A medical condition that is related to the Vestibular part of nervous system

1. VERTIGO
By
Haseeb Ullah 200
Muhammad Uzair Shafi 255

2. WHAT IS VERTIGO?

3. VERTIGO
 Vertigo is the illusion of movement of the body or
the environment

4.  Equilibrium is the ability to maintain
orientation of the body and its parts in relation to
external space.
 Disorders of equilibrium result from diseases
that affect
 central or peripheral vestibular pathways,
 the cerebellum,
 or sensory pathways involved in proprioception.
 Such disorders usually present with one of two
clinical problems: vertigo or ataxia

8. HAIR CELL

11. DDX
 The first step in DDX: localize the pathologic
process in peripheral or central vestibular
pathways
 Peripheral vestibular lesions affect the
labyrinth of the inner ear or the vestibular
division of the acoustic (VIII) nerve
 Central lesions affect the brainstem vestibular
nuclei or their connections
 Rarely, vertigo is of cortical origin, occurring as a
symptom associated with complex partial seizures

12. SYMPTOMS

13. SYMPTOMS
 Peripheral vertigo
 tends to be intermittent,
 lasts for briefer periods,
 and produces more distress than vertigo of central
origin
 Nystagmus is always associated, usually unidirectional,
never vertical
 Peripheral lesions commonly produce additional
symptoms of inner ear or acoustic nerve (tinnitus,
hearing loss)

14.  Central vertigo
 may occur with or without nystagmus; if nystagmus
is present, it can be vertical, unidirectional, or
multidirectional and may differ in character in the
two eyes.
 Central lesions may produce intrinsic brainstem or
cerebellar signs, such as motor or sensory deficits,
hyperreflexia, extensor plantar responses, dysarthria,
or limb ataxia

15. ONSET & TIME COURSE
 Establishing the time course of the disorder may
suggest its cause
 Sudden onset of disequilibrium occurs with
infarcts and hemorrhages in the brainstem or
cerebellum (eg, lateral medullary syndrome,
cerebellar hemorrhage or infarction)
 Episodic disequilibrium of acute onset suggests
transient ischemic attacks in the basilar artery
distribution, benign positional vertigo, or
meniere disease

16.  Chronic, progressive disequilibrium evolving
over weeks to months is most suggestive of a
toxic or nutritional disorder (eg, vitamin B12 or
vitamin E deficiency, nitrous oxide exposure)
 Evolution over months to years is characteristic of
an inherited spinocerebellar degeneration

17. PERIPHERAL VESTIBULAR
DISORDERS
 Benign Paroxysmal Positional vertigo
 Meniere’s Disease
 Vestibular Nuritis
 Labyrinthitis
 Vestibulotoxic drugs
 Head Trauma
 Perilymph fistula
 Syphilis
 Acoustic(VIII) neuroma

18. BPPV
 Positional vertigo occurs upon assuming a particular
head position
 No hearing loss or other neurologic symptoms
 It is usually associated with peripheral vestibular lesions
but also may be due to central (brainstem or cerebellar)
disease.
 Benign positional vertigo is the most common cause of
vertigo of peripheral origin, accounting for about 30% of
cases
 The most frequently identified cause is head trauma, but
in most instances, no cause can be determined
 The pathophysiologic basis of benign positional vertigo is
thought to be canalolithiasis - stimulation of
the semicircular canal by debris(crystalline) floating
in the endolymph

19.  The syndrome is characterized by brief (seconds
to minutes) episodes of severe vertigo that may
be accompanied by nausea and vomiting
 Symptoms may occur with any change in head
position but are usually most severe in the
lateral decubitus position with the affected
ear down
 Episodic vertigo typically continues for several
weeks and then resolves spontaneously; in some
cases it is recurrent
 Hearing loss is not a feature

20. The mainstay of treatment in
most cases of benign positional
vertigo of peripheral origin
(canalolithiasis) is the use of
employing the force of gravity to
move endolymphatic debris out
of the semicircular canal and
into the vestibule, where it can
be reabsorbed

21. MENIERE’S DISEASE (ENDOLYMPHATIC
HYDROPS)
 is characterized by repeated episodes of
vertigo lasting from minutes to days,
accompanied by tinnitus,aural fullness and
progressive sensorineural hearing loss
 Vertigo is of sudden onset and lasts for a few
minutes to 24 hours or so
 Onset is between the ages of 20 and 50 years in
about three-fourths of cases, and men are
affected more often than women

22. NORMAL EAR
Endolymphatic Hydrops

23.  Physical examination during an acute episode
shows spontaneous horizontal or rotatory
nystagmus (or both) that may change direction
 Audiometry shows low-frequency pure-tone
hearing loss, however, that fluctuates in
severity as well as impaired speech
discrimination and increased sensitivity to loud
sounds

24.  As has been noted, episodes of vertigo tend to
resolve as hearing loss progresses
 Treatment is with diuretics, such as
hydrochlorothiazide and triamterene
 The drugs listed in previous section may also be
helpful during acute attacks
 In persistent, disabling, drug-resistant cases,
surgical procedures such as endolymphatic
shunting, labyrinthectomy, or vestibular nerve
section are helpful

25. LABYRINTHITIS
 Circumscribed: seen in unsafe type of Chronic
suppurative otitis media(CSOM) & fistula test is
positive
 Serous: caused by trauma and infection(viral or
bacterial) adjacent to inner ear but without
actual invasion. There is severe vertigo &
Sensorineural hearing loss
 Purulent: is complication of CSOM. There is
actual bacterial invasion with total loss of
cochlear and vestibular functions. Vertigo is
due to acute vestibular failure. Nystagmus is
seen to opposite side due to destruction of
affected labyrinth

26. VESTIBULOTOXIC DRUGS
ALCOHOL
 Alcohol causes an acute syndrome of positional vertigo
because of its differential distribution between the cupula
and endolymph of the inner ear
 Alcohol initially diffuses into the cupula, reducing
its density relative to the endolymph
 This difference in density makes the peripheral vestibular
apparatus unusually sensitive to gravity and thus to
position
 With time, alcohol also diffuses into the endolymph,
and the densities of cupula and endolymph equalize,
eliminating the gravitational sensitivity
 As the blood alcohol level declines, alcohol leaves the
cupula before it leaves the endolymph
 This produces a second phase of gravitational
sensitivity that persists until the alcohol diffuses out of
the endolymph also.

27.  Alcohol-induced positional vertigo typically occurs
within 2 hours after ingesting ethanol in amounts
sufficient to produce blood levels in excess of 40
mg/dL.
 It is characterized clinically by vertigo and
nystagmus in the lateral recumbent position and is
accentuated when the eyes are closed
 The syndrome lasts up to about 12 hours and consists
of two symptomatic phases separated by an
asymptomatic interval of 1-2 hours
 Other signs of alcohol intoxication, such as
spontaneous nystagmus, dysarthria, and gait ataxia,
are caused primarily by cerebellar dysfunction.

28. AMINOGLYCOSIDE
 Aminoglycoside antibiotics are widely recognized
ototoxins that can produce both vestibular and
auditory symptoms
 Streptomycin, gentamicin, and tobramycin are the
agents most likely to cause vestibular toxicity, and
amikacin, kanamycin, and tobramycin are associated
with hearing loss
 Aminoglycosides concentrate in the perilymph
and endolymph and exert their ototoxic effects
by destroying sensory hair cells
 The risk of toxicity is related to drug dosage, plasma
concentration, duration of therapy, conditions (such
as renal failure)that impair drug clearance,
preexisting vestibular or cochlear dysfunction, and
concomitant administration of other ototoxic agents

29.  Symptoms of vertigo, nausea, vomiting, and gait
ataxia may begin acutely; physical findings
include spontaneous nystagmus and the presence
of Romberg sign
 The acute phase typically lasts for 1 to 2 weeks
and is followed by a period of gradual
improvement
 Prolonged or repeated aminoglycoside
therapy may be associated with a chronic
syndrome of progressive vestibular
dysfunction

30. SALICYLATES
 Salicylates, when used chronically and in high doses, can
cause vertigo, tinnitus, and sensorineural hearing loss-all
usually reversible when the drug is discontinued
 Symptoms result from cochlear and vestibular end-organ
damage. Chronic salicylism is characterized by headache,
tinnitus, hearing loss, vertigo, nausea, vomiting, thirst,
hyperventilation, and sometimes a confusional state
 Severe intoxication may be associated with fever, skin rash,
hemorrhage, dehydration, seizures, psychosis, or coma
 The characteristic laboratory findings are a high plasma
salicylate level (about or above 0.35 mg/mL) and combined
metabolic acidosis and respiratory alkalosis
 Measures for treating salicylate intoxication include
gastric lavage, administration of activated charcoal,
forced diuresis, peritoneal dialysis or hemodialysis, and
hemoperfusion

31. HEAD TRAUMA
 Head injury may cause concussion of labyrinth,
completely disrupt the bony labyrinth or VIII
nerve or cause a perilymph fistula
 Severe acoustic trauma such as that caused by
an explosion can also disturb the vestibular end
organ(otoliths) & result in vertigo

32. PERILYMPH FISTULA
 As a complication of stapedectomy or ear surgery,
when stapes is dislocated accidently, there is
leakage of perilymph into the middle ear through
the oval or round window.
 It can also result from sudden pressure changes
in middle ear or raised intracranial pressure.
 A perilymph fistula causes intermittent vertigo
& fluctuating sensorineural hearing loss,
sometimes with tinnitus and sense of fullness in
the ear.

33. SYPHILIS
 Syphilis of inner ear, both congenital or acquired,
causes dizziness in addition to sensorineural
hearing loss.
 Neurosyphilis (a tertiary acquired) can cause
central type of vestibular dysfunction

34. ACOUSTIC NEUROMA
 It arises fron CN VIII within internal acoustic
meatus.
 It causes only unsteadiness or vague sensation of
motion.
 Severe episodic vertigo, usually seen in the end
organ disease, is usually missing

35. CENTRAL VERTIGO

36. CENTRAL NERVOUS SYSTEM
DISORDERS
 The key to the diagnosis of CNS disorders in
patients presenting with dizziness are
 Central lesions may produce intrinsic brainstem or
cerebellar signs, such as motor or sensory deficits,
hyperreflexia, extensor plantar responses, dysarthria,
or limb ataxia
 the presence of other focal neurological symptoms
 identifying central ocular motor abnormalities

37. CENTRAL VESTIBULAR DISORDERS
INCLUDE:
 Vertebrobasillar insufficiency
 Wallenberg’s syndrome
 Basilar Migraine
 Neurodegenerative disorders
 Cerebellar Disease
 Multiple Sclerosis
 Epilepsy
 Cervical Vertigo

38. BRAINSTEM ISCHEMIA

39. BRAINSTEM ISCHEMIA
 Ischemia affecting vestibular pathways within
the brainstem or cerebellum often causes
vertigo
 Vertigo is the most common symptom with
Wallenberg syndrome(Lateral Medullary
Syndrome)
 infarction in the lateral medulla in the territory of the
posterior inferior cerebellar artery (PICA), but other
neurological symptoms and signs (e.g., diplopia, facial
numbness, hoarseness of voice, ataxia, sensory loss on
ipsilateral side of face and contraletral side of the body,
Horner syndrome) are invariably present

40.  Ischemia of the cerebellum can cause vertigo
as the most prominent or only symptom,
 Computed tomography (CT) scans of the
posterior fossa are not a sensitive test for
ischemic stroke

41.  Abnormal ocular motor findings in patients with
brainstem or cerebellar strokes include:
 (1) spontaneous nystagmus that is purely vertical,
horizontal, or torsional,
 (2) direction-changing gaze-evoked nystagmus
 (3) impairment of smooth pursuit,
 (4) overshooting saccades

42.  Patients with brainstem or cerebellar
infarction need immediate attention
because herniation or recurrent stroke can
occur
 However, because of the rarity of ischemia
causing isolated vertigo, MRI need only be
considered in patients with significant stroke
risk factors such as older age, known history of
stroke, transient ischemic attacks (TIAs),
coronary artery disease, or diabetes

43. MULTIPLE SCLEROSIS (MS)
 It is demyelinating disease affecting young adults
 Dizziness is a common symptom in patients with
multiple sclerosis (MS)
 A typical MS attack has a gradual onset,
reaching its peak within a few days
 Nearly all varieties of central spontaneous and
positional nystagmus occur with MS

44.  Posterior Fossa Structural Abnormalities
 Neurodegenerative Disorders
 Epilepsy
 Vertigo may occur as an aura in temporal lobe epilepsy
 Vestibular symptoms are common with focal seizures,
particularly those originating from the temporal and
parietal lobes.
 The key to differentiating vertigo with seizures from
other causes of vertigo is that seizures are almost
invariably associated with an altered level of
consciousness.

45. MIGRAINE
 Migraine is a vascular syndrome, producing
recurrent headaches with symptoms free
intervals
 Headache is usually unilateral & of the throbbing type.
 Dizziness has long been known to occur among patients with
migraine headaches
 benign recurrent vertigo is usually a migraine equivalent
 because no other signs or symptoms develop over time,
 the neurological exam remains normal,
 a family or personal history of migraine
headaches is common, as are typical migraine
triggers

46.  The key distinguishing factor between
migraine and Meniere disease is the lack of
progressive unilateral hearing loss in
patients with migraine
 Other types of dizziness are common in patients
with migraine as well, including nonspecific
dizziness and positional vertigo
 Though the diagnosis of migraine associated
dizziness remains one of exclusion, little else can
cause recurrent episodes without any other
symptoms over a long period of time

47. CERVICAL VERTIGO
 Vertigo may follow injuries to neck 7-10 days
after accident
 Examination shows tenderness in neck,spasm of
cervical muscles & limitations of neck
movements
 It may be due to disturbed vertebrobasilar
circulation, involvement of sympathetic vertebral
plexus or alteration of tonic neck reflexes

48. OTHER CAUSES OF VERTIGO
 Ocular Vartigo
 Normally, balance is maintained by integrated
information received from the eyes, labyrinths
and somatosensory system.
 A mismatch of information from any of these
organs causes vertigo and in this case from the
eyes
 Ocular Vertigo may occur in case of acute
extraocular muscles paresis or high errors of
refraction

49.  Psychogenic Vertigo
 This diagnosis is suspected in patients suffering
from emotional tension and anxiety.
 Symptom of vertigo is often vague in the form of
floating or swimming sensation or light-
headedness.
 No nystagmus or hearing loss

50. MANAGEMENT OF VERTIGO
Particle repositioning maneuvers
 Dix-Hallpike Maneuver
 Semont
 Epley

51. DIX-HALLPIKE MANEUVER

52. SEMONT MANEUVER

53. EPLEY’S MANEUVER

55. DRUGS USED IN THE
TREATMENT OF VERTIGO
 Antihistamines
 Meclizine
 Promethazine
 Dimenhydrinate
 Anticholinergics
 Scopolamine
 Diazepam
 Sympathomimetics
 Amphetamine
 Ephedrine