Differentials

Obsessive-compulsive disorder (OCD)

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SIGNS / SYMPTOMS

Onset is typically gradual over several months or years, although sudden onset of OCD has been reported. Age of onset is typically late adolescence to early twenties.[12]

Symptoms normally wax and wane with moderate changes of severity.

Often comorbid with general anxiety disorder.

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Clinical diagnosis.

Anorexia nervosa

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Onset is insidious and usually in the pubertal or postpubertal period.

More frequent in females than males.

Food restriction is due to fear of weight gain or body image distortion. Weight restoration is slow and relapse is common with a high mortality rate.

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Clinical diagnosis.

Laboratory tests, including CBC, electrolyte panel, thyroid function test, and liver function tests, are useful in the assessment of illness severity. Other tests include an ECG.

Avoidant-restrictive food intake disorder (ARFID)

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Onset can be gradual or acute.

Motivations contributing to food avoidance and restriction are due to the sensory properties of food and low appetite.[72]

Weight restoration is slow.

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Clinical diagnosis.

Tourette syndrome

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Gradual onset. Waxing and waning of tics in terms of frequency, severity, and distribution are not as drastic as seen in PANS.

Often co-occurs with attention deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), anxiety, mood disorder, impulse control disorder, and learning disorder. These comorbidities usually appear before the onset of tics.[73]

Age-related decline in severity of tics, ADHD, and OCD during adolescence.[74]

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Clinical diagnosis.

Tic disorders

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Concurrent severe neuropsychiatric symptoms are rarely present in tic disorder.[75]

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Clinical diagnosis.

Bipolar disorder

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Rare in prepubertal children.

Patients present with mood symptoms, and often with history of major or minor depressive episode.[76]

Up to 20% of bipolar patients have co-occurring obsessive-compulsive disorder (OCD) in their lifetime.[77][78]

High prevalence of hoarding/saving and multiple anxiety disorders. Generalized anxiety disorder and separation anxiety disorder are observed when OCD and bipolar disorder are comorbid.[79]

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Clinical diagnosis.

Sydenham chorea

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One of the major clinical manifestations of acute rheumatic fever.

Psychiatric symptoms may precede chorea by up to 2 weeks.

Frank chorea is present.

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Clinical diagnosis.

Autoimmune encephalitis

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Common features include an altered level of consciousness, confusion, new-onset memory and cognitive problems, and seizures.[67] Other features include rash and meningismus.

Patients typically present with a subacute onset of psychiatric symptoms, although acute presentations have been described.[67]

Hashimoto encephalitis may present with waxing and waning psychiatric symptoms (as opposed to relapsing-remitting as seen in PANS) and sleep disturbance before the development of seizures.[80]

Cognitive changes are typically more severe than in PANS.

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Lumbar puncture: positive antibodies (e.g., N-methyl-d-aspartate receptor [NMDA R] antibodies).[67]

MRI brain: may be normal or show hyperintense lesions (T2 and fluid-attenuated inversion recovery [FLAIR] sequences), increased diffusion on diffusion-weighted imaging (DWI) indicating edema, contrast enhancement on T1 post-contrast sequences indicating blood-brain barrier breakdown.

Electroencephalography (EEG): evidence of global dysfunction or seizures.

Systemic lupus erythematosus

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Psychiatric symptoms such as obsessive-compulsive disorder, if present, do not typically present abruptly.[81][82]

Signs may include malar (butterfly) rash, photosensitivity rash, and discoid rash.

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Antinuclear antibodies, double-stranded (ds) DNA, Smith antigen: elevated.

Anti-histone antibody: may be present in drug-induced lupus or neuropsychiatric lupus.

Sjogren syndrome

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Signs and symptoms include fatigue, dry eyes, dry mouth, autonomic nervous symptom dysfunction (altered vascular tone, esophageal or gastrointestinal dysmotility, cardiac rhythm abnormalities), neuropathic symptoms (burning, tingling, numbness), and proximal muscle weakness.[83]

Psychiatric symptoms such as obsessive-compulsive disorder, if present, do not typically present abruptly.

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Autoantibodies to: 60 kD (SS-A) Ro and La (SS-B).

Lip biopsy: salivary gland inflammation.

Schirmer test or rose bengal test: positive.

Electrical status epilepticus in sleep

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Global regression (e.g., loss of language and temporospatial skills). Motor deficits, resulting in ataxia, dystonia, and dyspraxia. Seizures are very common.[84]

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Marked activation of epileptiform activity during non-rapid eye movement (NREM) sleep to produce an electroencephalogram pattern of near-continuous spike-wave discharges.

Wilson disease

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Clinical manifestations are predominantly hepatic, neurologic, and psychiatric, with many patients having a combination of symptoms.

Kayser-Fleischer rings (gold-brown corneal pigments representing copper deposition) are seen in approximately 98% of patients with neurologic Wilson disease.

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Liver function tests: abnormal.

Serum ceruloplasmin level: low (<20 mg/dL).

24-hour urinary copper: >100 micrograms (>40 micrograms may suggest Wilson disease).

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