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_208_библиотеки_им_акад_М_И_Перельмана
.pdf
462 Laboratory Medicine in Psychiatry and Behavioral Science
Limbic encephalitis (LE)
Clinical findings LE is an autoimmune disorder characterized by the acute to subacute
development of psychiatric, cognitive, and/or epileptic symptoms at
-
tributed to inflammation in the brain’s limbic system (hippocampus,
amygdala, parahippocampal gyrus, cingulate gyrus, subcallosal gyri,
and related structures). Typical symptoms include severe impairment
in short-term memory, altered mental status (delirium, confusion,
psychosis), anxiety, depression, irritability, personality changes,
andseizures. Faciobrachial dystonic seizures are pathognomonic of
leucine-rich glioma-inactivated 1 (LGI1) encephalitis. Other signs/
symptoms reported in LE include autonomic disturbances, sleep prob
-
lems, ataxia, dystonia, myoclonus, aphasia, apraxia, obsessiveness,
and endocrine dysfunction. LE is caused by a reaction of theimmune
systemto cancer, non-cancerous tumors, infections, and other autoim
-
mune disorders. When LE represents a paraneoplastic syndrome, it
usually appears before the diagnosis of malignancy is made. The most
commonly associated cancer is small cell lung cancer, but breast, tes
-
ticular, and other cancers can be implicated.
According to published guidelines, the diagnosis of LE requires that
the following criteria be met:
• Subacute onset (rapid progression over <3 months) of working
memory deficits, seizures, or psychiatric symptoms suggesting
limbic system involvement
• Bilateral brain abnormalities on T2-weighted or FLAIR MRI re-
stricted to the medial temporal lobes
• Either CSF pleocytosis (WBC count >5/mm
3
) or EEG with epilep-
tic or slow-wave activity involving temporal lobes
• Reasonable exclusion of alternative causes
Laboratory testing MRI is performed (T2 and FLAIR) to evaluate medial temporal lobe
structures. MRI may be repeated or FDG-PET performed to evaluate
medial temporal lobe metabolism.
EEG is performed to screen for temporal lobe epileptiform or slow-
wave activity.
CSF is examined for pleocytosis. Usual CSF inflammatory markers
such as WBC and protein are not sensitive or specific for LE. Oligoclo
-
nal bands, if present, can increase the sensitivity for diagnosis.
Neuronal antibody detection is improved if both CSF and serum are
examined. Each laboratory has an encephalitis panel and algorithm for
reflex testing based on immunofluorescence patterns. Antibodies tested
include LGI1, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid
receptor (AMPAR), GABA-B receptor (GABA-BR), contactin-associated
protein-like 2 (Caspr2), metabotropic glutamate receptor subtype 5
(mGluR5), dipeptidyl-peptidase-like protein-6 (DPPx), NMDAR, glu-
tamic acid decarboxylase (GAD), Hu, Ma, Ri, collapsin response medi-
ator protein 5 (CRMP5), Sry-like high-mobility group box (SOX1),
amphiphysin, and adenylate kinase 5 (AK5).
If the patient is antibody-positive, a tumor survey is undertaken.
Abboud H, Probasco JC, Irani S, et al: Autoimmune encephalitis: proposed best practice recommenda-
tions for diagnosis and acute management.J Neurol Neurosurg Psychiatry 92(7):757–768, 2021
Budhram A, Leung A, Nicolle MW, Burneo JG: Diagnosing autoimmune limbic encephalitis.CMAJ
191(19):E529–E534, 2019
Chiveri L, Verrengia E, Muscia F, et al: Limbic encephalitis in a COVID-19 patient?J Neurovirol 27(3):498–
500, 2021
https://t.me/med1917
463 Diseases and Conditions
Limbic encephalitis (LE) (continued)
Graus F, Titulaer MJ, Balu R, et al: A clinical approach to diagnosis of autoimmune encephalitis.Lancet
Neurol 15(4):391–404, 2016
Kao YC, Lin MI, Weng WC, Lee WT: Neuropsychiatric disorders due to limbic encephalitis: immunologic
aspect.Int J Mol Sci 22(1):389,
Li X, Yuan J, Liu L, Hu W: Antibody-LGI 1 autoimmune encephalitis manifesting as rapidly progressive
dementia and hyponatremia: a case report and literature review. BMC Neurol. 19(1):19, 2019
Mahawish
Nissen MS, Ryding M, Meyer M, Blaabjerg M: Autoimmune encephalitis: current knowledge on sub-
types, disease mechanisms and treatment. CNS Neurol Disord Drug Targets 19(8):584–598, 2020
https://t.me/med1917
464 Laboratory Medicine in Psychiatry and Behavioral Science
Lyme disease
Clinical findings Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most
common tick-borne illness in the United States and is endemic in the
Northeastern states (Virginia to Maine), the upper Midwest (particu
-
larly Wisconsin and Minnesota), and Northern California, although
sporadic cases occur elsewhere. Lyme disease is transmitted only by
deer ticks, not by dog or wood ticks. The disease often begins with the
characteristic skin lesion known as erythema migrans at the site of the
tick bite. Within days to weeks, the spirochete may disseminate so that
the patient is at risk of developing cardiac, neurological, and/or rheu-
matological symptoms. Treatment with an antibiotic accelerates reso-
lution of the disease. If no treatment is given, the disease may resolve
spontaneously but can then recur.
The risk of contracting Lyme disease is highest in endemic areas when
the bite involves the tick genus Ixodes and the tick remains attached for
36 or more hours. The tick should therefore be removed promptly and
carefully with tweezers and should be saved for identification pur
-
poses. The tick itself should not be tested.
Signs, symptoms, and sequelae of Lyme disease:
• Constitutional symptoms that may be seen on presentation include
fever, chills, myalgias, fatigue, headache, and swollen lymph nodes.
• Lyme disease affects the nervous system in 10%–15% of cases, with
manifestations including lymphocytic meningitis, cranial neuritis,
painful radiculoneuritis, and mononeuropathy multiplex. During
active systemic infection, encephalopathy can be seen.
• Individuals diagnosed with Lyme disease also have a greatly in-
creased risk of psychiatric disorders including mood disorders,
suicidality, and completed suicide that is highest during the first
1–3 years after diagnosis. It should be noted that the converse is not
true; individuals diagnosed with psychiatric disorders do not nec-
essarily have an increased risk of Lyme disease, and testing in the
general psychiatric population has given rise to a great deal of con-
troversy.
• Symptoms that have been attributed to chronic Lyme disease may in
some cases be due to posttreatment Lyme disease, a syndrome char-
acterized by symptoms seen within 6 months of treatment that per-
sist for 6 months or longer. This posttreatment syndrome is thought
to arise from persistent immune activation, a hypothesis bolstered
by recent
11
C-DPA-713 PET studies of TSPO in affected patients ver-
sus healthy control subjects.
• Cardiac effects of Lyme disease include pericarditis, myocarditis,
and cardiac conduction disease that sometimes requires permanent
pacemaker implantation. Presenting symptoms in cardiac
involvement include dyspnea, chest pain, lightheadedness, syn-
cope, palpitations, and/or edema.
• In late-stage infection in which earlier stages were asymptomatic,
the presenting problem can be Lyme arthritis. In these cases, joint
pain and swelling can be persistent or intermittent and involve one
or a few large joints (particularly the knees). This syndrome may
persist for several years even in the absence of systemic symptoms.
https://t.me/med1917
465 Diseases and Conditions
Lyme disease (continued)
Laboratory testing Diagnosis of Lyme disease is made by serum antibody testing. In pa-
tients with CNS symptoms, CSF antibodies are also tested. Antigen
testing by PCR or culture is not recommended because of low sensitiv
-
ity. Testing is recommended for patients presenting with characteristic
neurological, cardiac, or rheumatological symptoms and in at-risk pa
-
tients exhibiting a rash that is not typical of erythema migrans. Routine
testing is not recommended for patients with known neurological con
-
ditions, cognitive decline, dementia, or psychiatric, behavioral, or de-
velopmental disorders.
Guidelines for testing are as follows:
• The tick should be saved for identification of species, but the tick
itself should not be tested.
• Asymptomatic patients with a tick-bite history do not require
testing.
• Patients presenting with an erythema migrans rash should be
treated immediately; confirmatory testing is not needed.
• Testing methods for the diagnosis of Lyme disease are of two types:
antigen testing for B. burgdorferi and antibody testing to detect im
-
mune response. As of this writing, antigen testing is not recom-
mended, in part because of the low sensitivity of existing assays.
• Antibody testing uses a two-tiered approach, with an initial en-
zyme immunoassay (EIA) followed by either a second EIA or West-
ern blot if the first EIA test is positive or borderline. This approach
works well for later stages of infection but has low sensitivity for
early infection. These assays do not distinguish active from inactive
infection, and seropositivity may persist for years, even after treat
-
ment and resolution of the clinical disease.
• Culture of B. burgdorferi has low sensitivity and requires lengthy
incubation and special media and expertise. It is not routinely used.
• For patients with skin lesions that suggest but are not typical of
erythema migrans, Lyme antibody testing is recommended on both
acute and convalescent serum samples (drawn 2–3 weeks later).
• To test for nervous system involvement (Lyme neuroborreliosis),
simultaneous sampling of serum and CSF for antibodies is recom
-
mended because sampling only CSF could yield spurious results
due to the passive transfer of antibodies from the blood to the CSF.
The two-tiered approach described above is used.
• At-risk patients with acute myocarditis or pericarditis of unknown
cause should undergo serum antibody testing for Lyme disease.
• In addition to serum antibody testing, an ECG should be performed
in patients evaluated for Lyme disease who have signs or symp
-
toms of carditis: dyspnea, edema, palpitations, lightheadedness,
chest pain, and/or syncope.
• Serum antibody testing is also used for possible Lyme arthritis. PCR
assay for B. burgdorferi can be used for evaluation of synovial fluid
samples in untreated patients with suspected Lyme arthritis but
cannot be used to show eradication of spirochetes after treatment.
• In patients who have persistent constitutional symptoms such as
high fever while being treated for Lyme disease, testing for co
-
infection with other organisms should be considered in consulta-
tion with an infectious disease specialist.
https://t.me/med1917
466 Laboratory Medicine in Psychiatry and Behavioral Science
Lyme disease (continued)
Arvikar SL, Steere AC: Diagnosis and treatment of Lyme arthritis.Infect Dis Clin North Am 29(2):269–
280, 2015
Chaconas G, Castellanos M, Verhey TB: Changing of the guard: how the Lyme disease spirochete sub-
verts the host immune response. J Biol Chem 295(2):301–313, 2020
Coughlin JM, Yang T, Rebman AW, et al: Imaging glial activation in patients with post-treatment Lyme
disease symptoms: a pilot study using [11C]DPA-713 PET. J Neuroinflammation 15(1):346, 2018
Dumes AA: Lyme disease and the epistemic tensions of “medically unexplained illnesses.” Med An-
thropol 39(6):441–456, 2020
Fallon BA, Madsen T, Erlangsen A, Benros ME: Lyme borreliosis and associations with mental disorders
and suicidal behavior: a nationwide Danish cohort study. Am J Psychiatry 178(10):921–931, 2021
Hinds K, Sutcliffe K: Heterodox and orthodox discourses in the case of Lyme disease: a synthesis of ar-
guments. Qual Health Res 29(11):1661–1673, 2019
John TM, Taege AJ: Appropriate laboratory testing in Lyme disease.Cleve Clin J Med 86(11):751–759, 2019
Lantos PM: Chronic Lyme disease.Infect Dis Clin North Am 29(2):325–340, 2015
Lantos PM, Rumbaugh J, Bockenstedt LK, et al: Clinical practice guidelines by the Infectious Diseases So-
ciety of America (IDSA), American Academy of Neurology (AAN), and American College of Rheuma-
tology (ACR): 2020 Guidelines for the Prevention, Diagnosis, and Treatment of Lyme Disease.Arthritis
Care Res (Hoboken) 73(1):1–9, 2021
Marques AR: Laboratory diagnosis of Lyme disease: advances and challenges.Infect Dis Clin North Am
29(2):295–307, 2015
Mead P, Petersen J, Hinckley A: Updated CDC recommendation for serologic diagnosis of Lyme dis-
ease. MMWR Morb Mortal Wkly Rep 68(32):703, 2019
Moore A, Nelson C, Molins C, et al: Current guidelines, common clinical pitfalls, and future directions
for laboratory diagnosis of Lyme disease, United States. Emerg Infect Dis 22(7):1169–1177, 2016
Nigrovic LE, Lewander DP, Balamuth F, et al: The Lyme disease polymerase chain reaction test has low
sensitivity.Vector Borne Zoonotic Dis 20(4):310–313, 2020
Pitrak D, Nguyen CT, Cifu AS: Diagnosis of Lyme disease. JAMA 327(7):676–677, 2022
Schriefer ME: Lyme disease diagnosis: serology. Clin Lab Med 35(4):797–814, 2015
Schutzer SE, Body BA, Boyle J, et al: Direct diagnostic tests for Lyme disease. Clin Infect Dis 68(6):1052–
1057, 2019
Shapiro ED: Clinical practice: Lyme disease. N Engl J Med 370(18):1724–1731, 2014
Tetens MM, Haahr R, Dessau RB, et al: Assessment of the risk of psychiatric disorders, use of psychiatric
hospitals, and receipt of psychiatric medication among patients with Lyme neuroborreliosis in Den
-
mark. JAMA Psychiatry 78(2):177–186, 2021
Uzomah UA, Rozen G, Mohammadreza Hosseini S, et al: Incidence of carditis and predictors of pace-
maker implantation in patients hospitalized with Lyme disease.PLoS One 16(11):e0259123, 2021
Waddell LA, Greig J, Mascarenhas M, et al: The accuracy of diagnostic tests for Lyme disease in humans,
a systematic review and meta-analysis of North American research. PLoS One 11(12):e0168613, 2016
Williams AL, Bevan J, Arnold MJ: Lyme disease: updated recommendations from the IDSA, AAN, and
ACR.Am Fam Physician 104(6):652–654, 2021
https://t.me/med1917
467 Diseases and Conditions
Major depressive disorder (MDD)
Clinical findings According to DSM-5, MDD is characterized by five or more of the fol-
lowing symptoms present during the same 2-week period and repre-
senting a change from previous function:
•
Depressed mood
• Marked loss of interest or pleasure in activities
• Change in appetite or weight
• Insomnia or hypersomnia
• Psychomotor agitation or retardation
• Fatigue or loss of energy
• Feelings of worthlessness or excessive/inappropriate guilt
• Reduced ability to think, concentrate, or make decisions
•
Recurrent thoughts of death, suicidal ideation, or suicide attempt
or plan
At least one of the symptoms above must be either depressed mood or
loss of interest or pleasure.
DSM-5 offers alternative diagnoses for depressive disorder due to an-
other medical condition or substance/medication-induced depressive
disorder, characterized only by a prominent and persistent period of
depressed mood or markedly diminished interest or pleasure in activ
-
ities. The importance of demonstrating a link between the depressive
episode and the medical condition or substance use is emphasized. In
practice, the abbreviated criteria for these secondary syndromes are
easy to meet, but the temporal link is not so easily established. More
-
over, it is self-evident that all patients presenting with d epression must
be evaluated for symptoms such as suicidality and for contributing
factors including undiscovered medical illness.
Depression commonly occurs in the context of established medical ill-
nesses such as diabetes, coronary artery disease, cerebrovascular insuf-
ficiency, cancer, epilepsy, multiple sclerosis, alcohol use disorder, SLE,
HIV infection, Huntington’s disease, and neurodegenerative diseases
such as Parkinson’s disease, Alzheimer’s disease, and FTD. Depression
also commonly follows stroke, heart attack, and TBI and is associated
with medications including glucocorticoids, β-blockers, calcium chan
-
nel blockers, statins, antiviral drugs, benzodiazepines, opioids, birth
control pills, isotretinoin, varenicline, reserpine, and methyldopa.
Laboratory testing Laboratory abnormalities may facilitate diagnosis of as-yet undis-
covered medical conditions that cause or contribute to depression or
predict later development of depression. These include anemia, mac
-
rocytosis, neutrophilia, abnormalities of liver function (elevated AST,
ALT, and GGT), abnormalities of renal function, various endocrine de-
rangements (involving thyroid, parathyroid, and adrenal glands), ele-
vated HbA1C, hypoglycemia, testosterone deficiency, adult growth
hormone deficiency, viral and bacterial infections, pancreatic cancer,
and vitamin B
12
or folate deficiency. Certain of these abnormalities are
sufficiently common that routine testing is indicated in patients pre-
senting with depression.
Basic screening tests for MDD include the following:
• CMP
• CBC with differential and platelets
https://t.me/med1917
468 Laboratory Medicine in Psychiatry and Behavioral Science
Major depressive disorder (MDD) (continued)
Laboratory testing
(continued)
• Vitamin B
12
and folate levels
• TSH
Based on the patient’s demographics, medical history, physical exam,
and specific signs and symptoms, the following tests should also be
considered:
• Urinalysis
• Urine toxicology screen
• RPR
• HIV testing
• Blood alcohol level
• Therapeutic medication levels (for TCAs or mood stabilizers)
• Urine pregnancy testing, if indicated
• ECG
• Brain MRI or head CT
• EEG
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Hsu WY, Chang TG, Chang CC, et al: Suicide ideation among outpatients with alcohol use disorder.Be-
hav Neurol 2022:4138629, 2022
Sealock JM, Lee YH, Moscati A, et al: Use of the PsycheMERGE network to investigate the association be-
tween depression polygenic scores and white blood cell count.JAMA Psychiatry 78(12):1365–1374, 2021
Wainberg M, Kloiber S, Diniz B, et al: Clinical laboratory tests and five-year incidence of major depressive
disorder: a prospective cohort study of 433,890 participants from the UK Biobank.Transl Psychiatry
11(1):380, 2021
https://t.me/med1917
469 Diseases and Conditions
Manganese poisoning
Clinical findings Manganese is an essential micronutrient that serves as a cofactor in
enzymatic reactions involved in metabolism, bone formation, repro
-
duction, immune response, scavenging of reactive oxygen species,
and blood clotting. The mineral is present in foods such as whole
grains, certain shellfish, legumes, and nuts and is also available as a
dietary supplement. It is absorbed in the small intestine and circulates
in the blood, to be taken up by tissues including the liver, pancreas,
kidney, and brain, with the highest concentrations in the globus pall-
idus and striatum. Manganese is eliminated mainly in the feces via
biliary excretion.
Because food is the primary source of manganese exposure in the gen-
eral population, toxicity is uncommon except in countries where pes-
ticide laws are lax. The most important source of toxic exposure is the
inhalation of air contaminated with particulate matter containing
manganese. Those who are at highest risk include miners, arc welders,
steelworkers, and dry-battery manufacturers and those living and
working in proximity to these industries. The potential toxicity of
manganese-containing gasoline additives such as MMT (methylcy-
clopentadienyl manganese tricarbonyl, which replaced lead as an
anti-knock agent) is unclear. Cases of manganese toxicity have been
reported among patients receiving long-term total parenteral nutri
-
tion, in those injecting methcathinone (“cat”) intravenously due to
poor purification procedures, and among individuals ingesting man
-
ganese-contaminated well water. The U.S. Environmental Protection
Agency has set a “health advisory level” for manganese in drinking
water of 0.3 mg/L.
Constitutional symptoms of manganese poisoning include apathy,
malaise, lethargy, weakness, headache, poor appetite, and sexual dys-
function. Although cardiovascular and pulmonary systems are af-
fected by toxicity, the most prominent symptoms are neuropsychiatric.
Psychiatric signs and symptoms include the following:
• Mood and personality changes: anxiety, irritability, euphoria, labil-
ity of mood
• Psychosis (“manganese madness”): agitation, hallucinations, delu-
sions with intact reality testing
• Behavioral changes: compulsive behaviors, pseudobulbar affect,
inappropriate jocularity, apathy, aggression, social withdrawal
• Cognitive impairment (usually mild) involving memory and judg-
ment domains
• Sleep disturbance (insomnia or daytime somnolence)
Specific motor signs and symptoms include the following:
• Parkinsonism
• Cogwheel rigidity
• Akinesia/bradykinesia
• Masked facies
• Tremor (intention type)
• Dysarthria
• Hypophonia
• Postural instability, retropulsion
• Hyperreflexia
https://t.me/med1917
470 Laboratory Medicine in Psychiatry and Behavioral Science
Manganese poisoning (continued)
Clinical findings • Dystonia (face, neck, and distal lower extremities)
(continued)
• Characteristic gait disorder (“cock walk,” a forward-tilting stance,
on tiptoes)
• Poor response to dopaminergic drugs
Laboratory testing Brain MRI can be used along with manganese levels and clinical signs
and symptoms to diagnose toxicity. MRI shows characteristic T1 hy
-
perintensities in the basal ganglia reflecting manganese accumulation.
The ratio of the signal observed in the globus pallidus to the signal ob
-
served in the frontal white matter multiplied by 100 yields the pallidal
index, which is a reliable marker of manganese load.
Reference levels for
• Serum: 0.0–2.0 μg/L
• Whole blood: 4.2–16.5 μg/L
• RBCs: by report
Serum levels are useful to indicate recent, active exposure.
Whole blood levels are useful for monitoring manganese accumulation
with total parenteral nutrition.
RBC levels are useful to indicate recent, active exposure and may be
useful in confirming long-term, low-dose exposure.
Values between 1 and 2 times the upper limit of normal (ULN) may be
due to normal biological variation and should be interpreted with cau
-
tion. Values >2 times the ULN correspond to toxicity. For monitoring
over time, samples should be taken no more frequently than the half
-
life of manganese, which is 40 days.
Abdel-Naby S, Hassanein M: Neuropsychiatric manifestations of chronic manganese poisoning. J Neurol
Neurosurg Psychiatry 28:282–288, 1965
ARUP Laboratories: Manganese, RBC, in Laboratory Test Directory. Salt Lake City, UT, ARUP Laborato-
ries, 2022. Available at: https://ltd.aruplab.com/Tests/Pub/2007254. Accessed February 2022.
ARUP Laboratories: Manganese, serum, in Laboratory Test Directory. Salt Lake City, UT, ARUP Labora-
tories, 2022. Available at: https://ltd.aruplab.com/Tests/Pub/0099265. Accessed February 2022.
ARUP Laboratories: Manganese, whole blood, in Laboratory Test Directory. Salt Lake City, UT, ARUP Lab-
oratories, 2022. Available at: https://ltd.aruplab.com/Tests/Pub/0099272. Accessed February 2022.
Balani SG, Umarji GM, Bellare RA, et al: Chronic manganese poisoning. J Postgrad Med 13:116–121, 1967
Chandra SV: Psychiatric illness
Crossgrove J, Zheng W:
Fitzgerald K, Mikalunas V, Rubin H, et al: Hypermanganesemia in patients receiving total parenteral nu-
trition. JPEN J Parenter Enteral Nutr 23(6):333–336, 1999
https://t.me/med1917
471 Diseases and Conditions
Manic episode
Clinical findings A manic episode is characterized by a distinct period of abnormally and
persistently elevated, expansive, or irritable mood and abnormally and
persistently increased activity or energy, lasting at least 1 week and
present most of the day, nearly every day (or for any duration if hospi-
talization is necessary). During this period, three or more of the follow-
ing symptoms are present (four or more symptoms if the mood is only
irritable): grandiosity, decreased need for sleep, pressured speech or in
-
creased talkativeness, flight of ideas or racing thoughts, distractibility,
increase
in activities that have a high
As with other secondary syndromes, the criteria for diagnosing a manic
episode due to another medical disorder are abbreviated, including
only the following (along with the usual exclusions and severity crite
-
rion):
• Prominent and persistent period of abnormally elevated, expan-
sive, or irritable mood and abnormally increased activity or energy
that predominates in the clinical picture
• Evidence from the history, physical examination, or laboratory
findings that the disturbance is the direct pathophysiological con
-
sequence
Medical conditions known to cause mania or hypomania include the
following:
•
Cerebral neoplasm
• Cushing’s disease
• Encephalitis/meningitis
• Epilepsy
• Multiple sclerosis
• Stroke
• SLE
• TBI
• Wilson’s disease
Numerous other endocrine, metabolic, and infectious conditions can
also be associated with mania/ hypomania. A first manic episode ap
-
pearing in late life is particularly likely to be secondary to a neurological
condition. Medications associated with mania include corticosteroids,
anabolic steroids, antidepressants, dopaminergic drugs, tumor necrosis
factor-α inhibitors, sympathomimetics, bronchodilators, amphetamines,
and certain herbal preparations. Abuse of alcohol and many illicit drugs
is also well known to be associated with mania.
Laboratory testing Laboratory testing is performed to exclude underlying medical condi-
tions that could be causing or contributing to the manic episode and to
help guide treatment. The following tests should be considered:
• CMP
• CBC with differential and platelets
• Urinalysis
• TSH
• RPR
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана