Fits, faints and funny turns presentation slides

1. FITS, FAINTS &
FUNNY TURNS
GROUP E2
RAMPRAVINDER, DACHANI, SYAHIRAH, SHIVANYA
MAY, ALICIA, SYARIFAH, SYAZWI, SOON HENG
PHANG TECK, EUGENE, GEETHA, SYAKIRAH

2. FITS

3. OUTLINE
DEFINITION
CAUSES
CLASSIFICATION OF FITS
HISTORY TAKING
INVESTIGATIONS
RESTRICTIONS
STATUS EPILEPTICUS
MANAGEMENT
IMPLICATIONS (SOCIAL, LEGAL, ETC)
DIFFERENTIAL DIAGNOSIS

4. DEFINITION

5. Definition
• SEIZURE
• any clinical event caused by an abnormal
electrical discharge in the brain
• EPILEPSY
• the tendency to have recurrent seizure.It is
a disorder characterized by the occurrence
of at least 2 unprovoked seizures.

7. Causes
PRIMARY GENERALIZED EPILEPSY
DEVELOPMENTAL(EG: HAMARTOMAS, NEURONAL MIGRATION ABNORMALITIES)
HIPPOCAMPAL SCLEROSIS
BRAIN TRAUMA/SURGERY
INTRACRANIAL MASS LESION(EG:TUMOUR, NEUROCYCTICERCOSIS)
VASCULAR(EG: CEREBRAL INFRACTION)
ENCEPHALITIS AND INFLAMMATORY CONDITION(EG: HERPES SIMPLEX)
METABOLIC ABNORMALITIES(EG: HYPONATRAEMIA, HYPOCALCAEMIA)
NEURODEGENERATIVE DISORDERS(EG:ALZHEIMER'S)
DRUG AND ALCOHOL WITHDRAWAL

8. Classification of
Fits

9. SEIZURES
GENERALIZED SEIZURES PARTIAL SEIZURE UNCLASSIFIED SEIZURES
! ABSENCE
! GENERALIZED
TONIC-CLONIC
SIZURES
! MYCLONIC
! TONIC AND ATONIC
SEIZURES
! SIMPLE
PARTIAL SEIZURE
! COMPLEX
PARTIAL SEIZURE

10. • GENERALIZED
• Absence
• Myoclonic
• Tonic-clonic
• Tonic
• Akinetic
• PARTIAL
• Simple partial
• Complex partial
• Partial seizure evolving to tonic clonic
• Apparent generalized tonic clonic
• UNCLASSIFIED (does not fall into either category)

12. SIMPLE PARTIAL SEIZURE
PARTIAL MOTOR SEIZURE
" ARISE FROM PRE-CENTRAL
GYRUS AFFECTING
CONTRALATERAL FACE ,ARM
OR LEG
PARTIAL SENSORY SEIZURES
SOME ATTACK BEGIN AT ONE PART OF
THE BODY(MOUTH,THUMB,TOE)
INVOLVED OTHER PART OF THE
BODY(JAKSONIAN SEIZURE)
IF LOCAL TEMPORARY PARALYSIS OF
THE LMP FELLOW CALL TODD'S
PARALYSIS
ARISE IN SENSORY CORTEX AND
CAUSE UNPLEASANT TINGLING
SENSATION OR 'ELECTRIC'
SENSATION IN CONTRA-LATERAL
FACE OR LIMBS

15. PETIT MAL (Absence)
• Starts in childhood
• Generalised discharge does not spread out
of hemispheres
• Abnormal electrical fail to effect muscle tone
(reason why no lost of posture)
• Since generalized, there is loss of consciousness
• Attack often mistaken with complex partial
seizure
• Shorter in duration and occurs more frequently
(20-30 times/day)

17. Tonic Clonic Seizure
• No aura as seizure can cause retrograde
amnesia
• Severely bitten tongue, bleeding after loss of
consciousness is pathognomic of generalized
seizure
• Body goes rigid and become unconscious
• Falls down, followed by clonic phase with
synchronous jerking of the limbs

18. Tonic Clonic Seizures
• After few seconds -->
rigidity replace by flaccid
state -->
persist for few minutes -->
regain consciousness -->
confused/disoriented
• Urinary incontinence and
tongue biting (+)
• Have headache, feels sleepy

19. VIDEOS

20. HISTORY
TAKING

21. History
taking
• Ask about type of seizure patient
experienced/ person who observed the
seizure
• Any aura present prior to incident?
• Enquire about possible triggers

22. Triggering factors
• Sleep deprivation
• Alcohol
• Recreational drug use
• Physical and mental exhaustion
• Flickering lights (ie:TV, computer)
• Infections and metabolic disturbances
• Uncommon: loud noises, hot baths, etc

23. Examination
EXAMINATION DIFFERENTIAL DIAGNOSIS
FEVER WITH STIFF NECK
" MENINGITIS
" SUBARACHNOID
HEMORRHAGE
" MENINGOENCEPHALITIS
PAPILLOEDEMA "↑ ICP
LOSS SPONTANEOUSVENOUS PULSATION " ICP
FOCAL NEUROLOGIC DEFECT(EG:ASYMMETRY OF
REFLEX OR MUSCLE STRENGTH)
" STROKE,POSTICTAL PARALYSIS
SKIN LESION(EG: SHAGREEN PATCHES, CAFE 'AU-LAIT) NEUROCUTANEOUS DISORDER
GENERALIZED NEUROMUSCULAR
IRRITABILITY(HYPER-REFLEXIA,TREMULOUSNESS)
" DRUG TOXICITY(EG:SYMPATHOMIMETIC)
" WITHDRAWAL SYNDROME(EG:ALCOHOL
OR SEDATIVES)
" CERTAIN METABOLIC
DISORDER(HYPOCALCAEMIA)

24. Tuberous sclerosis
Adenoma sebaceum

25. 25

26. INVESTIGATION
ARE THE ATTACK
TRULY EPILEPTIC
FROM WHERE IS THE
EPILEPSY ARISING
WHAT IS THE
CAUSE OF THE
EPIEPSY
AMBULATORY EEG
VIDEOTELEMETRY
" STANDARD EEG
" SLEEP EEG
" EEG WITH
SPECIAL
ELECTRODES
STRUCTURAL
LESION
" CT
" MRI
INFLAMMATORY
OR INFECTIVE
DISORDER
METABOLIC DISORDER?
" UREA N ELECTRODE
" LFT
" BLOOD GLUCOSE
" SERUM CAL,MG
" FBC/ESR/CRP
" CHEST- X-RAY
" CSF EXAMINATION
" SEROLOGY FOR
SYPHILIS, HIV,
COLLAGEN DISEASE

27. Routine Investigations I
• METABOLIC
• Blood glucose
• Serum electrolyte
• Magnesium, calcium levels
• Renal function test (RFT)
• Liver function test (LFT)

28. Routine Investigations II
• INFECTIONS/INFLAMMATORY
• Full blood count
• ESR
• CRP
• Serology for syphilis
• HIV
• Collagen disease
• Chest X-ray
• CSF examination

29. Electro-encephalography
(EEG)
• Diagnosis including the
type
for all patients with
unprovoked first fit
• Not very sensitive
• Only 50% have abnormal
interictal EEG
• Sensitivity improved by
sleep

30. Indications for brain imaging
• Epilepsy starting after age of 20 years
• Seizures have focal features clinically
• EEG shows a focal seizure source
• Control of seizures is poor or
patient deteriorates

31. To investigate the cause
• Find out whether
• Structural defect (MRI, CT)
• Metabolic causes
• Infective/inflammatory

32. IMAGING
• Magnetic Resonance Imaging (MRI)
• Computed tomography (CT)

33. Epileptic nature of attacks
• Ambulatory EEG
• Video telemetry
Where the epilepsy is arising
• Standard EEG
• Sleep EEG
• EEG with special electrodes
Investigations in suspected cases

34. Implications/Advise I
• Avoid working at height/
with heavy machinery, fire,
water
• Take bath when relative is
around /do not lock the
bathroom
• Recreational activities in
company of someone
• Discourage cycling until 6
months freedom from
seizure

35. Implications/Advise II
• Single day time seizure – for 1 year
• Free from seizure during sleep for
> 3 years
• Drug withdrawal- for 6 months
after withdrawal
• Vocational drivers- until off
medication & seizure free for > 10
years

36. Status epilepticus
• A seizure or series of seizures lasting
30minutes without the patient regaining
awareness between attacks.
• It is a life threatening medical
emergency

37. MANAGEMENT
OF SEIZURE

38. sz

42. Immediate management
!Ensure airway is patent.
!Give oxygen to offset cerebral hypoxia.
!Give intravenous anticonvulsants
- eg. Diazepam 10mg, only if convulsion are continuous or
repeated.
!Take blood for anticonvulsant levels (if known epileptic)
!Investigate cause

43. Management
• The goal of treatment in patients with epileptic
seizures is to achieve a seizure-free status without
adverse effects.
• The mainstay of seizure treatment is anticonvulsant
medication.
• The drug of choice depends on an accurate
diagnosis of the epileptic syndrome.

44. Guidelines for therapy I
•Start with one 1st line drug.
•Start at a low dose, gradually increase
dose until effective control of seizure is
achieved .
•Optimize compliance (use minimum
number of doses per day)
•If first drug fails, start second 1st line drug
whilst gradually withdrawing first drug.

45. Guidelines for therapy II
•If second drug fails, start 2nd line drug + 1st
line drug at maximum tolerated dose
(beware of interactions)
•If this combination fails, check compliance and
reconsider diagnosis.
•If this combinations fails, consider alternative,
non-drug treatment (eg. Epilepsy surgery, vagal
nerve stimulation)
•Do not use more than two drugs in
combination at any one time

46. Anti-epileptic drugs

47. Lifestyle modification
As soon as possible, patients should be made aware of the riskiness
of any activity where loss of awareness would be dangerous.
- Avoid activities such as :

48. -Only shallow baths ( shower) should be taken, preferably
with someone else in the house and with bathroom door
unlocked.
- Cycling should be discouraged until at least 6 months
freedom from seizures has been achieved.

49. Management of Status
Epilepticus
INTIAL
•Ensure airway is patent, give oxygen to prevent cerebral hypoxia
and secure intravenous access.
•Draw blood for glucose, urea and electrolytes, liver function and
store a sample for future analysis (e.g. drug misuse)
•Give diazepam 10 mg i.v. or rectally or lorazepam 4mg i.v.- repeat
once after 15 mins.
•Transfer to intensive care area, monitoring neurological condition,
blood pressure, respiration and blood gases, intubating and
ventilating patient if appropriate.

50. cont.
ONGOING
If seizure continue after 30mins
-i.v infusion (with cardiac monitoring) with one of :
•Phenytoin: 15mg/kg at 50mg/min
•Fosphenytoin: 15mg/kg at 100mg/min
•Phenobarbital: 10mg/kg at 100mg/min
If seziures still continue after 30-60 mins
•Start treatment for refractory status with intubation,
ventilation,
And general anaesthesia using propofol or thiopental.

51. cont.
• Once status controlled
• Commence longer term anticonvulsant medication with
one of:
- Sodium valproate 10mg/kg i.v. over 3-5 mins,
then 800-2000 mg/day.
- Phenytoin: give loading dose of 15mg/kg,
infuse at <50mg/min, then 300mg/day.
- Carbamazepine 400mg by nasogastric tube,
then 400-1200 mg/day
• Investigate cause

52. CONSEQUENCES
OF
MISDIAGNOSIS

53. Legal Consequences
DRIVING REGULATIONS
-Patients should be asked to stop driving after a
seizure and inform the regulatory authority if they
hold a driving license.
- After seizure, a temporary driving ban until seizure
free.
- Regulations differ from country to country.
- Many regulatory bodies also suggest refraining from
driving while withdrawing from anti-epileptic drugs.
- Notify the motor insurance company.

55. Economical Consequences
• Employers may refuse employment to
potential employees with epilepsy or
refuse advancement to existing
employees with epilepsy.
• Structural stigma can be perceived in
the policies of state institutions, which
systematically discriminate against or
restrict the opportunities available to
stigmatized group.
• Certain occupation, such as nursery
nurse or airline pilot are not open to
anyone who ever had an epileptic
seizure.

56. • Stigma and resultant psychosocial
issues are major hurdles that
people confront in their daily life.
• People with epilepsy, particularly
women, living in economically
weak countries.
• In a country where the majority of
marriages remain arranged,
families of people with epilepsy
may confront stigma when they
try to arrange marriages.

57. DIFFERENTIAL
DIAGNOSIS
OF
SEIZURES

58. Ddx I
• SYNCOPE
• (cardiac arrhythmia, vasovagal attack, etc)
• PSEUDO-SEIZURE
• (non-epileptic attack disorder)
• METABOLIC CONDITIONS
• (hypoglycemia, hyponatriemia)
• MIGRAINE
• (migraine with aura, etc)

59. Ddx II
• MOVEMENT DISORDERS
• (paroxysmal dyskinesia)
• VASCULAR CONDITIONS
• (TIA)
• SLEEP DISORDERS
• (cateplexy, nacrolepsy, night terror)
• PSYCHIATRIC DISORDERS
• (conversion, panic attack, breath holding spell,
malingering)

60. Syncope

61. VIDEO

63. Hypoglycemia
• Causes confusion, followed by loss of
consciousness (LOC)
• May cause convulsion, dysphasia, hemiparesis
• Comes with warning signs

64. Migraine

65. Panic attack
• Triggered by sudden sympathetic activation
and often hyperventilation
• Consciousness is usually preserved and
attacks easily recognized
•

66. FAINTS

67. OUTLINE
DEFINITION
ETIOLOGY
DIAGNOSIS
INVESTIGATION
MANAGEMENT

68. SYNCOPE

69. Definition:
Syncope is a total loss of consciousness due to
transient global cerebral hypoperfusion
characterized by rapid onset, short duration,
and spontaneous complete recovery.

70. Classification:
Syncope
Cardiogenic
Arrhythmia Structural
Non-
cardiogenic
Neurocardioge
nic
Orthostatic
hypotension

71. i. Cardiac Syncope
! ARRHYTHMIA
! Bradycardia
! Sinus node dysfunction- SICK SINUS SYNDROME
! AV block- Mobitz II and complete AV block
! Implanted device malfunction
! Tachycardia
! SVT
! VT
! STRUCTURAL
! Cardiac
! Severe aortic stenosis, hypertrophic
cardiomyopathy, myocardial infarction
! Others
! Pulmonary embolus, pulmonary hypertension,
acute aortic dissection

72. ii. Reflex (Neurocardiogenic/
Neurally-mediated) Syncope
! VASOVAGAL:
! Mediated by emotional distress: fear, pain, instrumentation,
blood phobia
! Mediated by orthostatic stress
! SITUATIONAL:
! Cough
! GI stimulation (swallow, defaecation, visceral pain)
! Micturition (post-micturition)
! Post-exercise
! Post-prandial
! CAROTID SINUS SYNCOPE (HYPERSENSITIVE CAROTID
SINUS SYNDROME)
! Atypical form (without apparent triggers and/or atypical
presentation)

73. CAROTID SINUS SYNCOPE (HYPERSENSITIVE CAROTID
SINUS SYNDROME)
BARORECEPTOR
is sensitive to
external pressure
BRADYCAR
DIA
VASODILATAT
ION

74. iii. Syncope due to orthostatic
hypotension
! Primary autonomic failure
! Pure autonomic failure, multiple system atrophy, Parkinson’s
disease with autonomic failure, Lewy body dementia
! Secondary autonomic failure
! DM, amyloidosis, uraemia, spinal cord injuries
! Drug-induced orthostatic hypotension
! Alcohol, vasodilators, diuretics, phenotiazines,
antidepressants
! Volume depletion
! Haemorrhage, diarrhea, vomiting

75. ANF = autonomic nervous failure
ANS = autonomic nervous system
OH = orthostatic hypotension.
Guidelines for the diagnosis and
management
of syncope (version 2009)-European Heart
Journal (2009)

76. Diagnosis of syncope
! QUESTIONS TO BE ANSWERED:
! Was loss of consciousness complete?
! Was loss of consciousness transient with rapid onset
and short duration?
! Did the patient recover spontaneously, completely
and without sequelae?
! Did the patient lose postural tone?
≥1 answer is NEGATIVE, then exclude
other form of loss of consciousness

77. Guidelines for the diagnosis and management
of syncope (version 2009)-European Heart Journal (2009)

78. History to ask……..
1. Prior to attack
! Position (supine, sitting or standing)
! Activity (rest, change in posture, during/
after exercise, during/immediately after
urination, defaecation, cough or swallowing)
! Predisposing factors (crowded/warm places,
prolonged standing, post-prandial period)
! Precipitating events (fear, intense pain,
neck movements)
2. Onset of attack
! Nausea, vomiting, abdominal discomfort,
feeling of cold, sweating, aura, pain in the
neck/shoulder, blurred vision, dizziness
! Palpitation

79. 3. About the attack (eyewitness)
! Way of falling (slumping/kneeling over)
! Skin color (pallor, cyanosis, flushing)
! Duration of loss of consciousness
! Breathing pattern (snoring)
! Movement (tonic, clonic, tonic-clonic, minimal
myoclonus or automatism) & its duration
! Onset of movement in relation to fall
! Tongue biting
4. About the end of attack
! Nausea, vomiting, sweating, feeling of cold, confusion,
muscle aches, skin color, injury, chest pain,
palpitations, urinary/faecal incontinence

80. 5. Other history:
! Recurrent syncope: 1st syncope episode, number
of spells
! Comorbid:
! Cardiac disease
! Neurological (Parkinsonism, epilepsy,
narcolepsy)
! Metabolic (DM)
! Medication (antihypertensive, anti-angina, anti-
arrhythmia, diuretic, QT prolonging agent, anti-
depressants)
! Alcohol

81. DAVIDSON’S PRINCIPLES&PRACTICES
OF MEDICINE

82. DAVIDSON’S PRINCIPLES&PRACTICES
OF MEDICINE

83. INVESTIGATIONS

84. • Carotid sinus massage
• Tilt testing
• OTHERS:
• EP testing
• signal averaged (V) ECG
• Echocardiography
• ETT
• cardiac catheterization
• neurological/psychiatric evaluation

86. Holter ECG

87. Carotid Sinus Massage

88. Carotid Sinus Massage
Protocol I
• Massage longitudinally, site of maximal impulse,
anterior margin SCM muscle level of cricoid
cartilage
• 5 –10 seconds, right first, then left after 1-2
minute break (Newcastle protocol 10secs)
• Continuous ECG and BP monitoring mandatory
• Neurological complication in 0.45% in a series of
1600 patients (5secs massage)

89. Carotid Sinus Massage
Protocol II
• Diagnostic if ventricular pause is more than three
seconds or if a decrease in systolic blood pressure > 50
mm Hg
• Contraindicated in patients with
• bruits
• history of transient ischemic attack
• cerebrovascular accident within the past three
months

90. Tilt Table Test

91. Tilt Table Testing
• Supine at least 20 minutes prior to tilt
• Tilt angle 70 degrees
• Passive phase min 20 to 45 minutes
• Use either intravenous isoprenaline or sublingual GTN
if passive phase is negative
• Pharmacological phase – 15 to 20 minutes
• End-point: induction syncope

92. Normal Test

93. Cardio-inhibitory
response

94. Vasodepressor response
BP drops from 150/70 to 50/30 but heart rate stays
same

95. Mixed response
BP drops from 150/60 to 50/20 while HR drops from 65
to 30bpm

97. Orthostatic hypotension
steady drop in BP and rise in HR

98. General Management I
• “Initial evaluation” that consists of
• history taking and physical examination, including
orthostatic blood pressure measurements and standard
electrocardiogram (rule out arrhythmia cause)
• Determine the severity and frequency of the episodes and
the presence or absence of heart disease
• Determining the mechanism of syncope is a prerequisite
for advising patients with regard to prognosis, and to
developing an effective mechanism-specific treatment

99. General Management II
• Base on good history, we could diagnose vasovagal
type syncope
• Most patients with syncope require only reassurance
and education regarding the nature of the disease and
the avoidance of triggering events

100. Neurally Mediated
(reflex) Syncope I
• Reassurance and education regarding the
nature of the disease and the avoidance of triggering
events
• Syncope in a high risk setting:
• Syncope is very frequent—for example, alters the
quality of life

101. Neurally Mediated
(reflex) Syncope II
• Syncope is recurrent and unpredictable (absence of
premonitory symptoms) and exposes patients to
“high risk” of trauma
• Syncope occurs during the prosecution of a “high
risk” activity (for example, driving, machine
operation, flying, competitive athletics, etc).

102. • Non-pharmacological “physical” treatments
• The prescription of progressively prolonged periods
of enforced upright posture (so-called “tilt-
training”) may reduce syncope recurrence
• Isometric counterpressure manoeuvres of the legs
(leg crossing), or of the arms (hand grip and arm
tensing)
• Induce a significant blood pressure increase during
the phase of impending vasovagal syncope
• Allow the patient to avoid or delay losing
consciousness in most cases

103. Pharmacological
Treatment
• Midodrine - first line of
treatment
•Fludrocortisone

104. Orthostatic Hypotension
• Drug-induced autonomic
failure is probably the
most frequent cause
• Principal treatment
strategy is elimination of
the offending agents,
mainly diuretics and
vasodilators

105. Cardiac Arrhythmias
• Must receive treatment
appropriate to the cause
• It is life-threatening and when
there is a high risk of injury
• Cardiac pacing, implantable
cardioverter-defibrillators,
and catheter ablation are the
usual treatments

106. Structural cardiac defect
• Treatment is best directed at
amelioration of the specific structural
lesion or its consequences.

107. 1. Kumar & Clarks Clinical medicine 8th edition by Parveen Kumar, Michael Clark
2. Davidson’s Principles and Practice of Medicine 21th edition by Nicki R.Colledge, Brian
R.Walker, Stuart H.Ralston
3. Diagnosis and treatment of syncope by Michele Brignole
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861366/
4. Syncope by Rumm Morag, MD, FACEP
http://emedicine.medscape.com/article/811669-overview
5. Syncope (Fainting) by American Heart Association
http://www.heart.org/HEARTORG/Conditions/Arrhythmia/
SymptomsDiagnosisMonitoringofArrhythmia/Syncope-Fainting_UCM_430006_Article.jsp
6. Evaluation of Syncope by ROBERT L. GAUER, MD
http://www.aafp.org/afp/2011/0915/p640.html
References

108. FUNNY TURNS

109. OUTLINE
DEFINITION AND SUBTYPES
DIFFERENTIAL DIAGNOSIS
HISTORY TAKING
CLINICAL EXAMINATION
VESTIBULAR EXAMINATION
NYSTAGMUS
SPECIAL EXAMINATIONS
DEMONSTRATION
PERIPHERALVS CENTRALVERTIGO
OTHER INVESTIGATIONS

110. Definition
and Subtypes

111. Philip D. Sloane, MD, MPH; Remy R. Coeytaux, MD; Rainer S. Beck, MD; and John Dallara, MD Dizziness: State of the Science Ann Intern Med. 2001;134:823-832.
Dizziness
subtype
Type of sensation Temporal
Characteristics
Other Specification
Vertigo A feeling one that one or One’s
surroundings are Moving (spinning)
Episodic vertigo
(seconds to days)
Continuous vertigo
(most of the time for
at least a week)
Characteristics, duration, and date of the first
episode, length of episodes; and exacerbating
factors.
Presyncope A lightheaded, faint feeling, as
though one were about to pass out.
Typically occurs in
episodes lasting
seconds to hours.
1) Has syncope ever occurred during an episode
2) Do episodes occur only when the patient is
upright, or do they occur in other positions?
3) Are episodes associated with palpitations,
medication meals, bathing, dyspnea, or chest
discomfort?
Disequilibrium Unsteadiness:
- felt in lower limb
- prominent when standing or
walking
- relieved by sitting or lying down
Usually present.
Although it may
fluctuate in intensity
Identify whether symptom occurs in isolation or
accompanies another dizziness subtype; describe
exacerbating factors.
Other
dizziness;
anxiety-
related, ocular,
tilting
environment ,
other
A feeling not covered by the above
definitions, may include swimming
or floating sensations, vague
lightheadedness, or feeling of
dissociation.
Present all the time
~ days/weeks/years
-Is dizziness a/w anxiety or hyperventilation?
- Was change in vision connected with dizziness
onset? - Environment is
tilting sideways (suggests an otolith problem?

112. !Nature
!Duration
!Associated
symptoms
!Precipitating
factors
!VNG
!VEMP (Ocul & Cer.)
!V-Hit
!EcohG
!Posturography
!Rotating Chair
!Subjective vertical
test
!Gen. exam.
!Eye exam.
!Aural exam.
!Neurology
exam.
!Specific test

113. • Peripheral vertigo
• Meniere’s disease
• BPPV
• Vestibular neuronitis
• Labyrinthinitis
• Vestibulotoxic drugs
• Head trauma
• Perilymph fistula
• Syphillis
• Acoustic neuroma
• Migraine
• Brainstem lesion
• Cerebellar lesion
Differential Diagnosis
PERIPHERALVERTIGO CENTRALVERTIGO

114. History Taking

115. •Chief Complaint
• dizziness
• lightheadedness
• headache
• floating
• pre-syncope
• whirling
• unsteadiness
•Nature
• spinning-vestibular
• unsteadiness-central lesion
• feeling faint-orthostatic
• unspecific-psychology

116. • Duration
• Seconds: BPPV
• Minutes: TIA
• Hours: Meniere’s
• Days: Neuronitis
• Years: Ototoxins
• Associated symptoms
• positional related, hearing disturbance,
headache, stress
• Precipitating symptoms/triggers

117. Duration
Duration of
episode
Suggested diagnosis
Seconds Peripheral: unilateral loss of vestibular fx, late stage
of acute vestibular neuronitis & MD
Seconds - minutes BPPV. perilymphatic fistula
Minutes – one hour Posterior transient ischemic attack; perilymphatic
fistula
Hours MD; perilymphatic; migraine.Acoustic neuroma
Days Early acute vestibular neuronitis, stroke, migraine,
multiple sclerosis
Weeks Psychogenic (constant ~weeks w/o Improvement)

118. Associated
symptoms I
Symptom Suggested diagnosis
Aural fullness Acoustic neuroma; Meniere’s disease
Ear or mastoid
pain
Acoustic neuroma; acute middle ear disease
(e.g; otitis zoster oticus)
Facial
weakness
Acoustic neuroma; herpes zoster oticus

119. Associated
symptoms II
Symptom Suggested diagnosis
Facial neurologic CPA tumour; CVA; MS
Headache Acoustic neuroma; migraine
Hearing loss MD; PLF; acoustic neuroma; cholesteatoma;
otosclerosis;TIA or stroke involving anterior
cerebella artery, herpes zoster oticus

120. Associated
symptoms III
Symptom Suggested diagnosis
Imbalance Acute vestibular neuronitis (usually moderate); CPA
tumor (usually severe)
Nystagmus Peripheral or central vertigo
Phonophobia,
photophobia
Migraine
Tinnitus Acute labyrinthitis; acoustic neuroma; Meniere’s
disease

121. Precipitating Factors
Provoking Factor Suggested diagnosis
Changes in head position Acute labyrinthitis; BPPV; CPA Tumour;
multiple sclerosis (MS); PLF
Spontaneous episodes AVN; CVA (stroke or TIA; MD ; migraine; MS
Recent URTI Acute vestibular neuronitis (AVN)
Stress Psychiatric or psychological causes; migraine
Changes in ear press.,
trauma, excess. straining,
loud noises
Perilymphatic fistula (PLF)

122. • Past Medical History
• vascular risk factors
• ear surgery
• Family History
• similar disorder
• migraine
• Drug History
• present and past exposures to ototoxins
• antihypertensives

123. Clinical
Examination

124. • General Medical Condition
• Blood pressure (lying and sitting)
• Cardiac arrhythmias
• Neck Examination
• Aural examination
• otitis media
• ear wax
• perforated ear drum
• cholesteatoma

125. • Eye Examination
• Visual acuity
• Nystagmus
• Neurological Examination (focused)
• cranial nerve palsies(Multiple sclerosis, acoustic
neuroma, advanced brain stem tumor or basilar
artery insufficiency)
• gait
• motor& sensory
• cerebellar: finger nose, dysdiadokokinesia

126. Cerebellar signs

127. Vestibular Examination
• to examine the vestibulo-ocular reflex (VOR) and
vestibulo-spinal reflex(VSR)
• A good vestibular function is when there is a robust
oculo-cephalic reflex and intact visual acuity with active
head movements.
• Decreased vestibular function is when there is absence of
oculocephalic reflex or a decrease in visual acuity with
head movements.

128. Nystagmus

129. Peripheral nystagmus I
• due to normal or diseased functional states of the vestibular
system
• maybe spontaneous, evoked or positional
• rotatory and inhibited by visual fixation
•GAZE INDUCED
• exacerbated as a result of changing one’s gaze toward
or away from a particular side which has an affected
vestibular apparatus

130. Peripheral nystagmus II
•POSITIONAL
• when a person’s head in a specific position eg: BPPV
•POST ROTATIONAL
• after an imbalance is created between a normal side and a
diseased side by stimulation of the vestibular system by
rapid shaking or rotation of the head
•SPONTANEOUS
• randomly regardless of the position of the patient’s head

131. Central nystagmus
• Occurs as a result of either normal or abnormal
processes not related to the vestibular organ.
• For example lesions of the mid-brain or cerebellum can
result in up and down beat nystagmus
• Purely horizontal or vertical and not suppressed by visual
fixation

132. Special Maneuvers
Hallpike Maneuver
Fistula Test
Caloric Test
Romberg Test

133. Hallpike Manoeuvre (Positional test) I
• Method:
• Patient sits on a couch
• Examiner holds patient’s head, turns it 45 degree to the
right and then places the patient in a supine position so
that his head hangs 30 degree below the horizontal.
• Patient’s eyes are observed for nystagmus.
• This test is repeated with head turned to left and then
again in straight head-hanging position.
• Useful when patient complains of vertigo in certain
head position
• Helps to differentiate a peripheral from a central
lesion

134. Hallpike Manoeuvre (Positional test) II
Peripheral Central
Latency 2-20 seconds No latency
Duration < 1 minute > 1 minute
Direction of
nystagmus
Direction fixed,
toward the
undermost ear
Direction changing
Fatiguability Fatiguable Non-fatiguable
Accompanying
symptoms
Severe vertigo None or slight

136. Fistula Test
• This test induce nystagmus by producing
pressure changes in the external canal
which are then transmitted to the
labyrinth.
• This test is performed by
• applying intermittent pressure on the tragus or by
• using Siegle’s speculum.

138. Fistula Test
• RESULTS:
• NEGATIVE: normal
• POSITIVE: erosion of HCC as in cholesteatoma,
fenestration operation, post-stapedectomy fistula or
rupture of round window membrane; also indicate the
labyrinth is still functioning.
• FALSE NEGATIVE: cholesteatoma covers the site of
fistula
• FALSE POSITIVE: seen in congenital syphilis and 25%
cases of Meniere’s disease

139. Caloric test
• Before the test, check both ear canals for tympanic perforation
and was to make sure they are normal.
• Test one ear at a time
• A small amount of cold water or air is gently delivered into one
ear.
• Nystagmus should be seen and they should move away
from the ear and slowly back.
• Next a small amount of warm water or air is delivered into the
same ear.
• Nystagmus should be seen but this time towards
the examining ear and slowly back.
• The other ear is tested in the same way

140. Caloric test
• Mnemonic: COWS; Cold Opposite, Warm Same
• Absent of nystagmus:
• weakness of the semicircular canal on the side being tested
• brainstem damage

141. Caloric Test

142. Romberg Test
• Patient is asked to stand with feet together and arms by
the side with eyes first open and then closed.
• In peripheral vestibular lesions, the patient sways
to the side of lesion.
• In central vestibular disorder, patient shows
instability.

143. Romberg Test
• If patient can perform this test without sway,“sharpened
Romberg test”, is performed.
• In this the patient stands with one heel in front of toes
and arms folded across the chest.
• Inability to perform indicates vestibular impairment.

144. Romberg Test

145. Peripheral
vs
Central
vertigo

146. Feature
Definition
Peripheral Vertigo
Vestibular end organs and their first
order neurons(vestibular nerve).
Cause lies in internal ear/8th
nerve. 85% of vertigo
Central Vertigo
Central nervous system after the
entrance of vestibular nerve in the
brainstem and involve vestibule-
ocular, vestibule-spinal & other
central nervous system pathways
Nystagmus Mix horizontal & tensional;
inhib. by fixation of eyes;
Fades after a few days; not
change direction with gaze
to either side
Purely vertical , horizontal, or torsional;
not inhibited by fixation of eyes ; last
weeks to months; change direction
With gaze towards fast phase of
Nystagmus
Imbalance Mild to moderate; able to walk Severe; unable to stand or walk
Nausea, vomiting May be severe Varies
Hearing loss,
tinnitus
Common Rare
Neurologic Sx
Rare Common
Latency
(follow. pro-
vocative)
Longer (up to 20 seconds) Shorter (up to 5 seconds)
Ddx
Peripheral neutitis, BPPV, Meniere’s
disease
Migraine,TIA, Stroke, Multiple
sclerosis, tumour

147. How do we know if vertigo is due to
a vestibular weakness?
• Case History
• onset
• duration
• ear symptoms
• Audiological and vestibular evaluation
• Pure tone and immittance audiometry
• Video- or electro-nystagmography
• Rotary chair testing
• Computerized dynamic posturography
• Vestibular-evoked myogenic potential (VEMP)
• Electrocochleography (ECoG)

148. • Audiological test
• Pure tone audiometry(PTA)
• Tympanometry
• Radiological Examinations
• CT Scan
• MRI Scan
• Laboratory Investigations
• FBC
• Blood sugar
• Lipid profile

149. References
1. Diseases of ear, nose & throat by PL Dhingra and Shruti
Dhingra (5th edition)
2. www.medscape.com

150. THE END
THANK YOU FOR YOUR
ATTENTION