14-vertigo and ataxia.ppsx

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Transcript 14-vertigo and ataxia.ppsx

Case
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A 46-year-old man with severe vertigo, nausea, and
vomiting was brought to the emergency
department. She reported that she had felt slightly
dizzy when she got out of bed that morning, and
that during the next several hours, she had
experienced increasing vertigo(illusion in rotation
way) and nausea, and eventually vomiting. Her
balance was impaired and she was having
difficulty focusing her eyes--"everything seems to
be jumping back and forth." with vertical
displacement of objects. There was no hearing loss
or other ear symptoms. Her history was significant
only for mild hypertension .
examination
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blood pressure was 150/80 mm Hg; her pulse was
88 b.p.m and regular , dehydrated from repeated
vomiting .
The patient was able to stand and walk, although
she tended to veer to the right and was obviously
unsteady. He had a brisk spontaneous nystagmus
that was horizontal-torsional ; increased in
amplitude when she looked to the left and
decreased when she looked to the right, but did
not change direction .
Cover-uncover testing indicated the presence of
skew deviation, with the right eye slightly lower
than the left in all directions of gaze.
The remainder of the physical examination was
unremarkable .
Vertigo , dizziness‫دوخة‬
versus ataxia= dysequilberium
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Definition of each and causes?
How we can differentiate between them?
 Concept map of approach ?
-type of symptoms and causes?
-str . involved=localization
-most likely cause -----investigation
-Treatments : symptomatic and specific?
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‫ دوخة‬Vertigo , dizziness
versus ataxia= dysequilberium
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1-Dizziness is non-specific broad term that includes
vertigo, pre syncope (lightheadedness, impending fainting
or giddiness ,dimming of vision) instability and
disequilibrium. Mechanisms?
Vertigo: One of common problem we face in neurology and
medicine.
It is illusion of movement of the body or environment .it is
often associated with sense of impulsion , visual illusion of
movement (oscillopsia), nausea ,vomiting ,or ataxia.
Vertigo must differentiated from non vertiginous dizziness
mentioned above that result from impair brain’s supply of
blood ,oxygen, or glucose ex: vasovagal ,orthostatic
hypotension ,cardiac ischemia and arrhythmias, hypoxia
and hypoglycemia ; all may culminate into loss of
consciousness and fall. If it is due to decresed cerebral
hypo perfusion is called syncope.
don’t forget hyperventilation where dizziness aggravated by
3 min. HV.
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2-Ataxia: is incoordination or clumsiness of movement that
is not due to weakness. it is caused by vestibular
,cerebellar , or sensory (proprioceptive) disorders. ataxia
can affect eye movement limbs, trunk or gait
------------------------------------------------------------------------------Draw concept map:
 When you diagnose vertigo as problem and depending on
H., examination &investigation:
 1st step is to differentiate between Central (due to lesion
affecting brainstem VN or their connection) versus
peripheral v (peripheral vest. lesion affecting labyrinth,
inner ear or v. division of 8th cranial nerve).
 central is more serious than peripheral
 Think about the etiology
 Treatment.
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Vertigo:
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Nausea &vomiting :
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Nystagmus
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Peripheral
often intermittent :sever
common
present: never vertical
Hearing loss &tinnitus:
Intrinsic BS signs include :
-M or S deficit
-dysartheria, ataxia
 Visual fixation:
Head thrust sign
 etiology:
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BPV, V.neuronitis , labyrinthitis
cerebellar H
Unidirectional
often present
absent
Inhibited
positive
central
often constant
usually less sever
uncommon
absent if present
vertical
uni or bi-directional
rarely present
typically present
no effect
negative
VB- ischemia ,MS.
.or infarction
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is in-coordination or clumsiness of movement that is not due to
weakness. it is caused by vestibular ,cerebellar
, or sensory
(proprioceptive) disorders. ataxia can affect eye movement limbs, trunk
or gait.
it result from same central or peripheral lesions that cause V.
Sensory ataxia and motor Ataxias.
Vestibular ataxia: nystagmus is frequently present ,usually unilateral most
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prominent on gaze away from side of lesion, dysartheria does not occur.
It is gravity dependent
: in coordination is not present in lying
position.
Romberg’s signs is positive.? It is sensory ataxias.
Cerebellar ataxia:
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cerebellar disease itself or it’s connection. We have limb ataxia
(hemisphere lesion) and truncal ataxia (vermis lesion)
frontal lobe lesion may give picture mimic ataxia resulting from
controlateral Cerebellar Hemisphere ?due to crossed connection
between frontal lobe and cerebellar H.
Cerebellar ataxia:
it characterized by limb or truncal ataxia
,dysartheria ,nystagmus often present with or
without other ocular abnormality like gaze paresis
and defective saccadic and pursuit movement.
vertigo may be present.
 The patient is unable to stand with feet together
whether eyes is closed or not.
 C/F OF cerebellar disease? Specific and non
specific. ?
Main causes :
 *Acquired :infection ,inflammatory , neoplastic
and demyelinating ; vitamin E dependent A.
 *inherited : Olivopontocerebellar degeneration ,
Frederich's ataxia. , spinocerebellar degeneration ,
metabolic like Wilson's disease.
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Sensory ataxia?
result from disorder that affect the proprioceptive
pathways in peripheral sensory nerve ,sensory root,
post. Column of spinal cord or m. lemniscuses.
Thalamic and parietal are rare causes of
controlateral sensory hemi-ataxia. clinically the
patient have:
 impaired vibration and position sense, depressed
ankle jerk
 able to stand with feet together when is opened
not if it is closed (Romberg’s sign).
 Limb ataxia in legs may present
 Vertigo, dysartheria and nystagmus are absent.
Main causes: polyneuropathy, posterior SC lesion as
in trepanomal disease , MS, Frederich's ataxia
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Approach?
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history : signs and symptoms vertigo or not , if ataxia which
type?
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onset &time course
medical H
Family H
general physical examination
neurological examination including:
Mental state
Gait &stance
Cranial nerves checking i.e.:
occulomotor,trochlear,abducent and acoustic nerves.
Check for PD which suggest increase ICP, or optic atrophy
in case of MS ,neurosyphilis ,B12 deficiency
Facial nerve affection ,corneal reflex associated with C-P
angle mass
Treatments