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Vertigo:clinical syndromes(sbo-3) 
Vertigo: an illusion of rotational motion, is due to asymmetry in vestibular nucleus activity. 
Dizziness : also called lightheadedness. 
What happens if one labyrinth is destroyed:Acute destruction or deafferation of one entire intact 
labyrinth,there is a spontaneous horizontal nystagmus ,with the slow phases toward the side of the 
lesion,vertigo,nausea,vomiting.These sign/symptom called acute unilateral vestibular 
deafferentation. 
Once vestibular compensation is complete ,so that there is a chronic stable unilateral vestibular 
deafferentation.The patients will no longer experience vertigo,&most will experience no symptoms 
at all. A minority of patients (20%) experience postural imbalance & visual instability. 
What happens if both labyrinth are destroyed If the two labyrinths are deafferented 
simultaneously,either suddenly or slowly ,the patient will not experience vertigo, since there is no 
left-right asymmetry in vestibular nucleus activity. 
The long term effects of bilateral vestibular deafferentation are the same irrespective of whether 
unilateral vestibular deafferentation occurred simultaneously or sequentially .The patient will 
experience the syndrome of chronic vestibular insufficiency,also known as Dandy’s syndrome.The 
three cardinal syndromes & signs of the CVI derive from reduced input to 
vestibulospinal,vestibuloocular &vestibulocortical pathway. 
1)The patient with CVI cann’t walk securely in the dark, particularly if the ground is uneven because 
of reduced input to vestibulospinal pathway. 
2)The patient cann’t see clearly while his or her head is moving quickly,because there is reduced 
input to vestibuloocular pathways,there is reduced retinal image stabilization(oscillopsia) with head 
movement. 
3)The patient will be disoriented when visual & propioceptive input is ambiguous. 
What happens if one labyrinth is stimulated stimulation of the lateral SSC produces 
horizontal beating nystagmus.Posterior SSC stimulation produces upbeating nystagmus,Superior SSC 
stimulation down beating nystagmus. 
When the entire labyrinth is stimulated ,the resulting nystagmus is predominantly horizontal ,since 
any vertical component is concelled by opposing action of the superior (anterior ) & posterior SSC 
on that side. 
BPPV or Dix-Hallpike manoeuvre>Transient upbeating nystagmus(posterior SSC) or horizontal 
nystagmus may occur. In patient with sound & pressure induced vestibular symptoms due to 
superior semicircular canal dehiscence,the induced nystagmus is down beating.
Peripheral vestibular diseases 
Vestibular neuritis: 
is a disordered in which there is sudden ,spontaneous, isolated, total or subtotal loss of afferent 
vestibular input from one labyrinth.It is common cause of the syndrome of spontaneous vertigo. 
Others synonynms:Vestibular neuronitis/Labyrinthitis/Acute unilateral peripheral vestibulopathy. 
Aetiology;result from a viral infection of the vestibular nerve.or selective neuronal loss in the 
vestibular ganglia due to viral infection.Furthermore, latent infection of the superior & inferior 
vestibular ganglia by herpes simplex virus type I. In most cases of vestibular neuritis only superior 
division of the vestibular is affected. 
Clinical manifestation; Acute spontaneous vertigo with nausea,vomiting, &postural imbalance. It is 
typically aggravated by head movement, 
Nystagmus;horizontal nystagmus. 
The head rotation test; invariable results in Catch up saccades with rotation of the head towards the 
affected side. 
Positive Fukuda test or unterberger test; The patients will characterically rotate towards the affected 
side when attempting to march on the spot with their eyes closed. 
Diagnosis is a clinical diagnosis. 
Management options 
Steroid &antiviral valacylovir( Suspected) 
Early mobilization & vestibular rehabilization is indicated. 
Outcomes &complications 
The acute uVD syndrome(unilateral vestibular deafferentation) invariable subsides over the 
following days,due to central vestibular compensation. 
In a small proportion of patients,subsequent attack on the opposite side a condition called bilateral 
sequential vestibular neuritis. 
20% of the patients develops typical posterior SSC type benign paroxysmal positioning vertigo on the 
affected side.The afferent from posterior canal often intact,since the inferior division of the 
vestibular nerve which also carries afferent from the saccule is usually spared. 
In some patients the opposite occurs,-the superior division which carries afferent from 
anterior(superior) & lateral SSC &uticle is spared. These patients can cause diagnostic confusion 
since no nystagmus, negative head impulse test.

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Verigo & vestibular neuritis(sbo 3)

  • 1. Vertigo:clinical syndromes(sbo-3) Vertigo: an illusion of rotational motion, is due to asymmetry in vestibular nucleus activity. Dizziness : also called lightheadedness. What happens if one labyrinth is destroyed:Acute destruction or deafferation of one entire intact labyrinth,there is a spontaneous horizontal nystagmus ,with the slow phases toward the side of the lesion,vertigo,nausea,vomiting.These sign/symptom called acute unilateral vestibular deafferentation. Once vestibular compensation is complete ,so that there is a chronic stable unilateral vestibular deafferentation.The patients will no longer experience vertigo,&most will experience no symptoms at all. A minority of patients (20%) experience postural imbalance & visual instability. What happens if both labyrinth are destroyed If the two labyrinths are deafferented simultaneously,either suddenly or slowly ,the patient will not experience vertigo, since there is no left-right asymmetry in vestibular nucleus activity. The long term effects of bilateral vestibular deafferentation are the same irrespective of whether unilateral vestibular deafferentation occurred simultaneously or sequentially .The patient will experience the syndrome of chronic vestibular insufficiency,also known as Dandy’s syndrome.The three cardinal syndromes & signs of the CVI derive from reduced input to vestibulospinal,vestibuloocular &vestibulocortical pathway. 1)The patient with CVI cann’t walk securely in the dark, particularly if the ground is uneven because of reduced input to vestibulospinal pathway. 2)The patient cann’t see clearly while his or her head is moving quickly,because there is reduced input to vestibuloocular pathways,there is reduced retinal image stabilization(oscillopsia) with head movement. 3)The patient will be disoriented when visual & propioceptive input is ambiguous. What happens if one labyrinth is stimulated stimulation of the lateral SSC produces horizontal beating nystagmus.Posterior SSC stimulation produces upbeating nystagmus,Superior SSC stimulation down beating nystagmus. When the entire labyrinth is stimulated ,the resulting nystagmus is predominantly horizontal ,since any vertical component is concelled by opposing action of the superior (anterior ) & posterior SSC on that side. BPPV or Dix-Hallpike manoeuvre>Transient upbeating nystagmus(posterior SSC) or horizontal nystagmus may occur. In patient with sound & pressure induced vestibular symptoms due to superior semicircular canal dehiscence,the induced nystagmus is down beating.
  • 2. Peripheral vestibular diseases Vestibular neuritis: is a disordered in which there is sudden ,spontaneous, isolated, total or subtotal loss of afferent vestibular input from one labyrinth.It is common cause of the syndrome of spontaneous vertigo. Others synonynms:Vestibular neuronitis/Labyrinthitis/Acute unilateral peripheral vestibulopathy. Aetiology;result from a viral infection of the vestibular nerve.or selective neuronal loss in the vestibular ganglia due to viral infection.Furthermore, latent infection of the superior & inferior vestibular ganglia by herpes simplex virus type I. In most cases of vestibular neuritis only superior division of the vestibular is affected. Clinical manifestation; Acute spontaneous vertigo with nausea,vomiting, &postural imbalance. It is typically aggravated by head movement, Nystagmus;horizontal nystagmus. The head rotation test; invariable results in Catch up saccades with rotation of the head towards the affected side. Positive Fukuda test or unterberger test; The patients will characterically rotate towards the affected side when attempting to march on the spot with their eyes closed. Diagnosis is a clinical diagnosis. Management options Steroid &antiviral valacylovir( Suspected) Early mobilization & vestibular rehabilization is indicated. Outcomes &complications The acute uVD syndrome(unilateral vestibular deafferentation) invariable subsides over the following days,due to central vestibular compensation. In a small proportion of patients,subsequent attack on the opposite side a condition called bilateral sequential vestibular neuritis. 20% of the patients develops typical posterior SSC type benign paroxysmal positioning vertigo on the affected side.The afferent from posterior canal often intact,since the inferior division of the vestibular nerve which also carries afferent from the saccule is usually spared. In some patients the opposite occurs,-the superior division which carries afferent from anterior(superior) & lateral SSC &uticle is spared. These patients can cause diagnostic confusion since no nystagmus, negative head impulse test.