SEEIZURE AND VERTIGO WITH BPPV

1. APPROACH TO SEIZURE

2. Introduction
 Seizure
 Transient occurrence of sign and symptoms
 Abnormal, excessive or synchronous neuronal activity in brain
 Epilepsy
 A chronic condition
 Rrecurrent, unprovoked seizures
 Incidence 0.3–0.5%
 Prevalence 5–30 persons per 1000.

4. Pseudo-seizures and Hysterical Seizures
 Pseudoseizures-
 paroxysmal attacks of non- epileptic etiology
 waxing and waning movements during a single attack
 prolonged tonic-clonic activity without postictal disorientation
 non-rhythmic pelvic thrusting
 non-physiological evolution of symptoms such as motor activity spreading
from one hand to the other without first affecting the ipsilateral face or leg.

8. 1. When did you experience the first seizure in your life?
 Early neonatal period
 perinatal insults
 metabolic disorders, and
 congenital malformation.
 Generalized seizures tend to present in early childhood/teenage
 Elderly with new onset seizures
 structural pathology such as a stroke or brain tumor

9. 2.Do you experience some kind of warning or unusual
feeling at onset, or immediately preceding the seizure?
 The warning symptoms perceived at the onset of a seizure -“aura.”
 Aura - indicates that the seizure is focal in origin.
 Temporal lobe epilepsy
 déjà vu
 Epigastric sensation
 Parietal lobe epilepsy
 Paresthesias
 Occipital lobe epilepsy
 visual distortions
 transient blindness

10. 3. What happens during the seizure?
 Is there head or eye deviation to one side?
 Seizures originating from the frontal eye fields may cause head and eye
deviation to the contralateral side
 Is there excessive eye blinking at the onset?
 Ocipital lobe seizures can present with excessive blinking at the onset,
negative visual symptoms or visual distortions

11. 3. What happens during the seizure?
 If automatisms occur, are these more pronounced on one side?
 Temporal lobe seizures -lip smacking
-oral and alimentary automatic behavior
 Most pronounced in the ipsilateral extremity, along with dystonic posturing
of the contralateral arm
 Does the patient bite his tongue or lose control of the bladder
function?
 More often seen with generalized seizures

12. 4.What happens immediately following the seizure? Postictal
 Generalized tonic-clonic seizure
 postictal sleep
 disorientation and lack of awareness of the surroundings
 Hemiparesis or hemiplegia following a seizure (Todd’s paralysis)
 focal seizure
 Aphasia with otherwise normal awareness
 language areas in the dominant hemisphere.
 Absence seizures
 brief or no postictal disorientation

13. 5. Is there a diurnal variation?
 Tonic-clonic and myoclonic seizures seen in primary generalized
epilepsies
 more common on awakening or in early morning.
 Temporal lobe seizures
 occur any time.
 Certain frontal lobe seizures
 nocturnal presentation

14. 6. Are there any known triggering factors?
 Sleep deprivation
 Flickering lights
 Menses
 Alcohol consumption
 Non-compliance of medication
 Use of antihistamines
 Stress
 Fever
 Exercise

15. 7. What is the seizure frequency?
 Response to treatment
8. What has been the max seizure-free period?
 To determine if any specific antiepileptic drug was more
efficacious than the others.

16. 9. Is there more than one kind of seizure?
 Different seizure types
10.Has patient sustained injuries related to seizures?
 Do not have auras/ enough time after aura to take preventive measures
11.What is the frequency of visits to the emergency?
 Degree of seizure control

17. PAST MEDICAL HISTORY
 Central nervous system infections-
 meningitis, encephalitis, Lyme disease, cysticercosis.
 Head injuries, especially associated with
 depressed skull fracture,
 intracerebral hemorrhage,
 loss of consciousness
 prolonged amnesia
 Brain tumor
 Cerebrovascular accident

18. SOCIAL HISTORY
 Level of education
 Job description
 construction worker, heavy equipment mechanic, driver
 Planning pregnancy in the near future
 Teratogenicity of antiepileptic drugs
 Lower efficacy of oral contraceptives with enzyme-inducing medication
(phenytoin, carbamazepine, and phenobarbital),
 Alcohol use
 risk factor for a first generalized tonic-clonic seizure
 interact with the metabolism of the antiepileptic drugs
 seizure exacerbation, especially after continued or binge drinking.

19. FAMILY HISTORY
 Specific epilepsy syndromes and Genetically mediated
neurological disorders that have seizures as one manifestation.
 Juvenile myoclonic epilepsy (JME),
 Familial neonatal convulsions,
 Benign rolandic epilepsy

20. DRUGS PRECIPITATING SEIZURE

21. Examination
 Asymmetries in the size of limbs or one half of the body (hemiatrophy)
 perinatal cerebral insult
 Marks or ulcerations on the side of tongue or oral mucous membranes
 Gingival hyperplasia
 Phenytoin
 Dupytrens contractures
 chronic use of barbiturates
 Dystonic posturing of one arm on stressed gait, such as walking on the sides of the feet
 remote insult to the corticospinal tracts
 Multiple bruises or injuries
 falls secondary to seizures
 End gaze nystagmus, diplopia and difficulty in tandem walking
 toxicity related to antiepileptic medications such as carbamazepine, phenytoin, and lamotrigine

22. Examination
Stigmata of neurocutaneous syndrome
 Neurofibramatosis
 café au lait spots
 iris hamartoms
 Tuberous sclerosis
 Ash leaf spots
 shahgreen patches
 subungal fibromas
 adenoma sebaceum
 Sturge-Weber syndrome
 port-wine stain (capillary hemangioma)

23. INVESTIGATING THE FIRST SEIZURE
 A seizure is a symptom of an underlying pathology.
 Investigations
 directed at identifying the precipitating etiology and conditions that can
be arrested, reversed, or treated.
 A detailed history and physical examination - provides direction to the extent of
investigations

25. Laboratory Investigations
 Hyponatremia, hypoglycemia, hypomagnesemia, uremia and
hepatic encephalopathy
 Serum and urine toxicology should be done when substance
abuse or drug overdose is suspected.
 In newborns and young children appropriate metabolic screen can
be requested

26. Neuroimaging
 CT scan
 subdural hematoma, subarachnoid hemorrhage, abscess, neoplastic
processes, and other space occupying lesions.
 MRI
 cerebral dysplasia
 mesial temporal scleroses
 when history and physical examination is suggestive of
focal pathology and the CT does not show the cause

27. Electroencephalogram (EEG)
 EEG tests the cerebral function rather than structure.
 Epileptiform discharges on the EEG-helps to classify the seizure types
 Focal and generalized slowing-focal and generalized disturbance of cerebral
function respectively.
 Focal disturbance
 strokes, tumors, and abscess.
 Generalized disturbance
 toxic, metabolic, or diffuse structural abnormalities

29. Treatment
 Treatment of underlying condition
 Avoidance of precipitating factors
 Antiepileptic drugs
 Refractory epilepsy

30. Antiepileptic drugs
Appear to act primarily by blocking the initiation or spread of seizures
1. Inhibition of Na+-dependent action potentials in a frequency- dependent manner
 (e.g., phenytoin, carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide,
rufinamide),
2. Inhibition of voltage-gated Ca2+ channels
 (phenytoin, gabapentin, pregabalin),
3. Facilitating the opening of potassium channels
 (ezogabine),
4. Attenuation of glutamate activity
 (lamotrigine, topiramate, felbamate),

31. Antiepileptic drugs
5. Potentiation of GABA receptor function
 (benzodiazepines and barbiturates),
6. Increase in the availability of GABA
 (valproic acid, gabapentin, tiagabine),
7. Modulation of release of synaptic vesicles
 (levetiracetam).
8. Inhibiting T-type Ca2+ channels in thalamic
neurons.
 ethosuximide and valproic acid

32. When to Initiate Antiepileptic Drug Therapy
 Recurrent seizures of unknown etiology or a known cause that cannot be reversed
 Patients with a single seizure due to an identified lesion such as a CNS tumor, infection, or
trauma, in which there is strong evidence that the lesion is epileptogenic, should be treated.
 Most patients with one or more of these risk factors should be treated
 an abnormal neurologic examination,
 seizures presenting as status epilepticus,
 postictal Todd’s paralysis,
 a strong family history of seizures,
 an abnormal EEG.

34. Surgical treatment
 Temporal lobe epilepsy
 temporal lobectomy
 amygdalohippocampectomy
 Focal seizures arising from extratemporal regions
 lesionectomy
 When the cortical region cannot be removed
 multiple subpial transection
 Hemimegalencephaly or other dysplastic abnormalities
 Hemispherectomy or multilobar resection
 Disabling tonic or atonic seizures, usually when they are part of a mixed-seizure syndrome
(e.g., Lennox-Gastaut syndrome).
 corpus callosotomy

35. Surgical treatment
 Vagus nerve stimulation (VNS)
 Implantable device
 Detects the onset of seizure and deliver an electrical stimulation
 Responsive NeuroStimulation
 Stereotactic radiosurgery,
 Laser thermoablation
 Deep brain stimulation (DBS)

36. When to Discontinue Therapy
 Withdrawal of therapy can be attempted after 2 years of seizure free
interval in a patient who meets all of the following criteria
1. complete medical control of seizures for 1–5 years
2. single seizure type, either focal or generalized
3. normal neurologic examination, including intelligence
4. normal EEG
 In most cases, it is preferable to reduce the dose of the drug gradually over
2–3 months
 Most recurrences occur in the first 3 months after discontinuing therapy

37. Epilepsy in pregnancy
 Pre-conception counselling
 folic acid 5 mg daily for 2 mths before conception
 Fetal malformation
 Single drug
 Carbamazepine and lamotrigine have the lowest incidence of major fetal malformations
 Sodium valproate has relatively higher risk
 Levetiracetam may be safe
 Learning difficulties in children
 Lower IQ with valproate
 Haemorrhagic disease of the newborn
 oral vitamin K 20 mg daily to the mother during the last month of pregnancy
 IM vitamin K 1 mg to the infant at birth
 Increased frequency of seizures
 carbamazepine levels may fall in the third trimester.
 Lamotrigine and levetiracetam levels may fall early in pregnancy
 adjust the dose regimen

39. ANATOMY OF THE INTERNAL EAR

40. HISTORY OF PRESENTING ILLNESS
• History and physical examination - the most important information
• Often, patients have difficulty describing the exact symptom experienced.
• The first step is to define the symptom

41. • Following questions should also be enquired:
– Symptom constant or episodic
– Accompanying symptoms
– How did it begin (gradual / sudden)
– Aggravating or alleviating factors?
– If episodic, what was the duration and frequency of attacks, and what were
the triggers?
• One key point is that any type of dizziness may worsen with position changes, but some
disorders such as BPPV only occur after position change.

42. Vertigo- Definition
• Not a disease, But a
symptom.
A feeling in which the
external world seems to
revolve around the
individual or in which the
individual itself seems to
revolve in space.

43. Vertigo & Dizziness
Specific term
Includes only
Vertigo
More common in
elderly
Vertigo Dizziness
Broad term
Includes vertigo,
syncope,
unsteadiness
All age groups

44. Types
Rotation
Rotatory
Non-rotatory
Patient’s
perception
Subjective
Objective
Stimulus
involved
Spontaneous
Induced

45. Physiological Vertigo
1. Balance between 3 stabilising sensory systems is lost.
2. Non-adaptation of vestibular system to unfamiliar head movements.
3. Unusual head & neck positions

46. Pathological Vertigo
Pathological
Vestibular
Peripheral Intermediate Central
Non-
vestibular
Occular Other

47. Peripheral & Central Vertigo

49. Central Vertigo
Vascular causes: Hypertension, Basilar artery insufficiency
Epilepsy: both disease & its treatment
Road Traffic Accident: Head trauma
Tumor: of brainstem, 4th ventricle & cerebellum
Infection: Meningitis, Encephalitis
Glial diseases: Multiple sclerosis
Others: Parkinsonism, Psychogenic

50. Peripheral Causes for Vertigo
• BPPV
• Vestibular Neuronitis
• Meniere’s disease
• Labrynthitis
• Vestibulotoxic Drugs
• Perilymph Fistula
• Head injuries & Surgical trauma
• Syphillis
• Acoustic Neuroma

51. • “Red flags” suggestive of a Central vestibular lesion :-
1. Other central signs or symptoms
2. Direction-changing nystagmus
3. Vertical nystagmus
4. A negative head-thrust test
5. A skew deviation or
6. Substantial stroke risk factors (Kattah et al. 2009)

52. Evaluation of Vertigo
Tests for
assessment of
Vestibular functions
Clinical tests Laboratory tests

53. Clinical Tests of Vestibular Function
1. Spontaneous Nystagmus
2. Fistula test
3. Romberg Test
4. Gait
5. Past-Pointing & Falling
6. Dix Hallpike Maneuver
7. Test of Cerebellar Dysfunction

54. Laboratory Tests
1. Caloric Test
2. Electronystagmography
3. Optokinetics
4. Rotational Test
5. Galvanic Test
6. Posturography

55. VESTIBULAR SUPPRESSANTS

56. CANAL REPOSITIONING THERAPIES (CRT)

57. EPLEY’S MANEUVRE FOR POSTERIOR CANAL BPPV

58. SEMONT MANEUVRE FOR TREATMENT OF POSTERIOR CANAL
BPPV

59. LEMPERT (BBQ) MANEUVRE FOR HORIZONTAL
CANAL BPPV

60. ROLL MANEUVRE FOR HORIZONTAL CANAL BPPV

61. GUFONI MANEUVRE FOR HORIZONTAL CANAL BPPV

62. DEEP HANGING MANEUVRE FOR ANTERIOR CANAL
BPPV

63. VESTIBULAR REHABILITATION THERAPY

64. BRANDT-DAROFF EXERCISES

65. CAWTHORNE COOKSEY EXERCISES
• Devised in 1940s
• Mainly for unilateral vestibular lesions
• Exercises performed are slow, gradually increasing speed as patient tolerates the movement
• The patient should experience an increase in symptoms with movement.
• Exercises performed for at least 1 minute, several times each day for adaptation to occur.
• Advantage - low-cost and effective.

66. Benign Paroxysmal Positional Vertigo
• Most common cause.
• Described by Barany
• Definition: Abnormal sensation of motion that is
elicited by certain provocative positions.
• These provocative positions usually trigger specific
eye movements i.e. Nystagmus
Rotational Geotropic
Latency: 1-
5 s
Duration:
20-30 s
Fatiguable
Associated
with
Vertigo
Reversible

67. Signs & Symptoms
Symptoms
• Sudden Onset
• Have few asymptomatic periods in between
• Dizziness triggered by head movements
• Classic BPPV: erect to supine, 45°
• During attacks, Rolling spin
• Symptoms dissipate within 20-30 s after a violent start.
Signs
• Neurological examination:
Normal
• Dix-Hallpike maneuver:
• Caloric Test: Normal or
Hypofunctional

68. Investigations
1. Electronystagmography(ENG)
2. Caloric Test
3. Audiometry
4. Posturography

69. Treatment
Medical
1. WAIT & WATCH
2. Vestibulo-suppressant medication
3. Vestibular Rehab: Cawthorne exercises
4. Canalith repositioning (CRP):
a. Epley Maneuver
b. Semont maneuver
Surgical
1. Labyrinthectomy
2. Posterior canal Occlusion
3. Singular neurectomy
4. Vestibular nerve section
5. Transtympanic Aminoglycoside

74. THANK YOU