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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_208_библиотеки_им_акад_М_И_Перельмана
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352 Laboratory Medicine in Psychiatry and Behavioral Science
Brain abscess
Clinical findings Brain abscess is a focal bacterial, fungal, or parasitic infection that be-
gins as an area of cerebritis and evolves into an encapsulated area of
pus. The condition develops from the spread of pathogens from adja
-
cent tissues or hematogenous dissemination. Patients at risk include
those with a history of trauma, dental abscess, otitis media, IV drug
abuse, endocarditis, immunodeficiency, or bronchiectasis. Abscess is
more common in males and in children, adolescents, and young adults.
Classic signs of brain abscess include fever, headache, and focal neu-
rological deficits, but seizures and altered mental status are also com-
monly seen, the latter presaging a poor outcome. Onset is usually
subacute. Specific focal signs depend on the location of the lesion(s),
with frontotemporal or frontoparietal areas most often affected. Mul
-
tiple lesions may be seen with a hematogenous origin.
If the abscess is left untreated, intracranial pressure may eventually
increase so that meningeal signs develop. Projectile vomiting can oc
-
cur. Rupture of the abscess into the ventricular space carries a high risk
of obstructive hydrocephalus and is fatal in up to 85% of cases.
Laboratory testing Sonneville et al. (2017) proposed an algorithm for the workup of sus-
pected brain abscess, as follows:
1. Presence of clinical signs/symptoms noted above.
2. While awaiting brain imaging, consider predisposing conditions
(e.g., endocarditis, dental infection).
3. Brain MRI if readily available. If not, urgent CT with contrast.
4. If CT does not detect abscess, perform MRI.
5. Obtain blood cultures before initiating antibacterial treatment.
6. Consider HIV testing, especially if lesions are bilateral (indicating
possible toxoplasmosis).
7. Stereotactic aspiration of all abscesses ≥ 2.5 cm. If no abscess
≥2.5 cm, at least one ≥1 cm.
8. Microbiology: routine, with or without molecular testing, and with
specific tests for tuberculosis, fungus, etc., as indicated.
Other laboratory abnormalities in affected patients include leukocyto-
sis and elevated ESR. Lumbar puncture is contraindicated. EEG may
show focal slowing. Follow-up EEG after treatment is recommended
because many patients develop seizures in the following year.
Brook I: Microbiology and treatment of brain abscess.J Clin Neurosci 38:8–12, 2017
Brouwer MC, van de Beek D: Epidemiology, diagnosis, and treatment of brain abscesses.Curr Opin In-
fect Dis 30(1):129–134, 2017
Cantiera M, Tattevin P, Sonneville R: Brain abscess in immunocompetent adult patients.Rev Neurol
(Paris) 175(7–8):469–474, 2019
Chow F: Brain and spinal epidural abscess. Continuum (Minneap Minn) 24(5):1327–1348, 2018
Sonneville R, Ruimy R, Benzonana N, et al: An update on bacterial brain abscess in immunocompetent
patients.Clin Microbiol Infect 23(9):614–620, 2017
https://t.me/med1917
353 Diseases and Conditions
Brain tumor
Clinical findings The most commonly diagnosed brain tumors are gliomas, menin-
giomas, and metastases from distant cancers such as melanoma and
lung, breast, or kidney cancer. These tumors range from benign, slow-
growing meningiomas to malignant, aggressive glioblastomas. Tumor-
related symptoms depend on the location, size, and growth rate of the
tumor as well as the extent of surrounding inflammation and edema.
Common neuropsychiatric symptoms include headache, fatigue, cog-
nitive changes, personality and behavioral changes, and focal signs
such as hemiparesis. Frequent complications include epilepsy, stroke,
venous thromboembolism, endocrine dysfunction, infection, and radi
-
ation necrosis secondary to treatment. Increasingly, genomic data are
used along with histopathological findings to inform the classification
and treatment of brain tumors.
Laboratory testing For patients with suspected brain tumors, MRI with contrast is used in
preference to CT unless there is some contraindication to MRI. The neu-
roradiologist should be
asked for specific information about the size,
constitution, surrounding tissue, and vascularity of the tumor, as well
as the
likely tumor type based on these characteristics and its location.
In selected cases (e.g., suspected lymphoma), if neuroimaging study
did not show any evidence of increased intracranial pressure, lumbar
puncture may be
performed to visualize cancer cells or tumor markers.
Biopsy of tumor tissue is usually accomplished via craniotomy at the
time the tumor is removed. Alternatively, stereotactic biopsy may be
used to confirm the diagnosis and identify the specific tumor type. This
involves insertion of a needle through a small hole rather than craniot
-
omy and is used for tumors thought to be radiation-sensitive or for
masses that are inaccessible to surgery.
EEG may show focal slowing or epileptiform activity around the site of
the tumor. Ictal (seizure) activity may be captured. At present, PET
scanning is not routinely used for brain tumor diagnosis but occasion
-
ally may be used for tumor grading or for more precise tissue targeting
for surgery. In treated cases, PET can also help distinguish delayed ra-
diation encephalopathy from recurrent tumor.
Other lab tests may be indicated in the diagnostic workup if metastatic
disease is suspected (e.g., if multiple tumor foci are identified) and the
primary remains unknown. These include CT of the chest, abdomen,
and pelvis; CT of the neck if thyroid cancer is suspected; mammogram;
ultrasound of the testes; and stool testing for occult blood. Certain
brain tumors are associated with SIAD; see Syndrome of Inappropri-
ate Antidiuresis entry for details of lab workup.
Louis DN, Perry A, Wesseling P, et al: The 2021 WHO Classification of Tumors of the Central Nervous
System: a summary. Neuro Oncol 23(8):1231–1251, 2021
McFaline-Figueroa JR, Lee EQ: Brain tumors.Am J Med 131(8):874–882, 2018
Ostrom QT, Wright CH, Barnholtz-Sloan JS: Brain metastases: epidemiology.Handb Clin Neurol 149:27–
42, 2018
Perez A, Huse JT: The evolving classification of diffuse gliomas: World Health Organization updates for
2021.Curr Neurol Neurosci Rep 21(12):67, 2021
Schiff D, Alyahya M: Neurological and medical complications in brain tumor patients.Curr Neurol Neu-
rosci Rep 20(8):33, 2020 [published correction appears in Curr Neurol Neurosci Rep 20(9):40, 2020]
Vargo MM: Brain tumors and metastases. Phys Med Rehabil Clin N Am 28(1):115–141, 2017
https://t.me/med1917
354 Laboratory Medicine in Psychiatry and Behavioral Science
Bulimia nervosa (BN)
Clinical findings BN is characterized by cycles of recurrent binge eating and recurrent
compensatory behaviors, such as self-induced vomiting, food restric
-
tion, and compulsive exercise. Affected individuals are not under-
weight but have a variety of health problems related to irregular eating
and purging. The disorder commonly begins in adolescence or young
adulthood and has a crude mortality rate of 2% per decade. Both the
incidence of BN and the severity of existing cases worsened during the
COVID-19 pandemic. Members of the LGBTQ+ community may be dis
-
proportionately affected by this condition.
Psychological symptoms of BN include a preoccupation with body
shape and weight, negative body image, feeling of loss of control over
eating, and excessive guilt, self-hate, and self-criticism. Executive func
-
tion impairment is identified on neuropsychological testing. Patients
are often seen as perfectionists, with their self-worth determined by
their current weight. Impulsivity and lack of emotional control become
highly problematic when the patient becomes self-injurious. Psychiat
-
ric comorbidities include major depression, anxiety disorders, sub-
stance abuse, and borderline personality disorder, and the risk of
suicide is significant.
Physical signs include weight fluctuation, dehydration, electrolyte
derangements, cardiac dysrhythmias, and amenorrhea or menstrual
irregularity. Osteopenia can develop with episodes of weight loss and
sex steroid suppression. With recurrent vomiting, scarring of the dor
-
sum of the hand, erosion of dental enamel, dental caries, throat and
mouth ulcers, parotid gland enlargement, Mallory-Weiss tears, and/or
esophageal rupture can be seen. Cardiac and skeletal myopathies can
occur secondary to abuse of syrup of ipecac. Laxative dependence and
rectal prolapse from recurrent diarrhea may develop.
Laboratory testing Electrolyte abnormalities in BN may include the following:
•Low magnesium
• Low potassium
• Low sodium
• Low chloride
• Elevated phosphate
• Metabolic alkalosis and elevated salivary amylase with vomiting
• Metabolic acidosis with laxative or diuretic use
Cardiomyopathy may be present on echocardiogram in cases of
chronic ipecac ingestion to induce vomiting.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Gibson D, Workman C, Mehler PS: Medical complications of anorexia nervosa and bulimia nervosa.Psy-
chiatr Clin North Am 42(2):263–274, 2019
Hay P: Current approach to eating disorders: a clinical update. Intern Med J 50(1):24–29, 2020
Hirst RB, Beard CL, Colby KA, et al: Anorexia nervosa and bulimia nervosa: a meta-analysis of executive
functioning.Neurosci Biobehav Rev 83:678–690, 2017
Strumia R: Dermatologic signs in patients with eating disorders. Am J Clin Dermatol 6:165–173, 2005
Treasure J, Claudino AM, Zucker N: Eating disorders. Lancet 375:583–593, 2010
Wade TD: Recent research on bulimia nervosa.Psychiatr Clin North Am 42(1):21–32, 2019
https://t.me/med1917
355 Diseases and Conditions
Catatonia
Clinical findings The DSM-5 classification of catatonia includes the following two cate-
gories:
1. Catatonia associated with another mental disorder (neurodevelop-
mental, psychotic, bipolar, depressive, or other disorder)
2. Catatonic disorder due to another medical condition
In addition, an unspecified catatonia and two other schizophrenia
spectrum categories are listed.
The clinical presentation of catatonia is dominated by at least three of
the following symptoms:
• Stupor—no psychomotor activity and/or not actively relating to
the environment
• Catalepsy—a limb remains in whatever position it is placed
• Waxy flexibility—resistance of a limb to movement by examiner
• Mutism—no or little verbal response (item is excluded if patient is
aphasic)
• Negativism—no response or opposition to instructions or verbal
stimuli
• Posturing—spontaneous, active maintenance of a posture against
gravity
• Mannerism—odd caricature of a normal action
• Stereotypy—frequent, repetitive, non-goal-directed movement
• Agitation that is not influenced by external stimuli
•Grimacing
• Echolalia—mimicking another’s speech
• Echopraxia—mimicking another’s movements
An instrument such as the Bush-Francis Catatonia Rating Scale can be
helpful in screening for catatonia and determining its severity. A care
-
ful history may implicate medications or drugs in the disorder.
A wide range of medical conditions have been found to underlie cat-
atonic disorder, including neurological conditions such as encephalitis,
non-convulsive status epilepticus, Parkinson’s disease, cerebrovascu
-
lar disease, head trauma, and brain neoplasm; metabolic conditions,
such as thyroid disease, renal failure, hepatic encephalopathy, keto-
acidosis, and electrolyte derangements; intoxication with substances
such as Ecstasy, amphetamines, and phencyclidine; and withdrawal
from benzodiazepines, alcohol, or other sedative-hypnotics. Of note,
COVID-19 infection has been associated with catatonic disorder with
underlying anti-NMDAR encephalitis.
Laboratory testing Recommended tests to exclude medical or substance-related causes of
catatonia include the following:
• CBC with differential and platelets
•CMP
•Creatine kinase
• Thyroid function tests
•Urinalysis
• Urine toxicology screen
• Brain imaging: MRI or CT
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356 Laboratory Medicine in Psychiatry and Behavioral Science
Catatonia (continued)
Laboratory testing
(continued)
• EEG (to exclude non-convulsive status epilepticus)
• CSF studies (if no evidence of increased intracranial pressure)
In addition, a fibrin D-dimer level is recommended to determine the
risk of venous thromboembolism. A greatly elevated
D-dimer level
may be found in immobile patients.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Brar K, Kaushik SS, Lippmann S: Catatonia update. Prim Care Companion CNS Disord 19(5):16br02023,
2017
Bush G, Fink M, Petrides G, et al: Catatonia, I: rating scale and standardized examination. Acta Psychiatr
Scand 93(2):129–136, 1996
Francis A: Catatonia: diagnosis, classification and treatment. Curr Psychiatry Rep 12:180–185, 2010
Rajan S, Kaas B, Moukheiber E: Movement disorders emergencies.Semin Neurol 39(1):125–136, 2019
Vasilevska V, Guest PC, Bernstein HG, et al: Molecular mimicry of NMDA receptors may contribute to
neuropsychiatric symptoms in severe COVID-19 cases. J Neuroinflammation 18(1):245, 2021
https://t.me/med1917
357 Diseases and Conditions
Central pontine myelinolysis (CPM)
Clinical findings CPM is a potentially fatal neurological condition most often caused by
overly rapid correction of hyponatremia, with shifts of small molecules
and fluid in the brain that result in the destruction of myelin. Although
the pons is particularly susceptible to injury, other areas of the brain
can be affected, resulting in extrapontine myelinolysis (EPM). The two
conditions are now subsumed under the term osmotic demyelination
syndrome (ODS).
Patients with chronic hyponatremia (>48 hours) are at higher risk of
ODS. Other populations at risk include those with alcohol use disor
-
der, malnutrition, history of liver transplant, eating disorders, serious
burns, or HIV/AIDS; elderly patients; and those undergoing renal di
-
alysis. Of interest to psychiatrists, severe hyponatremia can develop
when the club drug Ecstasy is consumed along with excessive free wa
-
ter intake, placing patients at risk of ODS with sodium correction.
Symptoms of ODS begin 2–3 days after hyponatremia is corrected,
with additional symptoms arising over the following 1–2 weeks, the
pattern partly dependent on the location of demyelination:
• General symptoms of ODS include encephalopathy, seizure, cata-
tonia, mutism, apathy, lethargy, primitive reflexes, cognitive dys-
function, and psychiatric symptoms such as depression, mania,
disinhibition, and emotional lability.
• EPM is characterized by movement disorders including the aki-
netic-rigid syndromes, tremor, dystonia, chorea, choreoathetosis,
myoclonus, opsoclonus, gait disorders, and ataxia.
• CPM is characterized by cranial nerve abnormalities (dysarthria,
dysphagia, pupillary and ocular motility disorders), delirium,
apathy, cognitive dysfunction, loss of reflexes, and the locked-in
syndrome (in which the patient is awake and aware but is unable
to move, show facial expression, speak, or communicate except by
eye movements).
With timely and effective intervention, morbidity and mortality of ODS
have improved, but one-third to one-half of patients will
still require
some at-home care, be fully dependent, or die from the condition. It is
also possible for affected patients to develop late-appearing symptoms
such as behavioral problems, intellectual impairment, or movement
disorders such as parkinsonism.
Predictors of poor outcome include
prior liver transplant as well as severe
hyponatremia (<114 mEq/L),
hypokalemia, and severe lack of awareness on presentation.
Laboratory testing Workup for the cause of hyponatremia (serum sodium <135 mEq/L)
is discussed in the Hyponatremia entry.
When ODS is suspected, brain MRI should be obtained as early as pos-
sible. Head CT could be used if brain MRI is not available, although
CT is significantly less sensitive. MRI with diffusion-weighted imag-
ing is most likely to show early changes. T2-weighted images show
hyperintense (bright) areas where demyelination has occurred.
Other laboratory tests include the following:
• Serum sodium performed serially during correction
• Serum potassium
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358 Laboratory Medicine in Psychiatry and Behavioral Science
Laboratory testing
(continued)
•LFTs
• Nutritional evaluation (serum vitamin B
12
, MMA, folic acid, and
phosphate)
Central pontine myelinolysis (CPM) (continued)
Filippatos TD, Makri A, Elisaf MS, Liamis G: Hyponatremia in the elderly: challenges and solutions.Clin
Interv Aging 12:1957–1965, 2017
Hoorn EJ, Zietse R: Diagnosis and treatment of hyponatremia: compilation of the guidelines.J Am Soc
Nephrol 28(5):1340–1349, 2017
Lambeck J, Hieber M, Drebing A, Niesen WD: Central pontine myelinosis and osmotic demyelination
syndrome. Dtsch Arztebl Int 116(35–36):600–606, 2019
Vladimirov T, Dreikorn M, Stahl K: Central pontine myelinolysis in a patient with bulimia: case report
and literature review. Clin Neurol Neurosurg 192:105722, 2020
https://t.me/med1917
359 Diseases and Conditions
Chronic fatigue syndrome (CFS)
Clinical findings CFS, also known as myalgic encephalomyelitis/chronic fatigue syn-
drome (ME/CFS), is characterized by disabling fatigue lasting 6 months
or longer, nonrestorative sleep, post-exertional malaise, and either cog
-
nitive dysfunction or orthostatic intolerance. Fatigue results in a sub-
stantial reduction or impairment in the ability to engage in premorbid
levels of occupational, educational, social, or personal activities. Fatigue
may be profound and is not alleviated with rest. Currently, the condition
is considered a complex, multisystem neuroimmune disease.
Other symptoms associated with CFS but not required for the diagno-
sis include sore throat, tender lymph nodes, myalgia, arthralgia, head-
ache, paresthesias, hypersensitivity to sensory stimuli, and other
symptoms of dysautonomia (nausea, palpitations, cold hands and feet,
irritable bladder, and irritable bowel).
Certain medical conditions exclude the diagnosis of CFS, including
untreated sleep apnea, cancer, hypothyroidism, major psychiatric dis
-
order (schizophrenia spectrum disorder, bipolar disorder, eating dis-
order, or substance abuse), and severe obesity. Other conditions that
do not exclude the diagnosis include fibromyalgia, somatic symptom
disorders, treated hypothyroidism, and slightly elevated antinuclear
antibodies. About one-third of individuals diagnosed with CFS also
meet criteria for fibromyalgia.
Despite substantial research effort, the cause of CFS is still unknown.
Evidence of increased intracranial pressure, reduced cerebral blood
flow, and endothelial cell dysfunction has been found, but a generally
accepted unifying hypothesis has not been advanced. Moreover,
although Epstein-Barr virus (EBV) and other pathogens have been
implicated in CFS, it appears that the condition is not caused by a sin-
gle infectious agent. Instead, it is thought that severe infections with
pathogens such as EBV, Ross River virus, or Coxiella burnetti may con-
tribute to later development of CFS in a subset of cases. The same may
be true for the post-acute sequelae syndrome of COVID-19 infection
(“long-haul” COVID-19).
Laboratory testing The basic workup for CFS includes the following tests:
• CBC with differential
•ESR
• CMP (with LFTs)
• Serum globulin
• Phosphorus
• TSH (ultra-sensitive)
•Urinalysis
In selected cases, the following tests may be indicated:
• Estradiol or testosterone level
• Echocardiogram (to determine ejection fraction)
• Polysomnography
• Maintenance of wakefulness test (to exclude narcolepsy)
• Arterial blood gases
• Lyme disease testing
• Rheumatoid factor, antinuclear antibody
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360 Laboratory Medicine in Psychiatry and Behavioral Science
Chronic fatigue syndrome (CFS) (continued)
Carod-Artal FJ: Post-COVID-19 syndrome: epidemiology, diagnostic criteria and pathogenic mecha-
nisms involved. Rev Neurol 72(11):384–396, 2021
Lim EJ, Son CG: Review of case definitions for myalgic encephalomyelitis/chronic fatigue syndrome
(ME/CFS).J Transl Med 18(1):289, 2020
Natelson BH: Myalgic Encephalomyelitis/Chronic fatigue syndrome and fibromyalgia: definitions, sim-
ilarities, and differences.Clin Ther 41(4):612–618, 2019
Sandler CX, Lloyd AR: Chronic fatigue syndrome: progress and possibilities. Med J Aust 212(9):428–433,
2020
Tleyjeh IM, Saddik B, Ramakrishnan RK, et al: Long term predictors of breathlessness, exercise intoler-
ance, chronic fatigue and well-being in hospitalized patients with COVID-19: a cohort study with
4 months median follow-up.J Infect Public Health 15(1):21–28, 2022
Wirth KJ, Scheibenbogen C, Paul F: An attempt to explain the neurological symptoms of myalgic enceph-
alomyelitis/chronic fatigue syndrome. J Transl Med 19(1):471, 2021
https://t.me/med1917
361 Diseases and Conditions
Chronic traumatic encephalopathy (CTE)
Clinical findings CTE is a neurodegenerative disease affecting those who have experi-
enced repetitive head trauma such as military personnel; football,
hockey and soccer players; boxers; and survivors of domestic abuse.
The cumulative head trauma burden must be substantial, even though
individual impacts may not have been associated with signs of concus
-
sion. CTE is characterized by cognitive, neuropsychiatric, and motor
impairments that are progressive, ultimately leading to functional de
-
pendence and dementia. Symptoms typically begin after a clear period
of stable functioning after head injury exposure ends. A definitive di
-
agnosis of CTE requires confirmation by neuropathological examina-
tion showing a
particular pattern of hyperphosphorylated tau
deposition in neurofibrillary tangles.
Core clinical features include the following:
• Cognitive deficits are common in CTE, mostly affecting episodic
memory, executive function, and attention.
• Language, visuospatial function, and other domains may also be
involved.
• Neurobehavioral dysregulation is also common and may be se-
vere, including explosiveness, impulsivity, rage, violent outbursts,
severe irritability, or emotional lability.
• Condition progressively worsens over a period of at least 1 year in
the absence of continued exposure to head injury.
Other signs and symptoms that are not included in the core
criteria
but
can support the diagnosis are as follows:
• Psychiatric: anxiety, pervasive worries, excessive fears, agitation,
obsessive-compulsive behavior, depression, apathy, anhedonia,
hopelessness, suicidal ideation and behavior, suspicion, delusional
jealousy, and paranoid ideation.
• Motor: gait and balance problems, dysarthria, parkinsonism (bra-
dykinesia, rigidity, resting tremor, and parkinsonian gait).
Laboratory testing A spectrum of pathology is seen, reflecting the progression of hyper-
phosphorylated tau deposition across time, with accompanying axo-
nal disruption and loss. What begins as focal perivascular tangle
formation in the frontal neocortex progresses to severe tauopathy in
-
volving widespread brain regions (including the medial temporal
lobe), enabling the staging of pathology from I to IV.
Clinical-pathological correlation has shown that early disease (patho-
logical stage I) is associated with headache and problems with atten-
tion and concentration. In pathological stage
II, additional symptoms
of depression, explosivity,
and short-term memory loss are seen. In
stage III, executive dysfunction and cognitive impairment are noted.
In stage IV, dementia with word-finding difficulty and aggression are
seen.
In severe CTE, other pathological changes are seen, including accumu-
lation of amyloid-β, α-synuclein, and TDP-43 (transactive response
DNA binding protein 43 kDa). Common comorbid pathological diag-
noses include motor neuron disease, Alzheimer’s disease, frontotem-
poral lobar degeneration, and Lewy body disease.
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