Page 850 - Clinical Small Animal Internal Medicine

818 Section 8 Neurologic Disease

can be observed in animals with neck pain. An animal systems. Some disease processes encompass both nocic-
VetBooks.ir with pain localized to the lumbosacral area will have its eptive/inflammatory and neuropathic pain mechanisms.
pelvic limbs tucked under the caudal abdomen.

Postural Reaction Deficits Loss of Nociception
Various postural reactions (paw replacement, hopping, Nociception (pain sensation) is considered the most
hemiwalking, wheelbarrow, extensor postural thrust) important prognostic indicator for functional recovery of
can further define the location and symmetry of the myelopathy. In dogs with thoracolumbar Hansen type I
weakness. Asymmetric weakness is common with vascu- intervertebral disc herniation, the majority of those with
lar, inflammatory, and compressive myelopathies. intact nociception have an excellent prognosis. Dogs with
loss of nociception longer than 24–48 hours prior to sur-
gery have a poorer prognosis for return of ambulatory
Spinal Reflex Abnormalities
function. If surgery is performed within 12–36 hours, the
Spinal, myotatic, and withdrawal reflexes can assist with prognosis is better for more rapid and complete recovery.
neuroanatomic localization to specific spinal regions In spinal fractures, however, animals with loss of nocicep-
(see Table 76.1). Presence of hypo‐ to areflexia of limb tion are assumed to have complete injury of neural tissues
reflexes can localize the lesion to within an intumes- and have a poor prognosis for recovery.
cence. The cutaneous trunci reflex can further assist
with localization of a thoracolumbar spinal cord lesion.
Acute Spinal Cord Dysfunction

Hyperesthesia
It is important to recognize specific physical and neuro-
Hyperesthesia denotes an unpleasant behavioral logic examination findings associated with acute spinal
response to a nonnoxious stimulus. As part of a routine cord injury. Neurogenic shock is a systemic complication
neurologic examination, spinal hyperesthesia is evalu- associated with severe cervical or cranial thoracic injury
ated by deep palpation of the spinal epaxial musculature to the spinal cord. This syndrome results from sympa-
and by detecting resistance with flexion‐extension and thetic loss (decreased blood pressure and heart rate result-
lateral movements. Testing for spinal hyperesthesia ing from unopposed vagal tone) and continual vagal tone.
should be performed near the end of the neurologic This phenomenon results in loss of spinal cord blood flow
examination. Spinal palpation should begin distal to the regulation and subsequent ischemia. Neurogenic shock
suspected lesion localization. Cervical spinal hyperes- resolves with fluid therapy and pressor agents.
thesia can be elicited by deep palpation of the cervical Spinal shock usually manifests as flaccidity of the limbs
spinal musculature near the vertebral transverse pro- distal to the lesion. The spinal reflexes are depressed to
cesses. Clinical signs include caudal flinching of the ears, absent. The bladder may be flaccid with urine retention
twitching spinal musculature, and behavioral signs of and the sphincter hypotonic. This phenomenon may
discomfort. The neck is manipulated by flexion, exten- mislead a neuroanatomic localization if neurologic
sion, and lateral movements. Normal animals have full examination is not reassessed. The duration of spinal
range of movement with no resistance. Resistance or shock is proportional to the degree of species encephali-
behavioral reluctance to move is evidence of spinal pain. zation and thus may last only a few hours in quadrupeds.
Meningeal pain often is diffuse but will commonly local- Cause may be cessation of tonic input of spinal neurons
ize to the cervical spine. Joint and muscle pain are by excitatory impulses in descending pathways.
assessed during palpation and evaluating range of motion The Schiff–Sherrington posture is characterized by
of the limbs. increased extensor tone of the thoracic limbs and flaccid
Differentials associated with spinal hyperesthesia paralysis of the pelvic limbs after acute T3–L3 spinal cord
include those associated with inflammation or compres- lesions. “Border cells,” which exert inhibitory influences
sion (e.g., intervertebral disc herniation, neoplasia). on extensor motor neurons of the thoracic limbs via the
Anatomic structures with nociceptors include the menin- fasciculus proprius, are predominantly located in the L2–4
ges, nerve roots, outer one‐third of the disc, joints, peri- spinal cord segments. Damage to these cells or interrup-
osteum, and muscle. Tissue damage or inflammation tion of the fasciculus proprius as it ascends through the
produces pain through stimulation of nociceptors that are thoracolumbar spinal cord causes release of thoracic limb
sensitive to mechanical, thermal, and chemical stimuli. extensor motor neurons and hypertonia. Despite the
Neuropathic pain occurs with injury to neural tissue and increase in extensor tone, the thoracic limbs are neuro-
represents abnormalities in transmission and somatosen- logically normal. Schiff–Sherrington posture does not
sory processing in the peripheral and central nervous indicate that the spinal cord lesion is irreversible.