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Chapter 25. Dizziness
503
Meniere’s Disease
The abnormal fluid balance of this condition can be managed based on the severity of disease. All patients should be referred for an ENT evaluation. Noninvasive treatments include salt restriction, diuretics, antihistamines, vestibular suppressants, and antiemetics. Patients should also be referred for vestibular rehabilitation. Patients with refractory or severe disease despite medical therapy may be candidates for invasive therapies such as intratympanic gentamicin or gluco­corticoids and, in some cases, surgical therapy [1].
Disequilibrium
The evaluation of a patient with disequilibrium involves looking for other disorders that are contributing to the symp­toms as treatment is focused on addressing the issues that underlie this condition. This may involve withdrawal of pre­cipitating medications, referral for ophthalmologic evaluation and corrective lenses for visual impairment, providing an ambulatory assistive device (cane or rolling walker), physical therapy evaluation, and the treatment of any metabolic, neu­rologic, or movement disorders that were unveiled during the evaluation.
Presyncope
The evaluation of patients with presyncope is the same as for patients who experienced true syncope. As with all other causes of dizziness, the history guides the clinician to the appropriate exam and relevant testing needed to secure the diagnosis. Any potentially offending medications that can safely be tapered or discontinued should be a priority. Patients with orthostatic hypotension can benefit from vol­ume replacement if they are volume depleted. Refractory orthostasis should prompt the clinician to consider auto­nomic dysregulation. In addition to management of underly-
504
R. Kennedy Jr
ing metabolic and endocrine disorders, medications such as midodrine or fludrocortisone can be initiated. Patient educa­tion with behavior modification should be provided to patients with a neurocardiogenic process. Patients with ath­erosclerotic cardiovascular disease history or risk factors, those with sudden or exertional syncope, and those who experience syncope in a supine position should undergo thor­ough evaluation and treatment for potentially malignant causes [13].
Lightheadedness
Hyperventilation syndrome often coupled with psychiatric disorders (anxiety and depression) is the main contributor to the vague and imprecise symptoms of lightheadedness. As previously noted, if the hyperventilation provocation test suc­cessfully recreates the patient’s symptoms, this can also be therapeutic and reassuring to the patient [1]. Conscious breathing exercises can control future events. If a mood dis­order is revealed during symptom evaluation, this should be treated with the appropriate agents, and the patient can also be referred to the relevant behavioral health specialist.
Clinical Pearls
• The patient’s initial, raw, unguided description of symp-
toms is the most important step in determining the cause
of dizziness.
• Movement worsens all types of vertigo, and even though
patients with peripheral vertigo may not want to move,
they are usually able to walk. In comparison, patients with
central vertigo experience greater impairment in gait and
posture and are often very ataxic and unable to walk.
• All patients with Meniere’s disease should be referred to
ENT early in the disease process as even though vertigo
attacks may be controlled in most patients, hearing loss
can be progressive.
Chapter 25. Dizziness
505
• Orthostasis can be caused by intravascular volume deple-
tion, many medications, and autonomic dysfunction.
• Visual impairment, deafness, peripheral neuropathy, mus-
cle weakness, and deconditioning can all contribute to
disequilibrium.
• The hyperventilation test for suspected lightheadedness
can be both therapeutic and diagnostic.
Do Not Miss This!
• These are findings on the physical exam that suggest
stroke in dizzy patients: normal bilateral vestibulo-ocular
reflexes (noted on head impulse test), skew deviation,
abnormal visual tracking (saccadic pursuit), and direction-
changing nystagmus.
• Syncope that occurs while supine, with exertion, or sud-
denly (without prodrome) should raise clinical suspicion
for malignant cardiac arrhythmias (VT, high-grade heart
block, prolonged sinus pauses) or structural cardiac abnor-
malities (severe aortic stenosis or HOCM).

References

1. Post RE, Dickerson LM.Dizziness: a diagnostic approach. Am Fam Physician. 2010;82(4):361–8.
2. Neuhauser HK, etal. Burden of dizziness and vertigo in the com­munity. Arch Intern Med. 2008;168:2118.
3. Kroenke K, et al. Causes of persistent dizziness. A prospec­tive study of 100 patients in ambulatory care. Ann Intern Med. 1992;117:898.
4. Stanton VA, etal. Overreliance on symptom quality in diagnos­ing dizziness: results of a multicenter survey of emergency physi­cians. Mayo Clin Proc. 2007;82:1319.
5. Baloh RW. Differentiating between peripheral and central causes of vertigo. Otolaryngol Head Neck Surg. 1998;119:55.
6. Hotson JR, Baloh RW. Acute vestibular syndrome. N Engl J Med. 1998;339:680.
7. Kerber KA, Baloh RW.The evaluation of a patient with dizzi­ness. Neurol Clin Pract. 2011;1:24.
506
R. Kennedy Jr
8. Wood KA, etal. Frequency of disabling symptoms in supraven­tricular tachycardia. Am J Cardiol. 1997;79:145.
9. Maarsingh OR, et al. Causes of persistent dizziness in elderly patients in primary care. Ann Fam Med. 2010;8:196.
10. Reilly BM.Dizziness. Clinical methods: the history, physical, and laboratory examinations. 3rd ed. Boston: Butterworths; 1990. p.220.
11. Furman JM, etal. Benign paroxysmal positional vertigo. N Engl J Med. 1999;341:1590.
12. Cohen HS, etal. Standing balance tests for screening people with vestibular impairments. Laryngoscope. 2014;124:545.
13. Sloane PD, etal. Management of dizziness in primary care. J Am Board Fam Pract. 1994;7:1.
Chapter 26
Headache
SchantalPolanco
Abbreviations
AVM Arteriovenous malformation CDH Chronic daily headache CVT Chronic venous thrombosis GCA Giant cell arteritis or temporal arteritis HC Hemicrania continua LP Lumbar puncture MO Medication overuse PH Paroxysmal hemicranias SAH Subarachnoid hemorrhage SDH Subdural hematoma SUNCT Short-lasting unilateral neuralgiform headache TAC Trigeminal autonomic cephalalgia TMJ Temporal mandibular joint TTH Tension-type headache;
S. Polanco (*) Albert Einstein College of Medicine, Jacobi Medical Center, Bronx, NY, USA e-mail: schantal.polanco@nychhc.org
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022 E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_26
507
508
S. Polanco

Introduction

Headache is a common neurological complaint in the outpa­tient setting [1]. The importance of proper diagnosis is crucial to our management. Most headaches are of benign etiology and fall under the category of primary headache disorders. Tension-type headache is more common than migraine head­ache [2]. However, migraine headaches tend to be disabling and cause functional impairment leading patients to seek medical assistance more frequently for this ailment [2]. Cluster headaches fall under the category of trigeminal auto­nomic cephalalgia and this disorder has a prevalence of less than 1% [3]. It is important to recognize the characteristics and diagnostic criteria of primary headaches to assist with management. As an initial first step in our assessment, it is important to focus on key aspects of the history and physical examination to exclude secondary causes of headache which may stem from other systemic, neurological, psychiatric, or traumatic etiologies. Once these “red flags” in the history and physical examination are excluded, one can focus on the more common primary etiologies of headache (Fig.26.1).
pneumonic?
Old with no “Red Flags”
Does it meet 4/5 *POUND
Chapter 26. Headache
disorder-refer to Table 2
Other Primary headache
No
TAC
*POUND pneumonic
Pulsatile
One day duration
Unilateral
TTH
Nausea association
Disabling intensity
509
Headache
New or “Red Flags”
No evidence of
secondary cause
Headache
Rule out Secondary
Yes=Migraine
Likely primary
headache with
atypical features
secondary headaches
Key history and suspected
1 month
Treat using recommendation
from Table 3 and reassess in
Signs of
infection
Any focal
or symptom
neurological sign
use
state or OCP
Pro-thrombotic
Thunderclap
>50
Age
consultation
Refer for neurological
diagnostic uncertainty
Persistent, MO or headache with
Encephalitis
Meningitis or
SAH CVT CVA
GCA
F . Headache algorithm
S. Polanco
510
Key History andPhysical Exam
A complete history and physical examination are essential in the assessment of any headache. When done properly, the potentially dangerous causes of headache which may warrant emergent intervention can be identified. The following fea­tures in the history have been underlined to highlight infor­mation which may support a secondary cause of headache (refer to Table26.1).
History
Age: New headache in a patient above 50years should raise
concerns for temporal arteritis, acute angle- closure glau­coma, and malignancy in the right context [1, 4–6], particu­larly if associated with visual disturbance, jaw claudication, polymyalgia, cough, or weight loss.
Onset and Characteristic: An abrupt onset of maximum inten-
sity is suggestive of an ominous or secondary cause for the headache. These symptoms fall under the umbrella term of “thunderclap headache” typically described by patients as “the worst headache of my life” and warrants immediate attention with imaging and lumbar puncture when imaging is nonrevealing and our clinical suspicion is high. Etiologies
T . Differential diagnosis as outlined by the International Headache Society
Primary headache Secondary headache based on “red flags”
1. Tension-type
headache (TTH)
2. Migraine
3. Trigeminal
autonomic cephalalgias (TACs)
Look for clues in your history, physical exam, laboratory studies, and imaging to guide your differential diagnosis when a secondary headache is suspected.
Chapter 26. Headache
T . (continued)
Primary headache Secondary headache based on “red flags”
4. Other primary
headache disorders
• Primary
cough headache
• Primary
exercise headache
• Primary
headache associated with sexual activity
• Primary
thunderclap headache
• Cold stimulus
headache
• External
pressure headache
• Primary
stabbing headaches
• Nummular
headache— Coin shaped
• Hypnic
headache—
1. Headache attributed to infection.
2. Headache attributed to trauma.
3. Headache attributed to a vascular disorder (CVA, SAH, SDH, arteritis, unruptured vascular malformation, carotid or vertebral artery disorder, genetic vasculopathy, pituitary apoplexy, and other acute intracranial disorders such as those resulting from an endovascular procedure or conditions less clearly understood such as reversible cerebral vasoconstriction syndrome.
4. Headache attributed to other nonvascular intracranial disorder (cerebrospinal fluid pressure—High or low), noninfectious intracranial inflammatory diseases, intracranial neoplasm, seizure, Chiari malformation)
5. Headache attributed to substance exposure, use, or withdrawal (including those prescribed, illicit, and contained in food).
6. Headache attributed to a disorder of homeostasis (hypoxia, hypercapnia, dialysis, hypertension, hypothyroidism, fasting, etc.)
7. Headache attributed to disorder of facial
or cervical structures.
8. Headache attributed to psychiatric disorder.
Only during sleep
• New daily persistent headache
511
512
S. Polanco
which may present this way include subarachnoid hemor­rhage, cavernous venous thrombosis, pituitary apoplexy, hypertensive emergency, arterial dissections, and acute angle-closure glaucoma, which require emergent interven­tion [1, 4, 5].
Duration and Relevant Past Medical History: Persistent or
progressive headache in a patient with a past medical history of cancer, HIV, Lyme disease, systemic vascular disorder, or hypercoagulable state warrants further workup of secondary causes. Additionally, patients with a past medical history of a primary headache such as migraine may be at increased risk of developing brain lesions including posterior circulation stroke-like lesions [7]. A new headache or prior changes in the characteris­tics of a known headache disorder warrant further investigation.
Medications: Use of anticoagulants, NSAIDs, steroids, or
drugs of abuse such as cocaine place patients at an increased risk of intracranial bleed and can be an indica­tion for neuroimaging [1]. The use of birth control pills is associated with increase in migraine severity but also an increased risk of CVT [8, 9].
Context: Headache in the setting of trauma, uncontrolled
hypertension, motor, sensory, cerebellar, personality, or cognitive change warrants imaging to further investi­gate the neurological symptom. The presence of sys­temic symptoms should precipitate additional considerations. In patients who were hospitalized with COVID-19, headache was considered a presenting symptom and this diagnosis should be considered in the appropriate clinical context [10].
Aggravating factors that raise intracranial pressure such as
exertion, cough, and lying down may reflect an intracranial etiology and require additional investigation [4].
Location: Careful history and palpation over maxillary and
frontal sinuses, orbits, temporal artery, TMJ, ears, occipi­tal nerve, and upper posterior neck can reveal pain from various secondary headaches and neuralgias [5].