FITS, FAINTS & FUNNY TURNS

GROUP E2RAMPRAVINDER, DACHANI, SYAHIRAH, SHIVANYAMAY, ALICIA, SYARIFAH, SYAZWI, SOON HENGPHANG TECK, EUGENE, GEETHA, SYAKIRAH

FITS

OUTLINEDEFINITION

CAUSES

CLASSIFICATION OF FITS

HISTORY TAKING

INVESTIGATIONS

RESTRICTIONS

STATUS EPILEPTICUS

MANAGEMENT

IMPLICATIONS (SOCIAL, LEGAL, ETC)

DIFFERENTIAL DIAGNOSIS

DEFINITION

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.

CausesPRIMARY 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

Classification of Fits

SEIZURES

GENERALIZED SEIZURES PARTIAL SEIZURE UNCLASSIFIED SEIZURES

! ABSENCE! GENERALIZED

TONIC-CLONIC SIZURES

! MYCLONIC! TONIC AND ATONIC

SEIZURES

! SIMPLE PARTIAL SEIZURE! COMPLEX PARTIAL SEIZURE

• 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)

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

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)

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

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

VIDEOS

HISTORY TAKING

History taking

• Ask about type of seizure patient experienced/ person who observed the seizure

• Any aura present prior to incident?

• Enquire about possible triggers

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

ExaminationEXAMINATION DIFFERENTIAL DIAGNOSIS

FEVER WITH STIFF NECK

" MENINGITIS

" SUBARACHNOID

HEMORRHAGE

" MENINGOENCEPHALITIS

PAPILLOEDEMA "↑ ICP

LOSS SPONTANEOUS VENOUS 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)

Tuberous sclerosis

Adenoma sebaceum

25

INVESTIGATION

ARE THE ATTACK TRULY EPILEPTIC

FROM WHERE IS THE EPILEPSY ARISING

WHAT IS THE CAUSE OF THE

EPIEPSY

AMBULATORY EEGVIDEOTELEMETRY

" 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

Routine Investigations I

• METABOLIC

• Blood glucose

• Serum electrolyte

• Magnesium, calcium levels

• Renal function test (RFT)

• Liver function test (LFT)

Routine Investigations II

• INFECTIONS/INFLAMMATORY

• Full blood count

• ESR

• CRP

• Serology for syphilis

• HIV

• Collagen disease

• Chest X-ray

• CSF examination

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

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

To investigate the cause

• Find out whether

• Structural defect (MRI, CT)

• Metabolic causes

• Infective/inflammatory

IMAGING• Magnetic Resonance Imaging (MRI)

• Computed tomography (CT)

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

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

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

Status epilepticus• A seizure or series of seizures lasting

30minutes without the patient regaining awareness between attacks.

• It is a life threatening medical emergency

MANAGEMENT OF SEIZURE

sz

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

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.

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.

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

Anti-epileptic drugs

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 :

-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.

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.

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.

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

CONSEQUENCES OF MISDIAGNOSIS

Legal ConsequencesDRIVING 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.

Economical Consequences• Employers may refuse employment to

potential employees with epilepsy or refuse advancement to exist ing 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.

• 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 marr iages remain arranged, families of people with epilepsy may confront stigma when they try to arrange marriages.

DIFFERENTIAL DIAGNOSIS

OF SEIZURES

Ddx I• SYNCOPE

• (cardiac arrhythmia, vasovagal attack, etc)

• PSEUDO-SEIZURE

• (non-epileptic attack disorder)

• METABOLIC CONDITIONS

• (hypoglycemia, hyponatriemia)

• MIGRAINE

• (migraine with aura, etc)

Ddx II

• MOVEMENT DISORDERS

• (paroxysmal dyskinesia)

• VASCULAR CONDITIONS

• (TIA)

• SLEEP DISORDERS

• (cateplexy, nacrolepsy, night terror)

• PSYCHIATRIC DISORDERS

• (conversion, panic attack, breath holding spell, malingering)

Syncope

VIDEO

Hypoglycemia

• Causes confusion, followed by loss of consciousness (LOC)

• May cause convulsion, dysphasia, hemiparesis

• Comes with warning signs

Migraine

Panic attack

• Triggered by sudden sympathetic activation and often hyperventilation

• Consciousness is usually preserved and attacks easily recognized

•

FAINTS

OUTLINE

DEFINITION

ETIOLOGY

DIAGNOSIS

INVESTIGATION

MANAGEMENT

SYNCOPE

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

Classification:

Syncope

Cardiogenic

Arrhythmia Structural

Non- cardiogenic

Neurocardiogenic

Orthostatic hypotension

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

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)

CAROTID SINUS SYNCOPE (HYPERSENSITIVE CAROTID SINUS SYNDROME)

BARORECEPTOR is sensitive to

external pressure

BRADYCARDIA

VASODILATATION

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

ANF = autonomic nervous failureANS = autonomic nervous systemOH = orthostatic hypotension.

Guidelines for the diagnosis and managementof syncope (version 2009)-European Heart Journal (2009)

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

Guidelines for the diagnosis and managementof syncope (version 2009)-European Heart Journal (2009)

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

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

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

DAVIDSON’S PRINCIPLES&PRACTICES OF MEDICINE

DAVIDSON’S PRINCIPLES&PRACTICES OF MEDICINE

INVESTIGATIONS

• Carotid sinus massage

• Tilt testing

• OTHERS:

• EP testing

• signal averaged (V) ECG

• Echocardiography

• ETT

• cardiac catheterization

• neurological/psychiatric evaluation

Holter ECG

Carotid Sinus Massage

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)

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

Tilt Table Test

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

Normal Test

Cardio-inhibitory response

Vasodepressor response

BP drops from 150/70 to 50/30 but heart rate stays same

Mixed response

BP drops from 150/60 to 50/20 while HR drops from 65 to 30bpm

Orthostatic hypotensionsteady drop in BP and rise in HR

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

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

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

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).

• 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

Pharmacological Treatment

• Midodrine - first line of treatment

•Fludrocortisone

Orthostatic Hypotension

• Drug-induced autonomic failure is probably the most frequent cause

• P r i n c i p a l t re a tmen t strategy is elimination of the offending agents, mainly diuret ics and vasodilators

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

Structural cardiac defect

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

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

FUNNY TURNS

OUTLINEDEFINITION AND SUBTYPES

DIFFERENTIAL DIAGNOSIS

HISTORY TAKING

CLINICAL EXAMINATION

VESTIBULAR EXAMINATION

NYSTAGMUS

SPECIAL EXAMINATIONS

DEMONSTRATION

PERIPHERAL VS CENTRAL VERTIGO

OTHER INVESTIGATIONS

Definitionand Subtypes

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 episode2) 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?

!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

• Peripheral vertigo

• Meniere’s disease

• BPPV

• Vestibular neuronitis

• Labyrinthinitis

• Vestibulotoxic drugs

• Head trauma

• Perilymph fistula

• Syphillis

• Acoustic neuroma

• Migraine

• Brainstem lesion

• Cerebellar lesion

Differential DiagnosisPERIPHERAL VERTIGO CENTRAL VERTIGO

History Taking

• Chief Complaint• dizziness

• lightheadedness

• headache

• floating

• pre-syncope

• whirling

• unsteadiness

• Nature• spinning-vestibular

• unsteadiness-central lesion

• feeling faint-orthostatic

• unspecific-psychology

• Duration• Seconds: BPPV

• Minutes: TIA

• Hours: Meniere’s

• Days: Neuronitis

• Years: Ototoxins

• Associated symptoms• positional related, hearing disturbance,

headache, stress

• Precipitating symptoms/triggers

DurationDuration 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)

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

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

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

Precipitating FactorsProvoking 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)

• Past Medical History

• vascular risk factors

• ear surgery

• Family History

• similar disorder

• migraine

• Drug History

• present and past exposures to ototoxins

• antihypertensives

Clinical Examination

• General Medical Condition

• Blood pressure (lying and sitting)

• Cardiac arrhythmias

• Neck Examination

• Aural examination

• otitis media

• ear wax

• perforated ear drum

• cholesteatoma

• 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

Cerebellar signs

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.

Nystagmus

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

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

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

Special Maneuvers

Hallpike Maneuver Fistula TestCaloric TestRomberg Test

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

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

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.

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

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

Caloric test

• Mnemonic: COWS; Cold Opposite, Warm Same

• Absent of nystagmus:

• weakness of the semicircular canal on the side being tested

• brainstem damage

Caloric Test

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.

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.

Romberg Test

Peripheral vs

Central vertigo

FeatureDefinition

Peripheral VertigoVestibular end organs and their first

order neurons(vestibular nerve). Cause lies in internal ear/8th

nerve. 85% of vertigo

Central VertigoCentral 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; notchange 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,

tinnitusCommon Rare

Neurologic SxRare 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

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)

• Audiological test

• Pure tone audiometry(PTA)

• Tympanometry

• Radiological Examinations

• CT Scan

• MRI Scan

• Laboratory Investigations

• FBC

• Blood sugar

• Lipid profile

References

1. Diseases of ear, nose & throat by PL Dhingra and Shruti Dhingra (5th edition)

2. www.medscape.com

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