ACVIM Required Literature - Neurology Flashcards
Describe the clinical, electrophysiologic, and pathologic features of EDM in a group of 15 related Lusitano horses.
- Neuro exam: 6 normal, 6 abnormal, 3 equivocal gait.
- Abnormal horses: ataxia and paresis 6/6, inconsistent menace response 4/6 abnormal and 1/3 equivocal.
- Low serum Vit E 15/15.
- Bilaterally symmetric, severe, neuro axonal degen in the gracilis, cuneatus medialis, cuneatus lateralis, and thoracicus nuclei and bilaterally symmetric axonal loss and demyelination mainly in the dorsolateral and ventromedial tracts of the spinal cord –> Dx of EDMN.
- The dz appears to have a genetic basis, and although vit E deficiency is a common finding, low serum vit E conc also may occur in apparently unaffected related individuals.
Ref: J. Vet. Intern. Med. 2011; 25(6):1439–1446.
Hypoglycin A, found in seeds of Acer negundo (box elder maple), appears to cause seasonal pasture myopathy in
North America. Acer negundo is uncommon in Europe. Are seeds of Acer pseudoplatanus (sycamore maple) a source of hypoglycin A in Europe?
Yes. Hypoglycin A was detected in all A. pseudoplatanus seeds in highly variable concentrations ranging from 0.04 to 2.81 ug/mg (mean 0.69) on AM farms and 0.10 to 9.12 ug/mg (mean 1.59) on control farms.
Ref: J. Vet. Intern. Med. 2014; 28(4):1289–1293.
What biochemical defect is identified in horses suffering from Atypical Myopathy?
- Multiple Acyl-CoA Dehydrogenase Deficiency (MADD).
- Enzymes impaired in MADD include dehydrogenases that catalyze b-oxidation of short-, medium-, and long-chain fatty acids, and dehydrogenases involved in amino acid and choline metabolism.
- Disruption of enzymatic pathways in MADD leads to accumulation of enzyme-specific substrates (acyl-CoAs) that can be eliminated as acylcarnitines or acylglycines (glycine conjugates). Hence, the presence of specific acylcarnitines in serum and glycine conjugates in urine directly reflects the intramitochondrial accumulation of corresponding acyl-CoA esters.
- Necropsy of 4 AM horses: affected muscle (4/4) showed degeneration with intramyofiber lipid accumulation, decreased free carnitine concentration, and increased carnitine esters. Serum acylcarnitine profiles (3/3) showed increases in short- and medium-chain acylcarnitines and urinary organic acid profiles (3/3) revealed increased ethylmalonic and methylsuccinic acid levels, and glycine conjugates, consistent with equine MADD.
Ref: J. Vet. Intern. Med. 2012; 26(4):1012–1018
List acid-base and shock variable derangements identified in horses with Atypical Myopathy.
- Tachycardia, tachypnea, and normal to increased PCV and BUN were common in AM cases.
- Respiratory, metabolic acid-base alterations, or both were mainly caused by respiratory alkalosis, lactic acidosis, and SID alkalosis, alone or in combination.
- The strong ion model provided a more accurate assessment than the traditional approach and identified mixed derangements.
Ref: J. Vet. Intern. Med. 2013; 27(1):186–193.
Describe the clinical presentation and aetiology of diaphragmatic paralysis in alpacas.
- The 11 alpacas ranged in age from 2 to 12 months.
- Fluoroscopic imaging confirmed the presence of bilateral diaphragmatic paralysis in the 7 alpacas that were imaged. - Arterial blood gas analyses showed hypercapnea, hypoxaemia, and low oxygen saturation.
- 7 died or were euth 2-60 days after onset of resp signs.
- Histo: phrenic nerve degen in the 6 alpacas that were necropsied and additional long nerves demonstrated degen in 2 of these animals, 2 had spinal cord lesions and 2 had diaphragm muscle abnormalities.
- No etiologic agent was identified in the alpacas.
- A variety of medical treatments did not appear to alter the outcome.
Ref: J. Vet. Intern. Med. 2011; 25(2):380–385.
Describe neurologic and clinicopathologic abnormalities in an alpaca with a pituitary adenoma in the pars distalis.
- First CSx were inappetence and obtundation.
- Alpaca had a tendency to walk compulsively and press its head and body against walls without directional preferences or circling. Cranial nerve reflexes, including menace response, were present and appeared within normal limits. Gait analysis indicated a slow pace with asymmetric hypermetria in the hindlimbs (L>R). Spinal reflexes were difficult to assess but appeared normal. In sternal recumbency, the alpaca would lower its neck and press its nose against the ground. Initial neurologic evaluation localized disease to the prosencephalon.
- CBC: hyperfibrinogenemia and a leukocytosis charac
by neutrophilia with a regenerative left shift. - Chem: azotemia, hyperglycaemia, elevated AST, hypohposphataemia; secondary to inappetence.
Ref: J. Vet. Intern. Med. 2012; 26(4):1073–1077.
Describe clinical signs, clinicpathologic and necropsy findings in lambs with hyperthermia (T>104F).
- All cases occurred between July and Sep, with a median heat index of 90.5 for the 3 days before presentation.
- Neruo signs included kyphosis, pelvic limb hyperext, treading of feet, muscle tremors and recumbency.
- CBC, serum chemistry, necropsy, rumen content, virology, brain MRI, liver copper, selenium, and vitamin E failed to identify a consistent etiology for the signs presented.
- The only common factor was high heat and humidity.
- Histo examination identified axonal degeneration and skeletal muscle necrosis in some lambs.
Ref: J. Vet. Intern. Med. 2013; 27(5):1242–1247.
Floppy Kid Syndrome affects kids in the first month of life and is assoc with high morbidity and mortality. The condition is characterszed by neurological signs that can be ascribed to increased plasma D-lactate concentrations. D-lactate-producing bacteria in the large intestine are thought to be involved. Is there a difference in the bacterial in faeces of goats with and without Floppy Kid Syndrome?
- Goat kids with FKS had a mean plasma D-lactate concentration of 10.9 mM compared with 0.3 mM in healthy kids, and significantly greater CFU counts for enterococci, streptococci, staphylococci, and lactobacilli.
- The groups of bacteria present in greater numbers in the faeces of goat kids with FKS include several D-lactate producing species, which makes dysbacteriosis a likely cause of the increased plasma D-lactate conc in FKS.
Ref: J. Vet. Intern. Med. 2013; 27(5):1283–1286.
Describe clinical signs, MRI findings and treatment in an alpaca with caudal occipital malformation syndrome.
- Very thin, dull, lethargic, anorexic.
- Neuro deficits: absent menace L eye, normal PLRs; conscious proprioceptive deficits were obs in all 4 legs.
- MRI: malformation of the caudal occipital bone with herniation/caudal displacement of the caudal cerebellum through the foramen magnum; syringohydromyelia.
- Medical therapy: PPN, fluids, antibiotics, and anti-inflammatory drugs, rumen transfaunation.
- Surgery: suboccipital craniectomy to decompress the foramen magnum; fibrous soft tissues and thickened dura overlying the caudal cerebellum and brainstem were removed. A temporalis facial graft was placed over the craniectomy defect.
- Full recovery; WNL 2 years post-Sx.
Ref: J. Vet. Intern. Med. 2014; 28(2):693–695.
What surgical procedure has been reported in alpacas who fail to respond to medical therapy for cervical vertebral stenotic myelopathy?
- A dorsal laminectomy of C7 and T1 via a dorsal midline approach was performed, and the spinous processes of both vertebrae were removed prior to removal of the overlying lamina.
- Free dorsal expansion of the spinal cord was ensured by resection of the ligamentum flavum.
- Six months after surgery, the alpaca had returned
to successful breeding. The patient was eventually euthanized 28 months after surgery because of neurologic deterioration but was still ambulatory at that time.
Ref: J. Am. Vet. Med. Assoc. 2015; 246(10):1122–1128.
Describe the clinical and pathological findings in a calf with cerebellar medulloblastoma.
- 1mo Holstein, had not stood since birth.
- Presented in lateral recumbency with spastic extension of all four limbs and opisthotonus.
- Mental status and consciousness were normal.
- Menace absent R eye, present L.
- L&R eye dorsomedial strabismus and In both eyes, upward deviation of the visual axis of the left eye (hypertropia) and inward deviation of the visual axis of the right eye (esotropia).
- Other CN tests were normal as were the spinal reflexes.
- Neurolocalisation: right side of the cerebellum
with bilateral involvement of the trochlear nerve and possibly, but less likely, of the other nerves innervating the extraocular muscles (oculomotor and abducent nerves). - PM Dx: Cerebellar meduloblastoma with bilateral trochlear nerve palsy caused by compression of the nerves at the level of their decussation.
Ref: J. Vet. Intern. Med. 2015; 29(4):1117–1121.
List the signalment, age and diagnoses of 43 cattle presenting to the University of Turin for a seizure disorder.
- Mean age: 8 months.
- Gender: 72% male, 28% female.
- Neuro exam soon after admission: 47% normal, 44% forebrain, 7% intracranial, 2% multifocal localisation.
- Reactive seizures (70%): 7% hypomagnesemia, 40% hypocalcemia and 53% hypomagnesemia-hypocalcemia.
- Structural seizures (30%): 62% cerebrocortical
necrosis, 31% inflammatory diseases and 7% Pb intox. - Survival: 83% survived, 12% euth, 5% died.
Ref: J. Vet. Intern. Med. 2015; 29(3):967–971.
Describe clinical and histopathologic characteristics of a central and peripheral axonopathy in Rouge-des-pre´ s (Maine Anjou) calves.
- Age of onset: 2 to 6 weeks.
- Initial signs of pelvic limb ataxia and paraparesis, progressed over 1-3 months to severe pelvic limb and truncal ataxia, moderate paraparesis –> recumbency.
- Animals alert, CN function normal, muscle atrophy was
not observed and spinal reflexes were normal. - Blood tests, CSF analysis, myelographic exam WNL.
- Neuropathology: neuronal fiber degeneration particularly in the dorsolateral and ventromedial funiculi of the spinal cord and in the peripheral nerves. Degenerative lesions also were obs in lateral vestibular and thoracic nuclei.
- Pedigree analysis suggested an inherited defect.
Ref: J. Vet. Intern. Med. 2011; 25(2):386–392.
Does repetitive stimulation of the common peroneal nerve aid in the diagnosis of botulism in foals?
- Stimulating electrodes were placed along the common peroneal nerve in healthy foals under GA and foals w botulism that were sedated.
- The active and reference electrodes were positioned over the midpoint and distal end of the extensor digitorum longus muscle, respectively.
- Repeated supramaximal stimulation of the nerve was performed utilizing a range of frequencies (1–50 Hz).
- A decremental response was seen at all frequencies in control foals. Decremental responses also were observed in affected foals at low frequencies. An incremental response was seen in all affected foals at 50 Hz.
- Decreased baseline M wave amplitudes with incremental responses at high rates are supportive of botulism.
- Repetitive nerve stimulation is a safe, simple, fast, and noninvasive technique that can aid in the diagnosis of suspected botulism in foals.
Ref: J. Vet. Intern. Med. 2011; 25(2):365–372.
What is the fatality rate in adult horses treated at referral hospitals for botulism? What factors increase or decrease the odds of survival?
- Overall survival rate was 48% (44/92 horses).
- Survival among horses that arrived standing was significantly higher at 67% and 95% for horses that
remained able to stand throughout hospitalisation. - Higher rectal temperature and dysphagia at admission, ability to stand and tx w anti-toxin inc the odds of survival.
- Abnormal respiratory effort or inability to stand had decreased odds of survival.
- Complications occurred in 62% but were not associated with nonsurvival; most to least freq: decubital ulcers, pneumonia, corneal ulcers, colic, cellulitis, salmonellosis, colitis or diarrhea, hyperlipemia or hyperlipidemia, thrombophlebitis, muscle abscess, FUO, facial paralysis.
Ref: J. Vet. Intern. Med. 2015; 29(1):311–319.
