Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2721_Библиотеки_им_академика_М_И_Перельмана
.pdf
4. Bagley CE, Annegers JF,
Lairson Dr, et al. Cost of
epilepsy in the United States: a
model based on incidence and
prognosis. Epilepsia, 1994; 35:
1230–1243.
5. Verity CM, Goldin J. Risk of
epilepsy convulsions: a national
cohort study. BMJ, 1991;
303(6814): 1373–1376.
6. Warden CR, Zibulewsky J,
Mace SE, et al. Evaluation and
management of seizures in the
out-of-hospital and emergency
department settings. Ann Emerg
Med, 2003; 41(2): 215–224.
7. Hirtz D, Thurman DJ, GwinnHardy K, et al. How common
are the “common” neurologic
disorders? Neurology 2007;
68:326–337.
8. Montouris GD, Jagoda AS.
Management of breakthrough
seizures in the emergency
department: continuity of
patient care. Curr Med
Research and Opinions, 2007;
23(7): 1583–1592.
9. Devi PU, Manocha A, Vohora
D. Seizures, antiepileptics,
antioxidants and oxidative
stress: an insight for
researchers. Expert Opin
Pharmacother, 2008; 9(18):
3169–3177.
10. Pashko S, McCord A, Sena
MM. The cost of epilepsy and
seizures in a cohort of
Pennsylvania Medicaid
patients. Medical Interface,
1993; November: 79–84.
11. Lozsadi DA, VonOertzen J,
Cock HR. Epilepsy: recent
advances. Neurol, 2010; 257:
1846–1951.
12. Huff JS, Morris DL, Kothari
RU, et al. Emergency Medicine
Seizure Study Group.
Emergency department
management of patients with
seizures: a multicenter study.
Acad Emerg Med, 2001; 8(6):
622–628.
13. Mace SE, Bent ST. Seizures. In:
Graff LG (ed.). Observation
Medicine: The Healthcare
System’s Tincture of Time.
https://webapps.acep.org/
WorkArea/Download
Assett.aspx?id=45885 (last
accessed July 27, 2012)
14. Stafstrom CE.
Pathophysiological
mechanisms of seizures and
epilepsy: a primer. In: Rho JM,
Sankar R, Stafstrom CE (eds.).
Epilepsy. Mechanisms, Models,
and Translational Perspective.
Boca Raton, FL, CRC Press,
2010; ch. 1: pp. 3–19.
15. Lung DD, Catlett CL, Tintinalli
JE. Seizures and status
epilepticus in adults. In:
Tintinalli J, Stapczynski JS,
Cline DM, et al. (eds.). New
York; McGraw-Hill Co., 2011,
ch. 165: pp. 1153–1159.
16. Huff JS, Fountain NB.
Pathophysiology and
definitions of seizures and
status epilepticus. Emerg Med
Clin N Am, 2011; 29: 1–13.
17. Shorvon S. The clinical forms
and causes of epilepsy. In:
Handbook of Epilepsy
Treatment. Malden, MA:
Blackwell Publishing, 2005;
ch. 1: pp. 1–59.
18. Kellinghaus C, Luders HO.
Classification of seizures.
In: Wyllie E, Cascino GD,
Gidal BE, Gookin HP (ed.).
Wyllie’s Treatment of Epilepsy:
Principles and Practice.
Philadelphia, PA: Wolters
Kluwer, 2011, ch. 10:
pp. 134–143.
19. Loddenkemper T.
Classification of the epilepsies.
In: Wyllie E, Cascino GD,
Gidal BE, Goodkin HP (eds.).
Wyllie’s Treatment of Epilepsy:
Principles and Practice.
Philadelphia, PA: Wolter
Kluwer, 2011; ch.18:
pp. 229–242.
20. Dichter MA. Overview: the
neurobiology of epilepsy. In:
Engel J. Jr., Pedley TA, Aicardi
J, et al. (eds.). Epilepsy: a
Comprehensive Textbook.
Philadelphia, PA: Wolters
Kluwer/Lippincott Williams &
Wilkins, 2nd ed., 2008, ch. 20:
pp. 217–218.
21. www.ncbi.nlm.nih.gov/books/
NBK2510 (last accessed July 25,
2012)
22. Heinemann U, Mody I, Yaari
Y. Control of neuronal
excitability. In: Engel J. Jr.,
Pedley TA, Aicardi J, et al.
(eds.). Epilepsy: a
Comprehensive Textbook.
Philadelphia, PA: Wolters
Kluwer/Lippincott Williams &
Wilkins, 2nd ed., 2008, ch. 21:
pp. 219–231.
23. King MA, Newton MR,
Jackson GD, et al. Epileptology
of the first-seizure
presentation: a clinical,
electroencephalographic, and
magnetic resonance imaging
study of 300 consecutive
patients. Lancet 352(9133):
1007–1011.
24. Hamiwka LD, Singh N, Niosi J,
et al. Diagnostic inaccuracy in
children with “first seizure”:
role for a first seizure clinic.
Epilepsia 2007; p 48(6):
1062–1066.
Seizures
040
21:05:10
Subpart IVD
Chapter
37
Clinical – Neurologic
Dizziness and Vertigo
Saurin Bhatt, MD
Dizziness is a common medical complaint
encountered in the outpatient setting. It is estimated that up to 18% of aggregate ambulatory
care visits are for the complaint of dizziness, with
an increasing prevalence toward older ages.
1,2
Inadvertently, dizziness results in billions of
dollars of health care costs and time lost from
work. Additionally, the duration of symptoms
may vary in time, potentially representing long
periods of morbidity. Dizziness, often a vague
complaint in itself, can represent a range of conditions from those easily treated disorders when
identified to several etiologies that represent significant morbidity and mortality. It is for this
reason that physicians have been looking for clinical decision strategies to help them determine the
severity of this patient complaint and then initiate
appropriate treatment. The goal of this chapter is
not only to help the clinician to determine the
correct diagnosis and treatment, but also aid in
the recognition of the significant disease processes
that require intervention and referral.
The emergency department (ED) and subsequently the observation unit (OU) turn out to be a
common triaging area for these patients, primarily due to the amount of resources available to
narrow down the complaint to a functional diagnosis. Depending on the patient, there may be a
variable workup, which can be extensive. A wellfunctioning OU will be able to coordinate patient
examination, testing, and specialist consultation
in an efficient manner to remain cost and time
effective for the hospital and patient. Due to the
extensive differential diagnosis of dizziness, additional evaluation may require many specialties,
including neurology, neurosurgery, otolaryngology, cardiology, psychiatry, geriatrics, toxicology,
and social work. The role of the physician in the
OU is to assimilate the information collected thus
far, add tests as needed, and properly disposition
the patient.
Many times, the first step in caring for the
patient involves elucidating the complaint itself.
This may include having the patient describe the
sensations he or she is feeling without using the
term “dizzy.” Particular caution needs to be exercised with women and geriatric populations, as
these populations may have atypical presentations
of disease. Elderly patients additionally may have
multiple concerning comorbidities, declining general health, polypharmacy concerns, or even
socioeconomic factors that can complicate evaluation, treatment, and disposition.
Classification and Differential
of Dizziness
The neurology literature has partitioned complaints of dizziness into four subtypes: presyncope,
vertigo, disequilibrium, and lightheadedness.
Please refer to Table 37.1 for a brief overview of
these four categories. Based upon the characterization of dizziness, further workup and evaluation
can proceed. This chapter will primarily focus on
vertiginous-based complaints, due to the significant morbidity and mortality associated with vertiginous complaints. Additionally, cardiac and
vasomotor evaluation and treatment that may be
associated with presyncope dizziness complaints
are discussed elsewhere. A large number of dizziness differentials require fairly basic treatment
once identified and will not be the focus of this
chapter.
History and Physical Examination
History
To help narrow a list of differential diagnoses, a
proper history and physical examination need to
be performed. History will help differentiate the
dizziness subtype.
041
21:05:18
There are specific historical factors that may
be helpful to the clinician in determining the
cause of the dizziness. For example, if the patient
states that there have been several episodes within
the past 6 months, consider that the patient may
have been experiencing transient ischemic attacks
(TIAs). If the patient offers a history of chiropractic manipulation, headache, or neck trauma, vertebral artery dissection should be considered.
A coexistent history of any other neurological
symptoms should prompt the clinician to consider a central cause of the dizziness.
If the patient by history by falls into the vertigo
category, it is often helpful to determine if the
complaint is suggestive of a peripheral or central
lesion. As is suggested by Table 37.2, certain historical and physical examination characteristics are
suggestive of a peripheral or central lesion. These
are causation predictors and not determinants of
the patient’s symptoms. It is prudent for the exam-
iner to not exclude a central cause solely due to the
presence of one or two weak peripheral characteristics. In fact, recent literature suggests that many
of these characteristics that are classically taught as
strongly predictive of peripheral or central causation are not as definitive as previously thought.
24
More so, some aspects of vertiginous complaints,
such as vomiting, can be found in both peripheral
and central causes and therefore is an unreliable
distinguishing characteristic.
For vertiginous complaints, asking about
timing, triggers, progression of symptoms, and
associated symptoms may be helpful. The
evidence-based literature describes acute vestibular
syndrome as a patient presentation lasting more
than 24 hours with accompanying symptoms that
include gait instability, nausea, vomiting, intolerance to head motion, and no focal neurological
findings. While this represents a specific subset of
dizzy patients, it also represents a specific set of
patients that have been researched and from which
treatment decisions have been made.
Physical Examination
Physical examination should be guided by history,
but almost always include the entire neurological
examination, in addition to the cardiovascular
Table 37.1 Differential Diagnosis of Dizziness
Information included from reference sources
3–7,13
Differentials of Dizziness
Dizziness
Subtype
Type of Sensation Temporal Characteristics Selected Differentials
Vertigo Spinning or motion
sensation
Episodic or continuous Benign paroxysmal positional
vertigo
Meniere’s disease
Labyrinthitis
Vertebrobasilar ischemia
Cerebellar infarction or
hemorrhage
Presyncope Feeling faint, or
about to pass out
Episodic, may last for seconds,
may be alleviated by lying down
Dehydration
Anemia
Cardiac ischemia
Infection
Hypo/Hyperglycemia
Disequilibrium Unsteady feeling in
the lower extremities
Continuous, but may vary in
intensity
Multiple sensory deficits
Peripheral neuropathy, Vision
loss
Lightheadedness Vague complaints,
nonspecific
Medication Related
Psychiatric disorders including
anxiety, depression, panic
attacks
hyperventilation
Dizziness and Vertigo
041
21:05:18
examination. Cranial nerves should be thoroughly
assessed as subtle neurological findings might be
present. An assessment of gait and the presence of
truncal ataxia (inability to sit upright in bed with
arms crossed) may help to distinguish between a
peripheral and central lesion. Cerebe llar tests are
also important for vertigo assessments, as cerebellar strokes may present with vertigo as the
only physical manifestation of the stroke. Patients
that complain of hearing abnormalities should
have a complete otologic exam, including external, internal, Rinne and Weber tests. (Figure 37.1,
37.2, 37.3) Concerns regarding cardiac disease
should include bruit examination and murmur
assessments.
Another high yield physical examination is
the complete eye examination. Nystagmus evaluation should always be performed in vertigo complaints, as its presence can provide significant
information regarding the etiology of the patient’s
vertigo complaint. An assessment should be made
in the patient’s full visual fields with the eyes
moved in all directions to fully assess all types of
nystagmus. Refer to Table 37.3 for nystagmus
characteristics, pattern type, and cause. The
proper description of nystagmus is in the fast
direction of movement. It is also important to
note that the lack of any nystagmus or a particular
type nystagmus does not rule out a stroke or
particular central cause. With the exception of
bidirectional nystagmus (further discussed later),
Table 37.2 Differentiation of Peripheral Versus Central
Vertigo
Information included from reference
sources:
2,4,7,13,16,20
Peripheral vs. Central Characteristics
Characteristic Peripheral Central
Onset Sudden Gradual
Frequency Episodic,
recurrent
Constant,
progressive
Duration Seconds,
minutes
Weeks, months
Nystagmus Horizontal Vertical
Triggered by
Movement?
Yes Symptoms may
worsen, but
generally are not
triggered with
movement.
Isolated
Hearing Loss?
Yes Other neurologic
findings are
usually present.
Fatigable Yes No
Associated
Symptoms
Tinnitus, N/V Neurologic/visual
Symptoms
Postural
Instability
No (may
lean
towards
lesion)
Yes
Figure 37.1 Normal Ear Anatomy
Saurin Bhatt
041
21:05:18
no clinical decisions should be made exclusively
on this physical examination finding. Even then,
bidirectional nystagmus should be used in conjunction with other findings to come to a clinical
conclusion of stroke.
Based upon recent literature, if there is a con-
cern that there is a central cause of the patient’s
vertigo, two additional physical examination tests
can be performed to help assess for a central
cause. According to Kattah et al.,
25
a three-step
examination is more sensitive than MRI within
the first 24 hours in determining stroke in patients
presenting with acute vertiginous symptoms. The
three components of this examination include
assessment of direction-changing nystagmus (also
called gaze evoking or bidirectional nystagmus),
horizontal head impulse testing, and assessment
for skew deviation (vertical ocular misalignment).
However, this has not been validated as of this
writing and therefore the presence of these findings should prompt urgent CT scan or MRI and
neurology specialist evaluation.
Testing for bidirectional nystagmus is an easy
test to perform. A patient with a positive test will
have nystagmus when looking to the left as well as
the right, suggesting a dysfunction of the gaze
Figure 37.2 Normal Inner Ear
Anatomy
Figure 37.3 Normal
Semicircular Canal
Dizziness and Vertigo
041
21:05:18
stabilizing mechanisms of the cerebellum and
brainstem.
Head impulse testing is a method for checking
an intact vestibular-ocular reflex. A head thrust
maneuver is performed by moving the head side
to side no more than 30 degrees in either side
from midline while the patient focuses on a fixed
object such as the examiner’s nose. The examiner
alters the pace of head thrusts to ensure that the
brainstem does not adapt to the movements.
A positive test is when the patient is able to focus
on the fixed object while the head thrusting is
performed in the presence of dizziness. Avoid this
maneuver in patients with known or suspected
cervical spine issues. The patient’s ability to fixate
on an object while having a vertiginous complaint
strongly suggests a central cause of symptoms.
The last test is for skew deviation. Once again
the patient is asked to focus on a fixed object. One
eye is covered and the covering is alternated
between eyes over a short time interval (several
seconds). If upon alternating the covered eye
there is a vertical misalignment, it is considered
a positive test for skew deviation.
Differential Diagnosis of Vertigo
The patient data after interview and exami nation
may point to a peripheral cause of the vertiginous dizziness. Peripheral causes can be further
differentiated by elucidating certain facts. The
first is to determine if the patient has any
migraine type symptoms. If so, the patient may
have a variant of migraines known as migrainous
vertigo, in which the treatment is standard
migraine treatment protocols (noted in Chapter 35, Headaches).
If no migraine type symptoms are present,
then the next step is to determine if the patient
has any hearing loss or tinnitus present (subjectively or objectively). If none is present, then
episodic events of dizziness may be considered
as benign paroxysmal positional vertigo (BPPV)
(Figure 37.4), whereas continuous dizziness is
termed vestibular neuritis. If the patient does
have hearing loss, episodic episodes likely represent Meniere’s disease (Figure 37.5), whereas
continuous episodes represent labrynthitis.
(Table 37.4)
BPPV (Figure 37.4) can be confirmed as well
as subsequently treated at the bedside by using
the Dix-Hallpike maneuver (Figure 37. 6). With
this maneuver, the patient is instructed to keep
his or her eyes open while being lowered from a
sitting to a lying position with the head positioned at 45° degrees to the left or right. The
head is brought to an extension to about 20° and
the eyes are observed. The patient with BPPV will
have an upbeating, torisonal ny stagmus in the
directionofthattheheadisturned.Ifthisfails
to elicit the nystagmus (usually delayed up to 30
seconds),anattemptcanbemadeintheopposite
direction after the patient’ssymptomshave
subsided.
Since the etiology of BPPV is due to debri s in
the semicircular canals (Figure 37.4), the Epley
maneuver (repositioning maneuver) can be used
to remove the debris (Figure 37.7). The Epley
Table 37.3 Nystagmus
Information included from reference
sources:
17
Nystagmus Evaluation
Pattern
Type
Nystagmus
Characteristic
Cause
Peripheral Upbeat torsional
nystagmus with
Dix-Hallpike
maneuver
Benign
paroxysmal
Positional
Vertigo
Peripheral Unidirectional
spontaneous
nystagmus
Vestibular
neuritis
Central Vertical
nystagmus
Strokes, Chiari
malformation,
multiple sclerosis
Central Direction
dependent
changes
Medications
(antiepileptic),
stroke, multiple
sclerosis
Central Downbeating
with Dix-Hallpike
Chiari
malformation or
cerebellar space
occupying
lesion
Central Intranuclear
ophthalmoplegia
Multiple
sclerosis, stroke
Physiologic Unsustained gaze
dependent
nystagmus
Saurin Bhatt
041
21:05:18
maneuver starts with the Dix-Hallpike maneuver
on the nystagmus elicited side. The patient’s head
is moved 90° in the opposite direction and held in
that position for up to 1 minute to allow the
patient to accommodate. The patient will now be
looking 45° in the opposite direction. Once the
patient has accommodated, the patient is rolled
further in the same direction onto his or her
shoulder, such that he or she is looking straight
into the ground. Finally, the patient is brought
back into a sitting position at the side of the bed.
This maneuver may be repeated, as needed, and
generally will alleviate the patient symptoms.
Follow up with otolaryngology (ENT) should
be provided for further treatment as needed.
Recurrence can occur, and the patient may need
specialized testing and treatment not possible in
the OU.
Labrynthitis and vestibular neuritis are diagnoses that usually will need ENT follow up for
vestibular rehabilitation exercises. (Table 37.4)
ENT consultation may be helpful to determine if
antibiotics or antivirals may be necessary based
upon the suspicion of symptom etiology as well
as for suppressant medication recommendations.
Of note, evidence-based literature suggests that
patients with vestibular dysfunction will in fact
learn to compensate over time, so that
Figure 37.5 Meniere’s Disease
Figures are courtesy of the Dr. Sharon
E. Mace of the Emergency Services Institute
of the Cleveland Clinic, the Art and Photo
Department of the Cleveland Clinic and
Amanda Mendelsohn (Figures 37.1–37.3) and
Bill Garriott (Figures 37.4–37.7)
Figure 37.4 Benign Paroxysmal
Positional Vertigo (BPPV)
Dizziness and Vertigo
041
21:05:18
suppression of this compensation via medication
for more than several days is not advised. If the
patient is unable to perform activities of daily
living (ADLs) or has a social situation that prevents discharge home, appropriate inpatient preparations should be made.
Meniere’s disease has a genetic predisposition.
It is treated acutely with diuretics, low salt diet,
and occasionally benzodiazepines, as the
causation of this disease is thought to be a fluid
imbalance within the inner ear. (Figure 37.3)
Again, ENT follow up would be recommended,
as persistent symptoms are managed differently.
History and physical examination often are
complemented with laboratory and radiographic
studies. Proper testing should be guided by the
patient’s presentation. For vertiginous complaints,
there often is little utility in obtaining laboratory
Table 37.4 Vestibular Causes of Vertigo
Benign Paroxysmal
Positional Vertigo
Labrynthitis Meniere’s Disease Vestibular Neuritis
Dizzy
Episodes
Episodic Continuous Episodic Continuous
Hearing
Loss
No Yes Yes No
Tinnitus No Can be present Yes No
Treatment Epley maneuver
Antihistamines
(diphenhydramine)
Anticholinergics
(meclizine)
Symptomatic:
antiemetics or
vestibular suppressant
including
benzodiazepines
Vestibular rehabilitation
exercises
Treatment if known
source: can include
steroids, antivirals, and
antibiotics (suspected
otitis media)
Symptomatic
treatment with
antiemetics or
vestibular suppressants
Diuretics, low salt
diet,
benzodiazepines,
anticholingerics
Vestibular
rehabilitation
exercises
Treatment if known
source: can include
steroids, antivirals
Symptomatic
treatment with
antiemetics or
vestibular
suppressants
ENT Follow-upYes Yes Yes Yes
Cause Otoconia (“ear rocks”),
crystals detach from
otolithic membrane
and collect in
semicircular canal
(usually posterior)
Inflammation of the
labyrinth of the inner
ear
Idiopathic;
symptoms are due
to excess fluid from
the labyrinth into
other areas of the
inner ear
Unknown,
associated with
preceding or
concurrent
infection in ~ half of
patients
Associated
symptoms
Nausea, vomiting Nausea, vomiting Nausea, vomiting Nausea, vomiting
Comment May reoccur
Most common
vestibular disorder
About 50% of dizziness
in elderly is due to
BPPV
Recovery can be
extended to several
months or years
depending on the
amount of damage
Triad: vertigo,
hearing loss,
tinnitus
Surgery for cases
resistant to medical
management
Usually without any
auditory symptoms
and no neurologic
symptoms other
than dizziness
Typical
Setting
> 50 yrs
idiopathic, due to agerelated dgeneration of
otolithic membrane
< 50 yrs trauma
Can be associated with
a viral or bacterial
upper respiratory
infection
Young to middleaged adults; many
times after a viral
infection
Sudden onset;
previously well
young or middleaged adult
Saurin Bhatt
041
21:05:18
data. Patients that fall into the dizziness categories
of presyncope, disequilibrium, and lightheadedness may benefit though from additional laboratory work, especially as it may help specialists rule
in other etiologies. For example, a geriatrician or
psychiatrist may request medical clearance via
ancillary testing for further care of the patient.
Other times, ambiguous histories supplemented
with laboratory data may demonstrate an easily
correctable diagnosis. Laboratory tests ordered
in the OU can also be obtained for trending
purposes and may provide assistance for later
patient care.
Radiographic studies in vertigo type complaints are almost always ordered and can be helpful in diagnosis and patient disposition. In terms of
radiographic studies a chest x-ray may be helpful if
there is a concern of an infectious cause of the
patient’s dizziness. Often CT is ordered to evaluate
for intracranial pathology. A common misconception, though, is to order a CT scan and to only use
those results to rule out stroke. Noncontrast head
CT is a very poor test to identify acute ischemic
cerebrovascular accident (CVA) in general, and is
even worse in identification of posterior fossa
strokes. MRI with Diffusion Weight Imaging
(DWI) is currently considered the gold standard
for identification of acute ischemic stroke. As
discussed previously, since there is a small percentage of posterior fossa strokes that m ay be
missed using this test, other aspects of the
patient’s history, physical examination, and specialist consultation may need to be incorporated
into the patient’s care. Neurology adm ission and
repeat imaging may be necessary if clinical suspicion is still high for a central process.
Central Causes of Vertigo
In an effort to aid the clinician in determining if
the presenting symptoms are of a stroke, characteristics of lesions along vascular distributions
Figure 37.6 Dix-Hallpike Maneuver
Dizziness and Vertigo
041
21:05:18
Figure 37.7 Epley Maneuver
Saurin Bhatt
041
21:05:18
Соседние файлы в папке Библиотека им академика М.И. Перельмана