DeLahunta Chapter 7 - GVE LMN Flashcards

1
Q

Where is the caudal commissure located and what structure decussate?

A

a. Rostral mesencephalon
b. The axons of the pretectal nuclei towards the contralateral GVE III CN

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2
Q

Name a common anatomic diagnosis for a lesion causing bilateral, internal/ external ophthalmoplegia.

A

Middle cranial fossae

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3
Q

Which are the most common neoplasia related with GVE LMN dysfunction of the III CN? And why? Which breed of dog has one of them been related to?

A

a. Germ cell neoplasm and meningiomas
b. Because these tend to expand laterally, compressing the oculomotor nerve axons.
c. GSD - 10.5326/jaaha-ms-6354

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4
Q

According to Pont et al (10.1111/vru.12478), oculomotor neuritis:
a-Mostly uni or bilateral?
b-In all cases affected the GSE/GVE axons?
c-Full recovery should be expected within 5 weeks and immunosuppressive doses of steroids improve the outcome.

A

a. Mostly uni or bilateral? Unilateral
b. In all cases affected the GSE/GVE axons? - false, not all cases presented with external
ophtalmoparesis.
c. Full recovery should be expected within 5 weeks and immunosuppresive doses of
steroids improve the outcome. (False – immunosupression has not been proven to
improve outcome)

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5
Q

Pharmacological testing of the mydriatic pupil – explain: the drug used, mechanism of action,
how to differentiate between preganglionic vs ganglionic lesion.

A

a. Direct acting parasympathicomymetic drugs (Pilocarpine)
b. If the lesion is in the ganglionic neuron – the pupil constrictor muscle will be
hypersensitive and the direct acting drug will produce a noticeable effect (miosis).

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6
Q

Name reasons for bilateral/unilateral protrusion of the third eyelid

A

a. Unilateral/ bilateral Horner syndrome
b. Unilateral/bilateral MM atrophy
i. Masticatory myositis (chronic phase)
ii. Trigeminal neoplasm affecting the mandibular branch
c. Cachexia
d. Tetanus
e. Dysautonomia (due to sympatehtic dysfunction)
f. Drugs (acepromazine)
g. Systemically unwell –
h. Idiopathic

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7
Q

According to the authors of the following paper: 10.1111/jvim.16588 what type of underlying disease was most commonly associated with Horner syndrome in dogs with cervical myelopathy? Which tract would be affected in these cases?

A

a. Non-compressive parenchymal lesions e.g. FCE
b. Lateral tectotegmento-spinal tract

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8
Q

Equine sympathetic paralysis syndromes - where is the lesion:
a) Horner syndrome + hyperidrosis of head/cranial neck
b) Horner syndrome + hyperidrosis to entire neck and cranial border of scapula
c) Horner syndrome + hyperidrosis until the thoracic limb entirely
d) Horner syndrome + hyperidrosis of entier ipsilateral body

A

a) T1-3 SCS, sympathetic trunk, cranial cervical ganglion

b) thoracic inlet (junction between root and thorax), sympathetic trunk, vertebral nerve

c) thoracic inlet, sympathetic trunk, vertebral nerve + branches of cervicothoracic ganglion to the brachial plexus nerves

d) CNS (midbrain, pons, medulla, C1-T1 lateral funiculus (lateral tectotegmentospinal tract -UMN)

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9
Q

What is the tympanic plexus, where is it located, why is it relevant?

A

a. Preganglionic GVE axons for IX
b. In the middle ear cavity close to the promontorium
c. Because ganglionic sympathethic fibers have been found to run associated with this
plexus (mostly in cats) - being a potential reason for Horner syndrome.

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10
Q

What do you know for canine dysautonomia based on this: https://avmajournals.avma.org/view/journals/javma/261/11/javma.23.03.0134.xml
a) Which was the mean age of the affected dogs?
b) Which were the most common GI signs?
c) Which were the most common ophthalmological signs?
d) Which histopathological changes would you expect in a PM examination?

A

Which was the mean age of the affected dogs?
i. 1y – subacute/chronic progressive presentation
b. Which were the most common GI signs?
i. Regurgitation and vomiting (87%)
c. Which were the most common ophthalmological signs?
i. Diminished PLR 55/79 (70%); Third eyelid elevation 51/79 (64%); Resting
mydriasis 21/79 (24%); 55/79 - abnormal STT (median 10-11 mm/min)
d. Which histopathological changes would you expect in a PM examination?
i. Neuronal degeneration: chromatolysis, pyknotic nuclei in ganglions of ANS

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11
Q

In equine grass sickness, ganglionic neurons for the GVE sympatehtic and parasympathetic system are usually affected; however, GSE nuclei for certain CNs have been described. Which are the most commonly affected? - Hahn et al DOI 10.1007/s004010000289

A

a. Trigeminal, Oculomotor, Facial and Hypoglossal nerves.

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12
Q

Describe the PLR pathway

A

Retina–> optic nerve –> optich chiasm –> crossing –> contralateral pretectal nucleus (some not crossing and go at the ispiplateral oculomotor nucleus)–> caudal commissure (crossing again) –> ipsilateral GVE oculomotro nucleus –> GVE oculomotor nerve –> ciliary ganglion –> ciliary nerve –> constrictor puppillae muscle

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13
Q

Which is the lateral tectotegmentospinal system?

A

This is an upper motor neuron (UMN) system that is part of the CNS portion of the autonomic nervous system. It begins in the hypothalamus and has components that continue caudally in the brainstem; it then continues in the lateral funiculus of the spinal cord. It terminates in the lateral gray horn from the T1 to L4–L5 spinal cord segments, where the UMNs synapse on the dendritic zones of the preganglionic neurons of the sympathetic-GVE-LMN system. The activity of this UMN system is necessary for the GVE-LMN to function. 1st order neuron.

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14
Q

Noxious stimuli or emotional responses may cause dilation of the pupils. Which are the pathways that cause mydriasis in pain and which in emotional/stress?

A

Noxious stimuli to the trunk and limbs use spinothalamic and spinotectal pathways to reach the sympathetic centers in the hypothalamus and activate the UMN that in turn projects caudally to the appropriate preganglionic sympathetic neurons in the cranial thoracic spinal cord to cause pupillary dilation.
Emotional responses use corticohypothalamic pathways to activate the sympathetic pathway.

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15
Q

What muscles of the eye are innervated by the sympathetic GVE neurons?

A

Oribitalis muscle (helps eye to protrude)
Ciliaris muscle (lens to focus)
Dilator pupillae (pupil to dilate)

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16
Q

Why xyromycteria occurs?

A

In contrast, parasympathetic denervation (FACIAL NERVE) would result in hyperkeratosis (xyromycteria) of the nasal planum secondary to a loss of moisture provided by the lateral nasal gland.

VS Dry discharge from the nose.
It is a result of loss of their sympathetic innervation to the nasal mucosa resulting in a decreased airflow caused by vasodilation, causing increased tissue rigidity of
the nasal mucosa and increased nasal gland secretion from disinhibition. The net effect may result in an accumulation of dried secretion, called crusts, within the naris.

17
Q

T or F: In all domestic animals sweating is decreased on the surface of the body that has been deprived of its sympathetic innervation.

A

F – expect for horse. The horse is unique among the domestic animals in that a sympathetic paralysis causes excessive sweating in the area of skin that is denervated.

18
Q

Causes of mydriasis

A

1) GVE oculomotor neuron, nerve, ganglion etc. lesion
2) retinal/optic nerve lesion
3) geriatric iris atrophy
4) mydriatic drug (phenylephirine, tropicamide)
5) toxin (belladona, cannabis) or opioids
6) glaucoma
7) cerebellar (ipsilateral -interposital; conralateral - fastigial)
8) sympatehtic hyperexcitability (purfur du petit)
9) constant compression to rostral midbrain (ICP)

19
Q

Causes of miosis

A

1) GVE sympathetic neuron lesion
2) iritis/uveitis
3) ocular dyscomfort in keratitis (oculopuppilary reflex through ophthalmic nerve)
4) drugs (pilocarpine)
5) acute rostral midbrain compresion (ICP)
6) forebrain lesion (causing release of UMN inhibition [supranucleaer lesion e.g. hypothalamic horner] and activation of GVE oculomotor neurons)

20
Q

Whcih are the neurotransmitters of the sympathetic and parasympathetic systems?

A

Sympathetic - norepinerphrine
Parasympathetic - acetlycholine

21
Q

State the sympathetic innervation to the eye

A

UMN (hypothalamus) –> lateral tectotegmental spinal tract until T1-3 SCS –> GVE LMN of T1-3 SCS –> spinal nerve roots –> rammus communicans –> thoracic and cervical sympathetic trunk –> vagosympathetic trunk (carotid sheath)–> cranial cervical ganglion –> (unsure pathway)
–> A) tympanic cavity along with tympanic plexus enters ventral to the tirgeminal ganglion (stylomastoid foramen)–> joining ophthlamic nerve –> eye

–>B) joins inernal carotid artery and nerve –> tympano-occipital fissure –>join ophthalmic nerve –> eye

-innervation of smooth muslces: a) orbitalis muscle, (b) ciliary muscle and (d) dilateor puppillae muscle

22
Q

Which is the reason for ptosis, enophthalmos and third eyelid protursion in Horner?

A

Orbitalis muscle - sympathetic paralysis means that all its 3 components paralyse:
1) sheet of circular fibers in the periorbita –> makes the eye protrude (dysfunciton = enophthalmos)
2) ventral sheet of longitudinal fibers (ventral rectus muscle) to the inferior eyelid + third eyelid (ptosis if dysfunction and third eyelid protrusion)
3) medial sheet of longitudinal fibers medial rectus muscle and trochlea) to superior eyelid + third eylied (ptosis if dysfunction)

23
Q

Why are horses sweating in sympathetic dysfunciton?

A

becaause due to over peripheral vasodilation
the sweating glands over work OR hypersensitive in norepinerprijne that circulates (sympathetic cholinergic innervation of swating glands)
NOT DENERVATION HYEPRSENSITIVITY AS TOO ACUTE TO HAPPEN

24
Q

Breed most common for idiopathic horner syndrome?

A

Golden retriever

25
Q

Which pharmacological testing is available to check for sympathetic denervation?

A

phenylephrine
less available cocaine, hydramphetamine

26
Q

Defaecation pathway

A
27
Q

Micturition pathway

A