Neuro Flashcards
What are the functions of nociception?
Warning the animal of actual damage to its tissues, predicting when tissue damage is likely to occur, and warning conspecifics of the presence of danger.
How does pain hypersensitivity manifests?
It manifests as hyperalgesia (exaggerated responses to painful stimuli) and allodynia (pain resulting from normally innocuous stimuli)
Mention the pad a that pain response takes.
It starts at the site of injury, where there is transduction of chemical signals from the noxious stimuli into electrical energy. This is followed by transmission of the electrical signal via nerve fibers up the spinothalamic tracts, where modulation may occur in the dorsal horn. Finally, the impulse is projected to the brain where pain perception occurs.
Why are local anesthetic poorly effective people in infected areas?
Local anesthetic shave poor effect in acidic environments such as infected tissues because these compounds are weak bases that must dissociate in an alkaline environment to exert their effect.
What are NMDA receptors?
.
Mention 2 compounds that are used to potential the effect of local anesthetics and how they work.
Magnesium sulfate .- it competitively antagonizes NMDA receptors and their associated ion channels, this reduces central sensitization caused by peripheral nociceptive stimulus
Sodium bicarbonate .- addition of sodium bicarbonate, significantly reduces pain produced by infiltration of lidocaine, likely due to the reduced acidity of the formulation. It also promotes solubility and stability
Describe the 5 grades of neurological gait deficit.
Grade 0: Normal gait
Grade 1: Very subtle deficits, observed by only an experienced clinician
Grade 2: Deficits apparent to an inexperienced clinician
Grade 3: Deficits apparent to laypersons
Grade 4: Severe deficits including stumbling, knuckling at the fetlock, falling
Grade 5: Recumbency and inability to rise
What would be the difference in neurolocalization from an animal that has mild to moderate and one with severe propioceptive and postural deficits?
Mild to moderate proprioceptive and postural deficits would most likely be caused by unilateral lesions rostral to the medulla oblongata (contralateral). Severe proprioceptive and postural deficits would most likely be caused by unilateral lesions in the medulla oblongata or spinal cord (ipsilateral).
What are the 2 types of cervical vertebral stenotic myelopathy (CVSM / Wobbler)?
Type I: There is focal or multifocal stenosis of the vertebral canal, principally (C1 - C6), it worsens on flexion ( dynamic stenosis). Typically younger horses (< 2 years).
Type II: There is bony and soft tissue impingement into the vertebral canal resulting from remodeling of the articular facets of the caudal cervical vertebrae (usually C5 - T1) and stenosis of the cranial vertebral orifice. It is present in all positions of the neck (static stenosis), may also have a dynamic component (worsens during hyperextension). Typically young to middle aged horses at the onset of wobbler signs.
Both syndromes likely involve some combination of aberrations in cartilage, bone development and external trauma that may precede clinical ataxia by many months (perhaps even in utero in the case of type I CVSM 1 ).
How do you calculate intravertebral sagittal ratios for cervical radiographs and what would be indiative of Wobbler?
Behind C2 it is calculated:
(minimal sagittal diameter of the vertebral canal) ÷ (maximal sagittal diameter of the cranial half of the vertebral body)
Both measurements are made perpendicular to the long axis of the vertebral canal.
A value for sagittal ratio (SR) <0.52 from C4 to C6 and <0.54 at C7 predicts spinal cord compression with 89% sensitivity and specificity for diagnosis of spinal cord compression according to the original description.
*In practice, cutoff values of 0.50 for C3-C6 and 0.52 for C7 can be used.
Even horses with static stenosis, (may predominantly have transverse compression), usually have at least one abnormal intravertebral SR.
What are the 2 clinical syndromes associated with Temporohyoid Osteoarthropathy (THO)?
- Non-neurologic - signs may be chronic, include difficulty chewing, nasal discharge, head tossing, ear rubbing, otorrhea, bit resentment, head shyness, and pain on manipulation of the head or ears.
- Neurologic - include acute onset of signs of facial and vestibular nerve dysfunction (ear droop, ptosis, hearing loss, muzzle deviation away from the affected side, corneal ulceration, head tilt toward the affected side, circling, ataxia, nystagmus, and collapse). Damage to the parasympathetic portion of the facial nerve may result in reduced lacrimation. Occasionally, dysphagia and rarely, seizures or sudden death may occur (secondary to fractures extending into the cranial vault).
Which is the diagnostic modality of choice to diagnose THO?
Endoscopy of the guttural pouches (equipment is readily available and evaluations can be performed in the conscious horse).
It has shown to be sensitive in detecting early and advanced, changes at the temporohyoid joint, including soft tissue inflammation and hemorrhage, osseous proliferation, enlargement of the stylohyoid bone, and previous sites of fractures.
- Always evaluate the contralateral guttural pouch, as some horses have bilateral disease.
Define and give the etiology of THO?
Temporohyoid osteoarthropathy is a bony proliferation at the junction of the stylohyoid and petrous temporal bones.
Several etiologies have been proposed but it is likely variable:
- Bony inflammation and remodeling secondarily to extension of otitis media/interna or upper respiratory tract infection.
- Due to primary DJD.
Regardless, there is bony proliferation of the tympanic bulla, proximal stylohyoid bone, and petrous temporal bones, often resulting in arthrosis of the temporohyoid joint and subsequent fracture of the stylohyoid and petrous temporal bones.
Fractures can extend to the basisphenoid and basioccipital bones, resulting in meningitis and brainstem disease (uncommon).
