Degenerative, Toxic, Bacterial CNS Disorders

Question 1

What results from secondary injuries (increased ICP, hemorrhage, ischemia) associated with traumatic brain injuries?

Answer 1

(Edema, neuronal and axonal injury, and cellular death)

Question 2

What are the most important diagnostics to perform in cases of TBI?

Answer 2

(Neurological examination and assessing hydration/blood pressure; otherwise rads and CT)

Question 3

What are the main treatment goals of a TBI?

Answer 3

(Decrease ICP while maintaining adequate cerebral blood flow (done with hypertonic saline and judicious fluid therapy), decrease inflammation and pain (flunixin, +/- gabapentin, acetaminophen), prevent sepsis if there is an open fracture (oxytet), maintain standing, and treat seizures if they occur)

Question 4

What is the main, obvious difference between equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (aka electronic dance music) [eNAD & EDM] and equine motor neuron disease [EMND]? Besides C/S.

Answer 4

(eNAD & EDM are genetic, EMND is not)

Question 5

What is the anatomical difference between eNAD and EDM? )

Answer 5

(eNAD lesions are confined to the caudal medulla oblongata, EDM lesions are more widespread and include demyelination within the ascending tracts of the spinal cord

Question 6

What type of inheritance pattern applies to eNAD and EDM?

Answer 6

(Autosomal dominant incomplete penetrance → if parent has it, foal will get it (autosomal dominant) but dz process can be intervened and prevented (incomplete penetrance))

Question 7

(T/F) Once clinical signs of eNAD and EDM are present, vitamin E supplementation will not improve neurological deficits.

Answer 7

(T, tho may halt progression of dz and will tx other vitamin E deficiency assc. dzs which can improve overall health and well-being)

Question 8

What is the target serum vitamin E value for prevention of eNAD and EDM in horses with higher risk?

Answer 8

(> 3 ug/ml)

Question 9

What are the clinical signs associated with eNAD and EDM?

Answer 9

(Symmetric ataxia and CP deficits in all limbs, will have an abnormal stance at rest, both thoracic and pelvic limbs will be weak and spastic with the pelvic limbs potentially being worse, and excessive hypermetria when head is elevated; variably some ppl note decreased menace and lack of fight/flight)

Question 10

Compare and contrast the clinical signs associated with subacute versus chronic equine motor neuron disease.

Answer 10

(Subacute → symmetrical muscle atrophy, muscle fasciculations, weight shifting, toe dragging, weakness; chronic → poor performance, failure to gain weight, symmetrical muscle atrophy not as severe as subacute)

Question 11

How is a definitive diagnosis of equine motor neuron disease obtained?

Answer 11

(By biopsying the sacrocaudalis dorsalis muscle)

Question 12

Equine dysautonomia (aka grass sickness) is an acquired degenerative polyneuropathy that predominantly affects neurons of which subsections of the nervous system?

Answer 12

(Autonomic and enteric)

Question 13

What are some signs that indicate facial nerve paralysis in a case of THO?

Answer 13

(Exposure keratitis (chronic non-healing corneal ulcer), decreased lacrimation, ear droop, and lip droop)

Question 14

What are some signs that indicate vestibular disease in a case of THO?

Answer 14

(Head tilt, nystagmus, strabismus, and base-wide ataxia)

Question 15

What are some differential diagnoses for CN VII and CN VIII signs?

Answer 15

(THO, guttural pouch dz, traumatic injury to base of the skull, otitis media/interna, EPM, and extracranial or brainstem neoplasia)

Question 16

What is the most sensitive diagnostic to pursue in a case of THO?

Answer 16

(CT, rads are least sensitive, then endoscopy, then CT)

Question 17

What is the surgical treatment for a THO?

Answer 17

(Ceratohyoidectomy → removal of the ceratohyoid releases pressure and eliminates movement at the temporohyoid joint)

Question 18

Horses with hyperammonemia will have bilateral forebrain dysfunction that may be permanent, particularly in chronic cases; what clinical signs will they exhibit?

Answer 18

(Behavior changes, circling, head pressing, central blindness, stertorous breathing, +/- seizures; will often have concurrent signs of hepatic insufficiency or enterocolitis)

Question 19

What is the purpose in treating hyperammonemia with oral lactulose?

Answer 19

(It acidifies the GI content which converts NH3 to NH4+ which will trap it in the lumen of the gut)

Question 20

What is the causative agent of equine leukoencephalomalacia?

Answer 20

(Fusarium moniliforme which typically colonizes corn)

Question 21

Fumonsin toxicity results in liquefactive necrosis and malacia of what portion of the CNS? )

Answer 21

(White matter → will have multifocal brain signs of circling, ataxia, blindness, and seizures

Question 22

What is the prognosis for equine leukoencephalomalacia?

Answer 22

(<10% of horses survive)

Question 23

What are some of the poor prognostic indicators for TBIs?

Answer 23

(If the fracture is basilar (7.5x more likely to not survive) or if the horse is recumbent for >4 hours (18x more likely to not survive))

Question 24

What does the prognosis for hepatic encephalopathy depend on?

Answer 24

(The severity of the underlying liver disease, for intestinal hyperammonemia → 39% survived to discharge and recovered)