch Reflex works
o A brisk tap on the patellar tendon stretches the primary sensory endings in muscle spindles located in the quadriceps femoris muscle, sending an impulse toward the posterior root ganglion via heavily myelinated, rapidly conducting group Ia fibers
o The central processes of these afferent axons synapse on and excite motor neurons in the anterior horn that innervate the quadriceps femoris muscle
o The result is a sudden contraction of these muscles and an extension (dorsiflexion) of the leg at the knee
Muscle Stretch Reflex Details
Because this reflex requires only one synapse and is a response to muscle stretch, it also may be called a monosynaptic stretch reflex or myotatic reflex
Reciprocal and autogenic inhibition is an extension of the simple stretch reflex
In reciprocal inhibition,
one group of muscles is excited and the antagonistic group is inhibited
• In this situation, the muscle spindle is stretches by a tap on the patellar tendon, and the impulse enters the spinal cord via a group Ia primary sensory fiber
• Ia primary sensory fiber branches and has excitatory terminations on the quadriceps femoris motor neurons and on group Ia inhibitory (glycinergic) interneurons
• As a result the quadriceps (extensor) contracts, whereas the interneurons inhibit spinal motor neurons innervating the hamstring (flexor) muscles, which remain passive
The receptors involved in autogenic inhibition are the Golgi tendon organ
This receptor responds to relatively high tension (higher than that needed to activate the muscle spindles)
Activation causes an increase in rate of firing of the group Ib sensory fibers that arise from this receptor
In the spinal cord, these fibers terminate on group Ib inhibitory (glycinergic) interneurons, which inhibit motor neurons that innervate the muscle attached to the tendon from which the afferent volley originated
Radiculopathy
is a result of damage to a nerve root
The most common cause is spondylolysis or intervertebral disc disease with resultant damage to one, or more, nerve roots
Due to the overlap of dermatomes on the body, compression of a single root may
not cause significant sensory loss
Main symptom experience by patients is perception of a sharp, burning pain (shooting pains) in the dermatomal distribution of the damaged spinal nerve
Cervical disc disease may result in
pain in the base of the neck, over the shoulder, or down the upper extremity
Lumbar disc problems may result in
low back pain or in pain radiating down the lower extremity, as in sciatica
Mononeuropathy is
deficits reflecting the distribution of a single anatomically defined peripheral nerve
Most common cause of mononeuropathy is
trauma; other causes include entrapment or compression syndromes (carpal tunnel syndrome)
Characteristic examples of traumatic mononeuropathy deficits and the damaged nerve are as follows:
1) Deviation of the tongue on protrusion - hypoglossal nerve
2) Loss of flexion adduction and extension of fingers - ulnar nerve
3) Loss of dorsiflexion of the foot and toes - deep peroneal nerve
4) Loss of pronation of the forearm and movements of fingers - median nerve
5) Loss of flexion of the toes - tibial nerve
Carpal tunnel syndrome
One of the more common entrapment mononeuropathies, in which the median nerve is compressed by fluid accumulation in the synovial sheaths of the carpal tunnel, creating a largely sensory deficit (although weakness of some finger muscles may occur)
Symptoms of carpal tunnel syndrome include
(1)numbness, (2)tingling, (3)pain from thumb, index, and middle finger
Treatment of carpal tunnel syndrome is
to section the transverse carpal ligament and relieve the pressure on the median nerve
Polyneuropathy includes
motor and sensory deficits that reflect damage to multiple peripheral nerves
Diabetes mellitus
One of the most common cause of polyneuropathy
Patients may experience numbness and a loss of pain and thermal sensations in the feet (affecting the longest fibers first), progressing up to about the knees, then the same deficits are perceived in the hands progressing up the forearm
In diabetes mellitus
the more distal portions of the fibers are affected first (distal axonopathy), starting in the lower extremity and then progressing to the upper extremity
The small-diameter myelinated and unmyelinated fibers are affected first followed by larger-diameter fibers as the disease progresses
Symptoms of Diabetes Mellitus
Since this sensory loss starts with the feet/legs and jumps to the hand/forearm it is common to describe this pattern as a stocking/glove sensory loss
Patients may also exhibit weakness of distal portions of the extremities and have hyporeflexia
Two examples of lesions that result in loss of function related to peripheral nerves are:
1) Sensory neuronopathy is a loss of cell bodies in the posterior root ganglion that results in a sensory loss that involves both distal and proximal portions of an extremity and may include most or all sensory modalitites
2) Motor neuronopathy is seen in a loss of anterior horn motor neurons with resultant flaccid weakness, muscle fasciculations, and eventual muscle atrophy
Brown-Sequard syndrome is
a functional hemisection of the spinal cord which results in a clinical picture that reflects damage to the lateral corticospinal tract, the ALS, and the posterior columns
A lesion on the right at C4 to C5 will result in:
1) Muscle weakness or paralysis (hemiparesis, hemiplegia) on the right side (corticospinal damage)
2) Loss of pain and thermal sensations on the left side (ALS damage-these fibers cross in the anterior white commissure)
3) Loss of proprioception, vibratory sense, and discriminative touch on the right (gracile and cuneate fasciculi injury)
Lesions to the lateral corticospinal tract, the ALS, and the posterior columns are frequently called
functional hemisections because the cord is not perfectly cut halfway across but may be injured/deformed by, for example, pieces of a damaged vertebrae
The net result is a loss of function on one half of the spinal cord
Cavitation of the central regions of the spinal cord,
as in a small syringomyelia, will frequently damage fibers crossing in the anterior white commissure
The Syringomyelia bundle
conveys fibers from the posterior horn across the midline to enter the ALS on the opposite side
A lesion of they syringomelia will
damage fibers coursing in both directions, resulting in a bilateral loss of pain and thermal sensations that correlate with the damaged levels of the spinal cord
If the lesion is in mid-to-low cervical levels the pain and thermal sensory deficits will fall over the shoulders and arm in a "cape distribution"
A large syrinx that involves the anterior white commissure and extends into the anterior horn results in
a bilateral sensory loss and weakness of the corresponding extremity
Because these lesions are usually in the cervical levels, extension of the syrinx into one anterior horn results in an ipsilateral weakness of the upper extremity; if both anterior horns are involved, the weakness is bilateral
In syringomyelia,
the cavity that develops in the central areas of the spinal cord does not have a lining of ependymal cells and is not an enlargement of the central canal; sometimes this is called noncommunicating syringomyelia to differentiate it from a cystic structure that may connect with the central canal (communicating syringomyelia)
Hydromyelia
Cavitation of the central canal (also called hydrosyringomyelia)
In patients with high cervical lesions,
preserving the ability to breathe becomes a major factor in care
High Cervical Cord Lesion
In addition to the potential for a total loss of sensation for the body below the lesion and of voluntary motor control below the lesion, the phrenic nucleus is located in the central regions of the anterior horn at levels C3 to C7
These phrenic nucleus innervates the diaphragm and in high cervical lesions is disconnected from the centers of the medulla that control breathing
Acute central cervical spinal cord syndrome,
commonly called the central cord syndrome, is an incomplete spinal cord injury
Acute central cervical spinal cord syndrome may result from
hyperextension of the neck (sometimes in patient with bony spurs on the vertebrae) that momentarily occludes blood supply to the cord via the anterior spinal artery
Deficits of Acute Central Cervical Spinal Cord Syndrome include
bilateral weakness of the extremities, more so of the upper than the lower, varying degrees and patterns of pain and thermal sensation loss, and bladder dysfunction
During recovery of Acute Central Cervical Spinal Cord Syndrome
o Function of the lower extremities returns first, bladder function next, and function of the upper extremities last
o Pain and thermal sensations may return at any time, and posterior column sensations are not affected•
Variations on the main themes of Acute Central Cervical Spinal Cord Syndrome may occur
e.g. a spinal cord hemisection at T8 would affect the body below that level but would spare the upper trunk and upper extremity; a lesion involving the posterior columns bilaterally would result in proprioceptive and discriminative touch losses below the level of the lesion but would spare pain and thermal sensations
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