DeLahunta Chapter 12 - Vestibular system Flashcards

1
Q

What is the origin and content of the bony and membranous labyrinth respectively? What is the name and origin of the ear ossicles?

A

Bony labyrinth: mesodermal and contains perilymph
Membranous labyrinth: ectodermal (otic placode) and contains endolymph

stapes, malleus, incus - neural crest

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2
Q

What is the crista ampullaris?

A

receptor of denritic zone of bipolar cells of vestublar ganglion

=hair cells with microvilli (stereocilia) and a single modified cilium (kinocilium) in the ampulla

Responsible for rotation

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3
Q

What is the embryogenic origin of the neurons of the vestibulocochlear nerve?

A

The neurons of the vestibulocochlear nerve are derived from otic placode ectoderm. The dendritic zones of the neurons of the vestibular portion of the vestibulocochlear nerve are in synaptic contact with the base of the hair cells.

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4
Q

What is the macula? Where are the maculae located? What is their function?

A

The macula is the receptor found in each utriculus and saccule, which are located in the bony vestibule.

Macula utricle - horizontal
Macula sacculi.- vertical

Both have hair cells
Both have statoconia (otoliths)

Utricle –> changes in head posture
Sacule –> vibrational stimuli and loud sounds

These structures are responsible for the sensation of the static position of the head and linear acceleration or deceleration. They function in static equilibrium. The macula of the utriculus may be more important as a receptor for sensing changes in head posture, whereas the macula of the saccule may be more sensitive to vibrational stimuli and loud sounds.

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5
Q

Where does the lateral vestibulospinal tract course and what is the clinical effect of stimulation of neurons with axons coursing through this tract?

A

Is a motor pathway starting for the lateral vestibular nuclei

in the ventral funiculus of whole spnal cord
synapses with interneurons in ventral grey column –>
-fascilitatory of ipsilateral a-GSE and g-GSE –> ipsilateral extensors
-inhibitory to a-GSE to flexors ipsiltaeral
-contralateral inhibition of a gSE of extenrso
–> ispilateeral extnesor tone and contralateral inhibition of tone

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6
Q

Which are the three possible terminations of neuronal cell bodies in the vestibular nuclei in the brainstem? (where are going the vestibular nuclei in the brainstem)?

A

1) MLF (rostrally) –> CN VI, III,IV
2) ARAS (vomiting centre)
3) conscious perception of balance to cerebrocortex (mibrain, contralateral MGN –> Thalamus–>temporal cortex)

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7
Q

What muscle is responsible for the simultaneous eyelid movement seen in some
patients with vestibular disturbance?

A

Levator anguli oculi medialis muscle (LAOM muscle) - because vestibular nuclei had interconnections wwith facial nuclus

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8
Q

In a recent paper on vestibular disease in dogs, what percentage of dogs
diagnosed with a peripheral lesion based on neurological examination had a
consistent lesion on MRI?
a- 98.4%
b- 88.4%
c- 77.4%
d- 67.4%

A

c

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9
Q

What is the proposed mechanism for the head tilt and loss of balance being
contralateral to the side of the lesion in cases of paradoxical (central) vestibular
system disease?

A

Paradoxical (central) vestibular disease is a unique syndrome in which the head tilt and loss of balance are directed toward the side opposite to the central lesion, which usually involves the caudal cerebellar peduncle. An explanation for this paradox in the direction of the clinical signs of vestibular system dysfunction is based on the rule that the direction of the head tilt and balance loss is toward the side of the least vestibular system activity. The description of the physiologic anatomy of the cerebellum in Chapter 13 explains that the Purkinje neurons that form a single layer of cells in the cerebellar cortex are the only neurons that project their axons from the cerebellar cortex. These neurons are all inhibitory neurons that release γ- aminobutyric acid at their telodendria. Most of these neurons terminate via their telodendria on neuronal cell bodies in the cerebellar nuclei, which are located in the central portion of the cerebellum known as the cerebellar medulla. The neurons in these cerebellar nuclei comprise most of the efferent axons that leave the cerebellum to terminate in various brainstem nuclei. An exception to this rule is a small population of Purkinje neurons, most of which are located in the cortex of the folia of the flocculus in the hemisphere and the nodulus in the vermis. The Purkinje neurons of these cortical areas have axons that leave the cerebellum directly as a component of the caudal cerebellar peduncle. Tey terminate in the vestibular nuclei, where they are inhibitory to the activation of these neuronal cell bodies. A lesion in the caudal cerebellar peduncle interferes with this inhibition, resulting in excessive discharge of vestibular system neurons on that side. The imbalance in vestibular system activation between the two sides is recognized as a head tilt and loss of balance to the side opposite to this lesion because as a rule the direction of the head tilt and balance loss is toward the side with the least activity of the vestibular system. This paradoxical syndrome is in contrast to lesions that cause a loss of activation of the neuronal cell bodies in the vestibular nuclei, as seen in disorders of the peripheral components of the vestibular system or within the vestibular nuclei themselves. In clinical practice, the side of this unilateral lesion will be determined on neurologic examination by the side of the postural reaction deficit or the side of the hemiparesis and ataxia, which is ipsilateral to the lesion. The caudal cerebellar peduncle lesion is contralateral to the direction of the head tilt in paradoxical (central) vestibular syndrome. The caudal cerebellar peduncle lesion that causes the paradoxical (central) vestibular syndrome also interferes with GP afferents that are entering the cerebellum. Their interruption causes ipsilateral ataxia and a deficit in postural reactions.

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10
Q

Older age was associated with which cause for peripheral and central vestibular
syndrome respectively based on two recent studies?
(Harrison2021 https://doi.org/10.1002/vetr.61
Orlandi2020 https://doi.org/10.1186/s12917-020-02366-8 )

A

Central: ischaemic infarct
Peripheral: idiopathic vestibular

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11
Q

Which has been reported as the most commonly isolated pathogen from cats
diagnosed with otitis media-interna? In which percentage of these cats may
otoscopic examination be found normal?
(Moore2018 https://doi.org/10.1177/1098612X187645 )

A

At total of 19 cats were identified. Sixty-three percent had no previous history of ear infection. Otoscopic examination was normal in 47% of cases. The most common bacterial isolate was Pasteurella multocida, which was identified in 24% of cases. Outcome was successful for 83% of cats managed with ventral bulla osteotomy (VBO) and in 66% of cats managed without surgical intervention.

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12
Q

Which commonly used antibiotic has been associated with neurotoxicity
exhibited with vestibular signs, and what is the reported median time for
resolution of the clinical signs following treatment discontinuation?
(Tauro2018 https://doi.org/10.1111/avj.12772 )

A

Metronidazole – 3d

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13
Q

Please name some common breeds for congenital peripheral vestibular disease.

A

These breeds include the German shepherd dog,48 doberman pinscher, Akita, beagle, English cocker spaniel,3 and Burmese and Siamese cats

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14
Q

What unique disorder often accompanies otitis in horses especially if they have
exhibited a brief period of dysphagia?

A

Temporohyoid osteopathy

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15
Q

Which are the vestibular nuclei and where are they located?

A

4 - medulla oblongata
-Rostral vestibular nucleus
-Medial and lateral vestibular nucleus
-Caudal vestibular nucleus )

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16
Q

State one category of ototoxic drugs that can cause vestibular signs and why?

A

Degeneration of the vestibular or cochlear labyrinthine receptors or both may occur with high levels of aminoglycoside antibiotics. These drugs include streptomycin,
amikacin, kanamycin, neomycin, gentamicin, and vancomycin.

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17
Q

Which pathogenesis has been blamed in two related litters of doberman pincher puppies with congenital vestibular disease?

A

Lymphocytic labyrinthitis

18
Q

State which pathogens can cause central vestibular signs in a cat:

A

FIP
Toxoplasmosis
Myiasis of larva Cuterebra
Bacterial meningoencephalitis secondary to otitis interna/media

19
Q

15yo Standardbred mare with acute progressive abnormal gait, instability, left head tilt. Localisation of cerebellum or/and brainstem. What is your DDx?

A

Equine protozoal encephalitis (sarcocystis neurona)
Rabies
WNV
Eastern equine virus
EHV-1
Abscess
Neoplasm

20
Q

2yo F Holstein cow presented with acute progressive depression and head till and circling. Localisation: brainstem. What is your DDx (and which one is the most common)?

A

Listeriosis
Rabies
Abscess
Bacterial meningoencephalitis
Thrombotic meningoencephalitis

21
Q

How does the vestibular pathways reach the cerebellum?

A

Axons from the vestibular nuclei and some of the vestibular ganglia project to the cerebellum through the caudal cerebellar peduncle. These axons terminate in the flocculus of the hemispheres and nodulus of the vermis. Some axons have collaterals that synapse in the fastigial nucleus (most medial).

22
Q

Which SCS are responsible for vestibular signs?

A

C1-3 SCS
If more caudal: either spinocerebellar of vestibulospinal tracts OR antalgic

23
Q

What is the pathogenesis behind hypothyroidism and vestibular disease?

A

Hypothyroidism induced ischemic neuropathy of the vestibulo-cochlear nerve – rare cause of acute onset clinical signs. Result of hypothyroidism-induced atherosclerosis or increase blood viscosity due to hypertriglyceridemia involving the labyrinthine artery.

24
Q

What do cats have in the middle ear compared to dogs?

A

Septum bullae which in dogs is only a small ridge. The two compartments (dorsolateral and larger ventromedial) communicate near the tympanum.

25
Q

Please describe the MRI features of FIP in cats based on Crawford et al.,

A

1) FLAIR hyperintensity in the lateral ventricles
2) ventriculomegaly especially 4th ventricle enlargement
4) ependymal CE in the ventircular system
5) meningeal CE
5) foramen magnum herniation

26
Q

Which are the areas affected on the MRI in DOG vs cat with thiamin deficiency?

A

Both:
caudal colliculi
vest nuclei
cerebellar nodulus

DOG: Red nucleus, caudate nucleus, rostral colliculi

CAT: (especially) medial vestibular nuclei, LGN, periaqudectal GM, facial nulcei

27
Q

Differential diagnosis for peripheral vestibular disease in horses?

A

OMI-
Temporohyodi osteopathy
Temporal bone fracture
IPVD

28
Q

What is the pathogenesis of temporohyoid osteopathy, what is the treatment?

A

It accompanies otitis in horses. Ankylosis of this joint associated with proliferation of the long stylohyoid bone and probably the very small tympanohyoid bone which it articulates with the petrous portion of the temporal bone. There will be loss of mobility of the hyoid apparatus and secondarily risk of fracture of the petrous portion of the temporal bone. Endoscopically enlarged stylohyoid bone. Dysphagia because of involvement of the cranial nerve IX and X at the jugular foramen. Diagnosis via ventrodorsal radiograoh or CT. Treatment surgical and antibiosis. Surgery: the portion of the affected bone is removed or the entire ceratohyoid bone. Check tear production, temporary tarsorrhaphy if needed.

29
Q

Causes for central vestibular disease in horses?

A

Equine protozoal encephalitis. Rabies.
West nile virus.
Eastern equine virus.
Equine herpes virus 1 vasculitis and encephalopathy. Abscess. Neoplasia.

30
Q

Normal CSF protein level in horses and cow/small ruminants?

A

80 mg/dl in horses, 40 mg/dl in goats.

31
Q

Pathophysiology of listeriosis in cows, and how can this cause vestibular signs?

A

The infection is caused by the Listeria monocytigenes in cows typically younger than 1 year of age. It causes cranial nerve dysfunction, by entering the body through abrasion and laceration of the oral mucosa and gain access to the dendritic zones of general somatic afferent neurons in the branches of trigeminal nerves (GSA). Via retrograde transportation over the axons of trigeminal nerve, and through the ganglion reaches the pons, it attaches to the brainstem, It causes necrosis, neutrophils are scattered in medulla and pons. It causes non-suppurative inflammation in meninges. Clinical signs will involve facial paralysis, tongue paralysis. Dysphagia, jaw paresis, dysfunction of central of central vestibular and aras. Circling may be due to lesion in substantia nigra.

32
Q

Differential diagnosis for central vestibular disease in goats?

A

Listeriosis. Canine arthritis encephalitis. Viral encephalitis. Parelaphostrongylus tenuis myiasis. Abscess, neoplasm.

33
Q

Why congenital resting pendular nystagmus occurs, and in which species (breeds) and why?

A

Congenital pendular resting nystagmus means equal velocity in both directions. It is benign and does not interfere with vision.
hYPocrossing:
In Belgian shepherds is due to failure of developing optic chiasm (achiasma).
Excessive crossing of axons: In cats (Siamese breed, Persian tiger) due to excessive crossing of the ganglionic cell neurons in the optic chiasm. It can cause also resting strabismus.

In Guerney cattle herd and Chediak Hiashy cattle breed. Also due to bilateral retinal dysplasia this can happen.

34
Q

Which vestibular pathways explain head tilt, ispilateral abnormal tone, nystagmus, vomit/nausea?

A

1) medial vestibulospinal tract -> head/neck tilt
2) lateral vestibulospinal tract –> tone of half body
3) MLF –> EOM
4) projection to ARAS (vomiitg centre)

35
Q

Which lesions can cause paradoxical vestibular syndorme?

A

1) caudal cerebellar peduncle
2) floculonodular lobe of cerebellum
(not fastigial nucleus- ipsilateral)

36
Q

Which is a common ear neoplasm in cats?

A

SCC

37
Q

Alexander disease (fibrinoid encephalomyelopathy) : what is it?which breed and age?

A

Leukodystrophy
8mo
Labrador

38
Q

Causes of thiamine deficiencY?

A

1) raw fish/fish diet containing thiaminase
2) diet with sulfur preservatives
3) overcooked food (destroyed hiamine)
4) prolonged anorexia

39
Q

Which is the unique cause of unilateral MM atrophy in horse?

A

EPM

40
Q

Why propulsive circling may happen in listeria?

A

affection substantia nigra

41
Q

Which is the environmental cause of Listeriosis?

A

poorly prepared silage (ph>5.5)

42
Q

What is the histopathological hallmark of listeriosis?

A

microabsecses (neutrophilic necrotic foci) in caudal brainstem + nonsupurative menngitis