Neurology Flashcards
Describe a seizure and how they are classified.
An epileptic seizure is the clinical manifestation of excessive and hypersynchronous abnormal neuronal activity in the cerebral cortex. Neurotransmission is regulated by a balance between excitatory and inhibitory stimulation. Seizures occur when excessive excitation or loss of inhibition results in uncontrolled neuron depolarization. Seizure threshold (defined as the number of neurons that must be activated to induce a seizure) is higher in large and adult animals than in small and young ones.
Cluster seizures are ≥2 seizures lasting <5 minutes within a 24‐h period. If seizures last >5 minutes or if full recovery, between them, does not occur, the condition is defined as status epilepticus.
Seizures are either focal or generalized. They fall under idiopathic, structural, reactive, metabolic or unknown.
10.1111/jvim.12592
In a bovine study looking at seizures, what were the main classifications and etiology of seizures?
Most cases of seizures in our population of cattle are caused by metabolic disorders and that they can be readily managed, with complete remission of seizures. Some permanent visual deficits remained in a few animals with CCN, but the visual deficits did not preclude the possibility of breeding these calves.
The definitive cause of reactive seizures was diagnosed as hypomagnesemia (n = 2), hypocalcemia (n = 12), and hypomagnesemia‐hypocalcemia (n = 16). The cause of structural seizures was diagnosed as cerebrocortical necrosis (n = 8), inflammatory diseases (n = 4), and lead (Pb) intoxication (n = 1).
10.1111/jvim.12592
How do deficiencies of calcium and magnesium play a role in causing seizures?
Calcium is essential for the transmission of nervous impulses as well as cardiac and skeletal muscle contraction. Its deficiency causes hyperexcitability of the CNS, manifesting as tremor or tetany. Calcium homeostasis is closely related to normal concentrations of Mg2+. Magnesium is an essential cofactor for enzymatic reactions induced by parathyroid hormone (PTH) in bones, kidneys and intestine and for the secretion of the hormone itself.
Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low Ca2+ concentrations. The body responds to serum Ca2+ concentrations below the reference range with the secretion of PTH by the parathyroid glands, mobilizing Ca2+ from the bones, increasing its absorption in the intestines, and stimulating the production of vitamin D by the kidneys. The major initial effect when serum Mg2+ concentration decreases to <1.6 mg/dL is an altered cellular response to PTH, but when concentrations further decrease to <1.2 mg/dL, the secretion of PTH is completely inhibited.
10.1111/jvim.12592
What is the cause of equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy?
Genetic predisposition and deficiency of vitamin E (alpha-tocopherol specifically)
10.1111/jvim.13618
How can neuroaxonal dystrophy/equine degenerative myeloencephalopathy be treated or prevented?
Supplementation must occur in foals with an IM injection of d‐alpha‐tocopheryl acetate, a synthetic formulation of α‐TP, which is combined with selenium (Se), another potent antioxidant. At this time, E‐Se®1 is the only FDA‐approved injectable α‐TP and Se supplement for horses.
10.1111/jvim.13618
Can mares be treated with alpha-tocopherol during gestation to prevent a neuroaxonal dystrophy/equine degenerative myeloencephalopathy foal from being born?
No, a-TP does not pass through the placenta.
HOWEVER, mares that are affected warrant treatment in late gestation because foals receive a large amount of a-TP through colostrum.
10.1111/jvim.13618
How will administration of alpha-tocopherol and selenium in the first few days of life change whole blood, CSF Se, serum and CSF a-TP levels?
There is a transient and limited increase in whole blood, but not in CSF Se, or in serum and CSF α‐TP concentrations.
10.1111/jvim.13618
Where is the location of disorder in temporohyoid osteoarthropathy? What characterizes this disorder and what are some proposed etiologies? Clinical signs?
THO is disorder of the temporohyoid joint formed by the stylohyoid and petrous temporal bone.
The disorder is characterized by bony proliferation, fusion of the joint, and potential fracture of the involved or adjacent bones.
Proposed etiologies include inflammation, infection of the middle/inner ear secondary to a hematogenous or ascending infection from the upper respiratory tract, extension of external ear infection, and primary degenerative process.
Clinical signs vary from head shaking, apparent resentment of manipulation of the head or ears, resistance to the bit, difficulty eating, and neurologic deficits mainly consisting of facial and vestibulocochlear nerve dysfunction.
Vestibular and facial nerve dysfunction is commonly observed in horses with THO.
10.1111/jvim.13654
What are treatment options for THO?
Medical: Abx, NSAIDs, IV fluids and monitoring
Surgical: ceratohyoid ostectomy, ipsilateal stylohyoid ostectomy
10.1111/jvim.13654
Auditory loss and other nerve dysfunctions are a common in horses with THO. In a study evaluating neurologic return to function, what were the results?
Auditory loss appears to be permanent regardless of medical or surgical intervention.
The most common signs included auditory loss (100% of horses), vestibular and facial nerve dysfunction (83%), and exposure ulcerative keratitis (71%). Concurrent left laryngeal hemiparesis was observed in 61% of horses through endoscopy.
10.1111/jvim.13654
What is equine motor neuron disease?
This is a neurodengenerative disorder of the somatic lower neurons, resulting in progressive weakness, muscle atrophy and weight loss.
Etiology is unknown, but Vitamin E deficiency plays a role. Patients may have problems absorbing Vitamin E. Diet, management, environment and genetics may also play a role.
10.1111/jvim.13944
What muscle samples are best for diagnosing equine motor neuron disease?
M. sacrocaudalis dorsaslis medialis and M. gluteus medius
10.1111/jvim.13944
What are some post-mortem findings in 5 severely affected horses with EMD?
- Low serum levels of Vit E.
- Changes in muscle histopathology (neurogenic atrophy)
- Spinal cord lesions (neuronal chromatolysis in ventral horns
- Intestinal inflammation (catarrhal enteritis, edema and eosinophilic infiltrate) associated with the presence of giant ciliated protozoa
10.1111/jvim.13944
What histologic lesions are characteristic of NAD/EDM? What are those characteristic of EMND?
NAD/EDM: alterations detected histologically include dystrophic, often vacuolated, neurons and their axons, axonal spheroids with axonal loss and demyelination, neuronal loss, lipofuscin pigment accumulation, astrogliosis, and microgliosis.
EMND: loss of Nissl granules in the neurons of the ventral horn, particularly in the lumbar and sacral segments, as well as angular myofiber atrophy of both fiber types.
10.1111/jvim.13944
What is the importance of finding an eosinophilic enteritis in 5 severely affected horses with EMND?
Although a cause‐effect relationship is difficult to establish, intestinal inflammation might have led to reduced vitamin E absorption, thus favoring the development of MND. The main limitation of this study is the absence of an antemortem demonstration of vitamin E malabsorption. The giant protozoa observed in the intestinal mucosa shared morphologic characteristics with Balantidium coli.
The possible association between MND and eosinophilic enteritis reported here could provide new perspectives for the etiopathogenesis of EMND. Based on the cases reported here, it may be beneficial to include a detailed gastrointestinal evaluation in the diagnostic work‐up of young horses with MND.
10.1111/jvim.13944
