ppt

2. dizziness
• Is a non-specific term
• The most common disorders lumped under this term
include:
1. Vertigo
2. Presyncope
3. Disequilibrium
4. Non-specific ‘dizziness’
-the first & the most important step in the evaluation is
to fit the patient into one of these more specific
categories

3. vertigo
• Arises from an acute asymmetry of the vestibular
system
• Vestibular system includes:
1. The vestibular apparatus in the inner ear
2. The vestibular nerve & nucleus within the medulla
3. Connections to & from the vestibular portions of the
cerebellum

4.  Patient often experience as illusion of motion
 ‘self-motion’ or ‘motion of the environment’
 The most common perception is a spinning sensation
distinguishing vertigo from other types of
dizziness:
- Spinning quality - unreliable
- lack of it does not exclude

5. More useful:
1. Time course
- vertigo is never continuous
2. Provoking factors
- certain types of vertigo occur spontaneously, while
others are precipitated by certain maneuvers that
change head position or middle ear pressure(e.g.
coughing)

6. Positional vertigo vs. postural presyncope
- Are frequently confused
- Both are associated with dizziness upon standing
- If dizziness can be provoked by maneuvers that change
head position without lowering blood pressure =
positional vertigo

7. 3. Aggravating factors
- All vertigo is made worse by moving the head
- If head motion does not worsen the feeling, it is
probably another type of dizziness
Associated signs and symptoms
Vertigo is generally accompanied by
1. Nystagmus
2. Postural instability

8. Causes of vertigo
Peripheral causes
- Benign paroxysmal positional vertigo
- Vestibular neuritis
- Herpes zoster oticus(Ramsy Hunt syndrome)
- Meniere’s disease
- Labyrinthine concussion
- Recurrent vestibulopathy

9. - Acoustic neuroma
- Aminoglycoside toxicity
- Otitis media
central causes:
- Migrainous vertigo
- Brainstem ischemia
- Cerebellar infarction and hemorrhage
- Chiari malformation and multiple sclerosis

10. nystagmus Peripheral vertigo Central vertigo
direction unidirectional May reverse direction
type Horizontal with torsional Any direction
Effect of visual fixation suppresses Not suppressed
Other neurologic signs absent Often present
Postural instability Unidirectional instability
, walking preserved
Severe instability , pt
often falls when walking
Deafness or tinnitus May be present absent
Associated central
nervous system
abnormalities
none Extremely common (e.g.,
diplopia, hiccups, cranial
neuropathies, dysarthria)
Common causes BPPV,infection ,
vestibular neuritis,
Ménière's disease,
labyrinthine ischemia,
Vascular, demyelinating,
neoplasm

11. Dix-Hallpike maneuver
 Positional maneuvers are designed to reproduce
vertigo and elicit nystagmus in patients with a history
of positional dizziness
 These maneuvers are most useful in patients who do
not have symptoms or nystagmus at rest
 The Dix-Hallpike maneuver tests for canalithiasis of
the posterior semicircular canal, which is the most
common cause of BPPV

12.  With the patient sitting, the neck is extended and
turned to one side. The patient is then placed supine
rapidly, so that the head hangs over the edge of the
bed. The patient is kept in this position until 30
seconds have passed if no nystagmus occurs. The
patient is then returned to upright, observed for
another 30 seconds for nystagmus, and the maneuver
is repeated with the head turned to the other side.

14. brainstem signs: suggest central vestibular lesions
- Staggering
- Ataxia of gait
- Vomiting , headache, double vision ,visual loss
- Slurred speech
- Numbness of the face or body
- Weakness ,clumsiness , incoordination
- The absence of other neurologic findings does not
exclude a central process

15. presyncope
 Is the prodromal symptom of fainting or a near faint
 More common than syncope
 Pallor
 Usually occurs when pt is standing or seated upright &
not when supine
 History of cardiac disease
 Ask about : palpitation, chest pain , dyspnea

16. common cause of presyncope
1. Orthostatic hypotension
2. Cardiac arrhythmia
3. Vasovagal attacks

17. disequilibrium
• Is a sense of imbalance that occurs primarily when
walking
• May result from
1. Peripheral neuropathy
2. Musculoskeletal disorders interfering with gait
3. Cervical spondylosis
4. Parkinson’s disease
* Visual impairment typically exacerbate the sense of
imbalance

18. Non-specific dizziness
• Difficult for the patient to describe
• ‘ I am dizzy’, ‘ light-headed’
• Psychiatric disorders may be the primary cause of non-
specific dizziness in some cases
• Ask about: any cause for hypoglycemia, medications
like antidepressant & anticholinergic
• There are no physical signs that are diagnostic of non-
specific dizziness
• Most are healthy , young

19. Treatment of vertigo
 Bed rest
 Vestibular suppressant drugs
e.g. dimenhydrinate , promethazine
 Tranquilizers e.g. diazepam
 Disease specific treatment

20. Summary
• Most pts with dizziness have vertigo
• Vertigo is illusion of movement
• Nystagmus suggests that the cause of dizziness is
vertigo
• Hearing loss & tinnitus suggests peripheral vertigo
• Brainstem signs suggest central vertigo
• Presyncope: sensation of impending faint(occur in
upright posture)

21. summary…con’t
• Dizziness that represent disequilibrium or a sense of
imbalance may be the presenting symptom of
peripheral neuropathy , PD, or cervical myelopathy
• Non-specific dizziness is ill described and has a wide
differential diagnoses that may include milder forms
of vertigo, presyncope, and disequilibrium, as well as
medication side effect, psychiatric disorders, and
metabolic derangements
• Elderly patients often have multiple etiologic
contributors the their dizziness

22. The confusional state
 Confusion is a mental & behavioral state of reduced
comprehension , coherence, and capacity to reason
 Delirium is a state of confusion that is accompanied
by agitation ,hallucination , tremor and
illusions(misperception of environmental sight, sound
, or touch)

23. Causes of confusion & delirium
• Meningitis and encephalitis
• Systemic infections
• Head injury
• Seizures
• Drug toxicity or withdrawal
• Metabolic disorders resulting from hepatic, renal ,
pulmonary , or cardiac failure
• Chronic dementing disease

24. • Detailed medical history
• Physical examination
- orientation
- memory
- focal signs
- meningeal irritation signs
- astrexis
• Laboratory tests(RBS, serum elecrolyte, RFT, LFT,
CBC, U/A, neuroimaging, LP, B/F)

25. Coma & related disorders of
consciousness
 Coma is deep sleeplike state from which the patient
cannot be aroused
 Stupor : can be awakened by vigorous stimuli
 Drowsiness : easy arousal & the persistence of
alertness for brief period
 Vegetative state: an awake but unresponsive state

26. Vegetative state
 Eyelids are open(giving the appearance of
wakefulness)
 Yawning , grunting & swallowing as well as limb&
head movements persist ,but there are few, if any,
meaningful response to the external and internal
environment
 It is ‘awake coma’
 Respiratory & autonomic functions are retained. It has
poor prognosis
 Common causes : cardiac arrest & head injury

27. Clinical states prone to be
misinterpreted as stupor or coma
 Akinetic mutism: awake pt who is able to form
impression and think but remains immobile & mute
cause : damage to medial thalamic nuclei , frontal
lobes & hydrocephalus
 Abulia: mental & physical slowness and lack of
impulse to activity that is in essence a mild form of
akinetic mutism, with the same anatomic origins

28. Catatonic : hypomobile & mute syndrome associated
with a major psychosis
- Appears awake with eyes open
- No voluntary or responsive movement
- eyelid elevation is actively resisted
- Blinking occurs in response to visual threat
- Catalepsy(retain limb posture in which they have been
placed by the examiner)

29. Catatonic…cont’d
 Have some memory of events that occurred during
their catatonic stupor
 Superficially similar to akinetic mutism, but clinical
evidence of brain damage is lacking

30. Locked-in state
 Pseudocoma
 Awake patient
 No means of producing speech or volitional limb, face
and pharyngeal movements
 Vertical eye movements and lid elevation remain
unimpaired, thus allowing the patient to signal
Cause: infarction or hemorrhage of the ventral pons ,
which transects all descending corticospinal and
corticobulbar pathways

31.  Similar awake but deefferented state occurs as a result
of total paralysis of the musculature in severe cases of :
1. Guillain-Barre syndrome
2. Critical illness neuropathy
3. Pharmacologic neuromuscular blockade

32. Etiologies & pathopysiology of
coma
 The ascending reticular activating system(RAS) is a
network of neurons originating in the tegmentum of
the upper Pons and midbrain, believed to be integral
to inducing and maintaining alertness

33.  These neurons project to structures in the
diencephalon, including the thalamus and
hypothalamus, and from there to the cerebral cortex
 Injury to the cerebral hemispheres can also produce
coma, but in this case, the involvement is necessarily
bilateral and diffuse, or if unilateral, large enough to
exert remote effects on the contralateral hemisphere or
brain stem.

34. causes
 Infections
 Metabolic derangements
 Cerebrovascular diseases
 Intoxications
 Trauma
 Postictal seizure
 Cerebral mass
lesions,herniations(transfacial,transtentorial,
foraminal)

35. history
 From witnesses
 What was the time course of the loss of consciousness?
 Abrupt: Subarachnoid hemorrhage, seizure
 Gradual: brain tumor
 Fluctuating: subdural hematoma, recurrent seizure,
metabolic encephalopathy
 Focal signs precede the loss of consciousness?:
structural lesions

36.  History of TIA or seizure?
 Fever: infection (history of travel to malaria endemic
area?)
 Headache: intracranial lesion or infection
 Recent falls?: subdural hematoma
 Recent confusion or delirium might indicate a metabolic or
toxic cause
 Drugs used? Prescription or non-prescription
 Are there medical or psychiatric conditions in the past?
 Alcohol or drug abuse?

37. General examination
 Extreme hypertension
- Hypertensive encephalopathy
- Hypertensive intracerebral hemorrhage
 Hypotension
- sepsis
- Hypovolumia
- Cardiac failure

38.  Fever : infection
 Hyperventilation: acidosis
 Cheyne-stokes: bicerebral dysfunction
 Apneustic breathing= pontine lesions
 Skin
- petechia= bleeding diatheses,meningococcemai
- jaundice = liver disease

39. Neurologic assessment
Level of consciousness
 Glasgow coma scale: indicates the severity (prognosis)
 Components:
 Eye opening(E)
 Best verbal response(V)
 Best motor response(M)
 Scale : 3-15

40.  The components of the GCS should be recorded
individually e.g.E2V3M4=GCs of 9
 Mild brain injury= 13 or higher
 Moderate injury = 9- 12
 Severe brain injury= 8 or less

41. Motor examination
 Spontaneous and elicited movements
 Muscle tone
 Reflexes
 Decorticate posturing: dysfunction at the cerebral
cortex level
 Decerebrate posturing: dysfunction below the red
nucleus ( has poor prognosis )
 Asterixis: metabolic encephalopathy
 Meningeal irritation signs( meningitis,
subarachnoid hemorrhage)

42. Fundescopy
 Subhyaloid hemorrhage: indicates subarachnoid
hemorrhage
 Papilledema indicates increased intracranial pressure
or malignant hypertension
Pupils
 Normally reactive & round pupils of midsize (2.5-
5mm) essentially exclude midbrain damage

43. Disruption of the pupillary light reflex in comatose
patients usually occurs because of either:
1. Downward herniation of mesial temporal structures
from an expanding supratentorial mass or
2. Primary brainstem lesions
In either of these the third cranial nerves or their
nuclei in the midbrain are injured. This gives
unreactive & enlarged pupil (>6mm)

44.  Pontine lesion = very small pupil(<1mm) , but reactive
 Opiate overdose= very small pupil
 Severe midbrain damage=bilaterally dilated and
unreactive

45. Eye movements
 Large cerebral lesions produce a persistent conjugate
deviation of the eyes toward the side of the lesion
 The eyes look toward a hemispheric lesion & away
from a brainstem lesion
 Persistent eye deviation may also suggest seizures, in
this case the eye deviation is away from the side of the
lesion

46.  In the comatose patient, bilateral conjugate roving eye
movements which appear full indicate an intact
brainstem and further reflex testing in not required
 Oculocephalic maneuver ( doll’s eye): positive
doll’s eyes = the eyes turn in opposite direction
 Caloric testing:
With brainstem lesions, both the vestibuloocular
reflex are absent or abnormal

47.  Corneal reflex : the response is lost if the reflex
connections between the 5th and 7th cranial nerves
within the Pons are damaged

48. Laboratory testing & imaging
 Random blood sugar
 Blood film for hemoparasites, CBC
 Lumbar puncture ( infection, subarachnoid
hemorrhage)
 Serum electrolytes
 Renal and liver function tests
 Cranial CT and MRI, EEG
 Chemical-toxicological analysis of blood and urine

49. treatment
 ABC
 Cervical spine injuries must not be overlooked!
 Oropharyngeal airway/ endotracheal intubation
 Oxygen supplementation
 Maintain iv access
 Dextrose 50ml of 50%, thiamine 100mg
 Naloxone & flumazenil if drug toxicity is suspected

50. Treatment…cont’d
 Treat increased intracranial hypertension e.g.
Mannitol
 Control hyperthermia
 Treat hypotension , severe hypertension
 Empiric antibiotic ( if meningitis is suspected)
 Antimalaria : based on the clinical suspicion
 Definitive therapy depends on establishing the precise
diagnosis

52. Questions & Discussion