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Titi Musk > Tina Neurology/neuromusc: 5 > Flashcards

Tina Neurology/neuromusc: 5 Flashcards

1
Q

types of muscle fibers

A

Type 1 fibers: lower glycogen and glycolytic capacity and higher lipid and oxidative capacity than type 2 fibers. Tonic motor neurons with a slow discharge rate supply type 1 fibers.

Type 2a fibers: intermediate properties whereas type 2x fibers have higher glycogen, higher glycolytic, and lower lipid and oxidative capacity than type 1 and 2a fibers.

fast discharging phasic motor neurons supplying type 2a and 2x fibers.

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2
Q

in selenium deficiency, which laboratory parameter can be testet to confirm deficiency when the horse has received selenium before blood collection?

A

Glutation peroxidase activity

Als selenhaltiges Enzym spiegelt die GPx-Konzentration die Selenversorgung des Tieres der letzten 2 - 3 Wochen wider.

Daher kann GPx keine akute Unterversorgung mit Selen anzeigen.

Überversorgung kann nicht anhand der GPx-Konzentration diagnostiziert werden.

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3
Q

RER: prevalence in TB racehorses around the world

other predispositions?

A

5-6.5%

mares> geldings

nervous horses

high grain diet

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4
Q

Preventative medications for RER

A

low dose tranquilizers

Dantrolene sodium: receptor antagonist to ryanodine receptor -> decreasing free intracellular Calcium concentration

Phenytoin: block of voltage gated Sodium channels in the motorcortex

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5
Q

Malignant hyperthermia

pathophysiology

A

Malignant hyperthermia (MH) occurs in Quarter Horses and Paint Horses (1%) as a result of an autosomal dominant mutation in exon 46 of the skeletal muscle ryanodine receptor 1 gene (RYR1). The mutation lowers the activation and heightens the deactivation threshold of the ryanodine receptor, which intermittently can result in a dramatic efflux of calcium from the sarcoplasmic reticulum, increasing myoplasmic calcium and producing a contracture.

Anaerobic glycogen metabolism is activated, lactate is produced, excessive heat is gener-
ated, and massive muscle necrosis ensues.

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6
Q

clinical signs of malignant hyperthermia and when do they occur?

can it be prevented?

A

hyperthermia (104.9°F [40.5°C]),

hypercapnia (PaCO2 of 274 mm Hg), and

acidosis

-> during anesthesia - prevention via dantrum

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7
Q

What is PSSM?

A

PSSM1 is caused by an autosomal dominant missense mutation in GYS1 at codon 309 in glycogen synthase.

Result: higher than normal activity of glycogen synthase both at basal states and when activated by glucose-6-phosphate.

– draft horses from continental Europe, 6-10% QH, 6-8%: Pinto and appaloosa

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8
Q

Clinical and histopathological signs of PSSM

A

persistent elevations in serum CK and AST are common in symptomatic horses OR

minimum tripling of CK 4hours after exercise test (15min)

muscle biopsies: numerous vacuoles and crystalline PAS positive and amylase resistant inclusions in fast twitching fibers

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9
Q

fibrotic myopathy

A

affects semimembranosus/tendinosus

trauma resulting in classic gait abnomality (slamming hind leg on the floor)

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10
Q

Gegenstueck von PSSM (auch enzymatisch bedingte erkrankung)

A

Glycogen branching enzyme deficiency

QH foals - premature stop codon in exon 1 of the -gbe1 gene

-> letal

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11
Q

Nutritional myodegeneration

A

deficiency of selenium and/or vit E (=Alpha tocopherol) in young rapidly growing foals

-> Selenium is key component of gluthation peroxidase (GSH-Px) that prevents oxidative damage of the muscle

cardiorespiratory and skeletal form

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12
Q

Vitamin E Deficient Myopathy

A

can be a disease by itself: with characteristic alterations in mitochondrial distributions (reversible)

(without the hallmark of EMND: neurogenic atrophy in sacrocaudalis dorsalis medialis muscle biopsies) or a predecessor to the development of equine motoneuron disease

  • > reduced performance and muscle loss
  • > ttx: natural liquid RRR Alpha Tocopherol
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13
Q

Bacterial associated myositis

A

usually Clostridium perf

clinical disease usually by Alpha toxin

OR

Streptococc equi equi associated generalized rhabdomyolysis in QH

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14
Q

infarctive purpura hem

what happens to muscles

diagnosis

tx?

A

severe form of purpura with high fatality rate-> infarctions occur initially in skeletal muscle

deposition of immune complexes composed of IgM/A and streptococcal M protein

  • > diagnosis: serum titers for ELISA M Protein
  • > high dose corticos and Peni
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15
Q

Immune mediated myositis

A

in QH breeds: rapid onset of severe atrophy particularly affecting epaxial and gluteal muscles, and high serum CK and AST activities

  • > as a result of lymphocytic destruction of myofibers by CD4+ and to a lesser extent CD8+ cells.
  • > may occur after rhabdomyolysis, infection with S. equi, or vaccination.
  • > dx: muscle biopsy of epaxial and gluteal muscles early in the disease process (to see lymphocytes)
  • > corticosteroids - reversable
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16
Q

systemic calcinosis

A

should be suspected if a horse presents with

  • muscle atrophy,
  • malaise,
  • respiratory distress, or
  • renal insufficiency
  • with evidence of hyperfibrinogenemia and an
  • elevated Ca × P (>66; reason in horses for electrolyte overload unknown)product. -> high fatality rate

histopath: resembles IMM; however, multinucleated giant cells are consistently present, and dystrophic calcification of muscle fibers is also evident.

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17
Q

Toxic causes of Rhabdomyolysis

A
  • Tremetone containing plants (snakeroot, rayless goldenrod) -> stays active in hay!
  • Atypical myopathy -> Acyl CoA dehydrogenase inhibitor (MCPA CoA)
  • Sicklepod

…

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18
Q
A
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19
Q

Myopathies associated to general anesthesia

A
  • focal/
  • generalized postanesth myopathy: maybe bc of lesions resulting from hypotension and hypoxia
    • ->take CK at least 4hrs after sx
  • Malignant hyperthermia
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20
Q

DDs for muscle fasciculations

A
  1. Pain, Anxiety
  2. Weakness:
    1. Botulism
    2. Vit E def
    3. EMND
  3. Increased motor neuron firing
    1. electrolyte abnorm
    2. focal nerve irritation
    3. Stiff horse syndrome
    4. shivers
    5. Neuromyotonia
  4. Abnormal sarcolemma conductivity
    1. HYPP
    2. Myotonia congenita
    3. Myotonia dystrophica
21
Q

Myotonia

Which channels

A

acquired or congenital diseases that share the feature of delayed relaxation of muscle after mechanical stimulation or voluntary contraction caused by abnormal muscle membrane excitability.

Congenital: skeletal muscle chloride channel (myotonia congenita) or sodium chan-
nel (hyperkalemic periodic paralysis).

Acquired: infestation with the spinous ear tick Otobius megnini.

The cause of many cases of myotonia in horses, especially dystrophic forms, remains unknown.

22
Q

HYPP

A

F1416L mutation in the SCN4A gene encoding the

alpha subunit of the sodium channel. =>

resting sarcolemma potentials that are closer to firing

23
Q

treatment HYPP

A

For horses with recurrent episodes of muscle fasciculations even with dietary modification,

  • *acetazolamide** (2–3 mg/kg orally, every 8–12 hours) or hydrochlorothiazide (0.5–1 mg/ kg orally, every 12 hours) may be indicated.
  • > both increase renal potassium excretion. Acetazolamide also stabilizes blood glucose and potassium by stimulating insulin secretion.
24
Q

clinical signs of hypocalcemia (muscles)

A

Clinical signs are similar to those seen with tetanus and include a stiff, stilted gait, muscle fasciculations (especially temporal, masseter, and triceps muscles), trismus, dysphagia, salivation, anxiety, profuse sweating, tachycardia, elevated body temperature, cardiac arrhythmias, synchronous diaphragmatic flutter, convulsions, coma, and death.

EXTRACELLULAR CALCIUM INHIBITS VOLTAGE DEPENDENT SODIUM CHANNELS -> absence of calcium results in hyperexcitability

25
Q

pathogenesis of diaphragmatic flutter

A

Synchronous diaphragmatic flutter (SDF), or “thumps,” arises when fluid and electrolyte imbalances disrupt the membrane potential of the phrenic nerve. The phrenic nerve begins to discharge in concert with atrial depolarization with subsequent contraction of the diaphragm.

EXTRACELLULAR CALCIUM INHIBITS VOLTAGE DEPENDENT SODIUM CHANNELS

26
Q

Botulism

types of toxins?

A

C.botulinum toxin A-F

Europe: mostly C

type B most commonly in silage

type C with contamination w/ carcasses

27
Q

Mechanism of action of tetanus toxin

A

migrates retrograde on motorneurons to the spinal cord where it acts on the synapse of inhibotory interneurons by cleaving VAMP (synaptobrevin) - a protein required for exocytosis of glycin and GABA

28
Q

Mechanism of action of botulinum toxin

A

INHIBITs PREsynaptic ACh release at neuromusc endplate

acts on synaptic endplate of motorneurons by cleaving

  • SNAP-25 (serotypes A,E) or
  • VAMP (B,D,F,G) or
  • Syntaxin (C)

and therefore the release of ACh at the neuromusc endplate

29
Q

name the sensory cranial nerves

A

Olfactory CN I Olfaction

Optic CN II Vision

Vestibulocochlear CN VIII Balance and hearing

30
Q

cranial nerves: only motor

A

Oculomotor CN III Extraocular eye muscles Parasympathetic to eye

Trochlear CN IV Extraocular eye muscles

Abducens CN VI Extraocular eye muscles

Accessory CN XI Pharyngeal and laryngeal muscles; cervical muscles

Hypoglossal CN XII Lingual muscles

31
Q

cranial nerves: mixed

A
32
Q

types of white matter fiber systems in the cerebrum

A

projection fibers carry information to and from the cerebrum to form connections with the brainstem and spinal cord, principally through the internal capsule.

Commissural fibers carry information across the midline between the left and right cerebral hemispheres, mostly through the prominent corpus callosum.

Association fibers form more subtle pathways that connect structures within one hemisphere, within and between lobes.

33
Q

skizze: Arrangement of gray and white matter in the spinal cord

A

1, Dorsal gray column; 2, lateral gray column; 3, ventral gray column; 4, dorsal funiculus; 5, lateral funiculus; 6, ventral funiculus.

34
Q

cerebral functions by lobes

A

frontal lobe likely the motor cortex and association area involved in planning actions and movement.

parietal lobe is found just caudal to the motor cortex and consists of somesthetic regions and cognitive association areas involved in perceiving sensory input,

temporal lobe ventrolateral to the parietal lobe. auditory information is processed

occipital lobe processes visual information.

35
Q

Describe the basic mechanisms and role of the cerebellum in the nervous system

A

The cerebellum receives general proprioceptive information from the periphery along with information from both the pyramidal and extra motor systems. Information about head position and movement also enters the cerebellum.

The Purkinje cells in the cortex monitor and process all the incoming information. When activated as a result of the net summation of all the afferent impulses, the Purkinje cells send normally inhibitory impulse to the appropriate cerebellar nuclei.

The cerebellar nuclei in turn stimulate upper motor neurons (UMNs) in the brainstem, which in turn project to LMNs in the spinal cord as well as the cerebral cortex to produce coordinated movement.

36
Q

the fibers of which cranial nerves exit the brainstem at the medulla oblongata?

A

The fibers of cranial nerves VI through XII exit the brainstem on the ventral surface of the medulla oblongata

37
Q

skizziere die dorsalwurzel des spinalkanals

A

furr seite 13

38
Q

difference UMN and LMN

A

Motor neurons in the higher levels of the CNS are defined as upper motor neurons, and motor neurons that send their axons to provide motor innervation to peripheral targets are defined as lower motor neurons. The descending tracts of the spinal cord are formed by axons of UMNs that descend through the brain and spinal cord to provide a regulatory influence on the lower motor cells.

39
Q

define the extrapyramidal motor system

A

The extrapyramidal motor system is so named because the nuclei and tracts contained within this division do not contribute to formation of the pyramids seen on the ventral surface of the medulla oblongata. Anatomically, the extrapyramidal part of the motor system is composed of a myriad of nuclei and tracts located within all divisions of the brain.

In general, the extrapyramidal system principally provides regulatory influence on the LMNs that are responsible for muscle tone and posture.

40
Q

The clinical signs that are considered to be hallmarks of UMN disease include

A
  • hypertonus (“spasticity”),
  • hyperreflexia (commonly examined in small animals but almost impossible to elicit in ambulatory adult horses),
  • UMN paresis.

The most straightforward way to test for UMN paresis in horses is to firmly, and consistently, pull on the horse’s tail as it is walking in a straight line; an animal with UMN paresis will not be able to initiate the ipsilateral limb extension required to counteract this maneuver and particularly patients with acute spinal cord compression can be remarkably easy to pull over.

41
Q

difference between UMN and LMN paresis

A

Schwäche: UMN paresis differs from LMN paresis by the preservation, and often increase, of reflexes and muscle tone.

42
Q

who is more likely to have PSSM 1 compared to 2?

A

GYS 1-neg:

28% of QH

90% WB

100% arabians

43
Q

Which breeds are predisposed to PSSM

A

60% of percherons and belgians drafts

6-8% of Quarter HOrses

44
Q

Problems with diagnosis of PSSM via muscle biopsies?

A

False positives possible!

so only test horses that are suspicious

amylase + PAS staining

45
Q

Warmbloods with PSSM show predominantly

A

abnormal gait:

lameness!!!

46
Q

PSSM 2: does it affect performance in well managed horses?

A

53% said that horses are not performing up to expectiation

valberg

47
Q

microscopic features of myofibrillar myopathy

A

immunohistochemically for desmin: stains very strongly

48
Q

HYPP different grades?

A

homozygots are more severely affected and can have upper airway collapse, protrusion of third eyelid and generally more severe clinical signs

emergency treatment:

Ca -> decreases treshhold

dextrose -> to move K in cells

Titi Musk (8 decks)

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