Criteria
The presence of one or more non-bizarre delusions that persist for at least one month.
The delusions are not due to the direct physiological effects of a substance or a general medical condition.
Somatic type. The person’s conviction that there is an infestation on or on the skin, internal parasite (contrary to all medical evidence).
Differential Diagnosis
The diagnosis of Delusional Disorder is made only when the delusion is not due to the direct physiological effects of a substance or a general medical condition. A delirium, a dementia, and Psychotic Disorder Due to a General Medical Condition may present with symptoms that suggest Delusional Disorder.
For example, simple persecutory delusions (e.g., "someone comes into my room at night and steals my clothes") in the early phase of Dementia of the Alzheimer's Type would be diagnosed as Dementia of the Alzheimer's Type, With Delusions.
A Substance-Induced Psychotic Disorder, especially due to stimulants such as amphetamines or cocaine, cross-sectionally may be identical in symptomatology to Delusional Disorder, but can usually be distinguished by the chronological relationship of substance use to the onset and remission of the delusional beliefs.
Diagnostic criteria for 297.1 Delusional Disorder
A. Nonbizarre delusions (i.e., involving situations that occur in real life, such as being followed, poisoned, infected, loved at a distance, or deceived by spouse or lover, or having a disease) of at least 1 month's duration.
B. Criterion A for Schizophrenia has never been met. Note: Tactile and olfactory hallucinations may be present in Delusional Disorder if they are related to the delusional theme.
C. Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired and behavior is not obviously odd or bizarre.
D. If mood episodes have occurred concurrently with delusions, their total duration has been brief relative to the duration of the delusional periods.
E. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.
Delusional parasitosis
3 kinds - primary, secondary, organic
What they warn about:
Characteristics they say are universal but dismiss without evaluation or observation.
Compulsively gather evidence to present to health professionals for help
Injure themselves to extract objects
Bring scabs or debris excoriated from the skin as evidence for inspection
Refers to cutaneous symptoms like biting, crawling, or stinging.
Commonly seek attention if dermatologist or doctors and different therapies for a cure
Experiencing psychological distress
What the doctors fail to understand or do:
It’s an uncommon condition. Very uncommon.
They should be referred to psychiatric only after all other medical possibilities ruled out with regular physicians, specialists, and are showing psychiatric signs that meet the criteria.
Doctors should never be allowed to lie to patients.
CT or MRI may be reserved for patients with an atypical clinical presentation, neurological findings, or an unusual/treatment-refractory course. A normal baseline CT or MRI scan, however, is reassuring and can help patients and families accept that medical and neurological causes of illness have been excluded.
Endocrine diseases. Endocrine diseases are the prototype for systemic illnesses that affect the brain and lead to a wide variety of neuropsychiatric symptoms.
Thyroid disease in the form of hyperthyroidism or hypothyroidism (myxedema madness) can be associated with psychosis.
Steroid-producing tumors, located in either the adrenal gland (Cushing disease) or other tissues (eg, ectopic Cushing syndrome from small-cell lung cancer) need to be considered, particularly in cases of refractory psychosis.
Insulinomas can present with an array of psychiatric symptoms, including confusion and bizarre behavior that can be falsely attributed to psychiatric illness.
A pheochromocytoma is yet another rare hormone-producing tumor that characteristically produces episodic anxiety states but can present with psychosis.
Metabolic diseases. Among the metabolic disorders, only acute intermittent porphyria (AIP) is sufficiently common to be routinely considered in patients with psychosis, particularly if abdominal complaints (colicky pain, severe constipation) and peripheral motor neuropathy are present.
AIP is an autosomal dominant disease of heme synthesis that results from defects in the enzyme porphobilinogen deaminase (PBGD). These defects could result in an accumulation of the porphyrin precursors, porphobilinogen (PBG) and aminolevulinic acid (ALA). A diagnosis of AIP is therefore suggested by an excess of ALA and PBG in urine and a concomitant decrease in PBGD enzyme activity in erythrocytes. The course of AIP is episodic, and patients are well between episodes. Fasting, alcohol, and a host of porphyrogenic medications can trigger episodes.
Tay-Sachs disease (GM2 gangliosidosis type 1) and Niemann-Pick disease type C are rare storage disorders that have adult-onset variants. Psychosis is one of the possible symptoms.
Autoimmune. Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease for which 2 CNS symptoms, psychosis and seizures, have long been recognized as diagnostic criteria by the American College of Rheumatology.
Psychosis has been well documented to occur in a significant minority of patients as a result of the immune disease itself, unrelated to medical treatment. For example, in a cohort study of 520 consecutive SLE patients, Appenzeller and colleagues found that 11% of patients with SLE had psychosis secondary to brain involvement. Moreover, psychosis correlated with markers of SLE disease activity. By contrast, psychosis as a result of corticosteroid treatment was diagnosed in only 5% of patients, and psychosis was thought to be from a primary psychiatric disorder in fewer than 1% of cases.
Other autoimmune disorders to be considered include Hashimoto encephalopathy and paraneoplastic syndromes. Hashimoto encephalopathy is associated with autoimmune thyroiditis and recurrent episodes of psychosis. It is exquisitely corticosteroid-responsive, and prompt treatment leads to rapid recovery.
Paraneoplastic limbic encephalitis (PLE) can cause neuropsychiatric symptoms that are the result of autoantibodies directed toward neuronal intracellular or cell membrane antigens.
Although PLE is most commonly associated with small-cell lung cancer, many other tumors have been implicated. A young woman who presents with psychosis that progresses to seizures, autonomic instability, and unresponsiveness should have a workup for ovarian tumors because she might have encephalitis associated with N-methyl d-aspartate (NMDA) receptor antibodies. Considering PLE in progressive or poorly responsive neuropsychiatric syndromes is critical so that a tumor search is initiated.
Infections. Immigrant populations or travelers can present with diseases associated with psychosis that would be considered uncommon in the United States (eg, cerebral malaria, toxoplasmosis, neurocysticercosis, sleeping sickness).
In addition to the patient’s geographic locale and travel history, immune status can help identify likely infectious agents.
HIV infection and neurosyphilis are treatable diseases that affect the brain. They can present with psychosis and should specifically be considered in all patients with psychosis.
In contrast to neurosyphilis, the link between chronic psychosis and another spirochetal disease, neuroborreliosis, is controversial, although it has been linked to acute psychosis in a case report. Be mindful that patients with encephalitis can inadvertently present to a psychiatric service if psychiatric symptoms dominate the clinical picture.
Among the viral infections, herpes simplex encephalitis is the most urgent to consider because any delay in administering acyclovir worsens prognosis.
Narcolepsy. Narcolepsy is characterized by the tetrad of excessive daytime sleepiness, cataplexy, sleep paralysis, and hypnagogic hallucinations (ie, vivid auditory or visual illusions that occur when falling asleep). However, the full tetrad is present in only 10% of patients. In some patients, prominent psychosis-like experiences occur throughout the day and overshadow other symptoms of narcolepsy that can lead to a mistaken diagnosis of schizophrenia.
In one small series of 69 patients in a state hospital, 7% of patients with a diagnosis of schizophrenia were found to have narcolepsy. The treatment of narcolepsy with stimulants can further complicate the picture because psychosis can result from the medical treatment. The diagnosis of narcolepsy requires a nocturnal sleep study followed by a multiple sleep latency test (MSLT) to identify reduced daytime sleep latency and sleep onset rapid eye movement (SOREM) periods. Human leukocyte antigen testing and cerebrospinal fluid levels of hypocretin-1 can further assist in making the correct diagnosis.
Seizures. The link between seizures, particularly temporal lobe epilepsy, and psychosis is well established. Epidemiological studies have shown a higher rate of schizophrenia in patients with epilepsy and vice versa. Psychosis in the setting of seizures can occur during the ictal, postictal, and interictal phases. Ictal psychosis can occur in complex partial or absence status epilepticus. Postictal psychosis emerges close to the seizure and can last several days or weeks, rarely morphing into a chronic psychosis. Interictal psychosis typically emerges after a decade of poorly treated or poorly responsive epilepsy and is characterized by intense dysphoric affect in addition to psychosis. Earlier development of interictal psychosis suggests individual vulnerability as opposed to epilepsy-related damage.
Confusion, episodic violence, and catatonia are clinical symptoms that should raise suspicion for seizures. If a seizure or epilepsy is suspected, the diagnosis needs to be pursued appropriately. A normal, routine interictal EEG is insufficient to exclude epilepsy. Serial EEGs and optimal lead placement improve the chances of making a diagnosis of epilepsy. Frontal lobe seizures, in particular, can be very difficult to diagnose. A high index of suspicion based on history (abrupt onset and cessation of bizarre motor automatisms and vocalizations but little if any postictal confusion) combined with EEG monitoring and alternative electrode placement (eg, pharyngeal leads) can succeed in making this diagnosis.
Space-occupying lesions. Primary or secondary brain tumors can cause psychosis as their first manifestation and should be considered in elderly patients, particularly if there is a persistent headache or other neurological signs, including seizures. However, in the case of “silent” indolent-growing tumors, such as frontal meningiomas, neurological examination findings are often normal. Tumor histology is not as important as rapidity of growth and location for the clinical presentation. Temporal lobe location is thought to increase the likelihood of psychosis, although it must be stressed that no lesion location in the brain reliably produces psychosis. Causal attribution of psychosis to incidental neuroimaging findings (eg, cysts or vascular malformations in the temporal lobes) is therefore often unclear. Conditions that increase intracranial pressure, such as normal pressure hydrocephalus, have been associated with psychosis as well.
Strokes. Rarely, psychosis can be the presenting symptom of a stroke. In some cases, stroke-related seizure activity is responsible for the psychosis. The sudden onset of complex visual hallucinations should lead to consideration of 2 lesion-related conditions: peduncular hallucinosis caused by focal midbrain (peduncular) lesions and the Charles Bonnet syndrome following occipital infarction. However, in both conditions, causes other than a stroke are possible.
Head injury. A history of head injury is a risk factor for the development of a chronic psychotic syndrome that can be clinically indistinguishable from schizophrenia. Head injury–related psychosis is typically a mostly paranoid-hallucinatory syndrome that develops insidiously several years after injury. Patients experiencing psychosis can appear blunted and withdrawn, and it is critical not to ascribe apparent negative symptoms to brain damage but to consider active psychosis. The severity of head injury (as judged by the duration of loss of consciousness) and a family history of psychosis are 2 variables associated with the emergence of psychosis following head injury.
Demyelinating diseases. Diseases that disrupt the integrity of white matter tracts in the brain can lead to psychosis, likely to be caused by the functional disconnectivity of critical brain regions. Demyelinating diseases would be expected to be associated with psychosis if (1) the disease affects the brain as opposed to the brain stem and spinal cord, and (2) the “right” brain regions are disconnected.
Multiple sclerosis, the most common demyelinating disease, is associated with psychosis more often than can be expected by chance, although the rate of psychosis is low. Inherited leukodystrophies, such as metachromatic leukodystrophy (MLD) and adrenoleukodystrophy (ALD), on the other hand, are associated with a high prevalence of neuropsychiatric symptoms, including psychosis. MLD in particular is associated with a very high rate of psychosis, perhaps as high as 50%.66MLD is an autosomal recessive disorder caused by a deficiency in the lysosomal enzyme, arylsulfatase A.
ALD is an X-linked disorder in which very-long-chain fatty acids accumulate because of defective peroxisomal oxidation. While inherited leukodystrophies are typically diagnosed in childhood because of their aggressive clinical course with systemic and neurological symptoms, adult-onset cases can present with a predominantly psychiatric picture. The diagnosis of a demyelinating disorder is suggested by abnormal findings on MRI scans. Clinical red flags for inherited leukodystrophies include progressive cognitive decline, other neurological findings (eg, seizures or a neuropathy), or other systemic findings (eg, adrenal insufficiency in patients with ALD).
Basal ganglia disorders. Rare, inherited basal ganglia disorders associated with psychosis include Wilson disease, Huntington disease, and Fahr disease. Wilson disease is a disorder of copper metabolism that leads to copper deposits in the liver and the lenticular nucleus of the brain (hence the term “hepatolenticular” degeneration). Since early diagnosis and treatment can prevent irreversible end-organ damage, screening with 24-hour urinary copper and serum ceruloplasmin levels should be considered in psychotic patients, particularly if patients show evidence of liver abnormalities. Kayser-Fleischer rings of the cornea as detected by slitlamp examination are not always present in neuropsychiatric Wilson disease.
The diagnosis of Huntington disease, an autosomal dominant disorder, is usually not difficult because most patients will have a family history. Psychosis can precede the motor symptoms of Huntington disease and delay its recognition. While Huntington disease will eventually declare itself clinically, a definite diagnosis can be made earlier with genetic testing.
Fahr disease is characterized by bilateral basal ganglia calcifications and neuropsychiatric symptoms, including psychosis. However, basal ganglia calcification can also be an incidental CT finding of unclear significance.
Hallucinations, particularly visual hallucinations, are a common problem associated with Parkinson disease. Their etiology is likely to be multifactorial and includes disease severity and dementia as well as treatment with levodopa.
Nutritional deficiencies. Vitamin B12 deficiency is easily correctable and should be specifically excluded in all patients. Psychosis from vitamin B12 deficiency can predate anemia and the typical spinal symptoms. Thiamin deficiency is easily correctable as well; therefore, thiamin must be given in the appropriate setting (ie, alcoholism). Niacin deficiency (pellagra) is rare in the United States; symptoms include psychosis in addition to diarrhea, dermatitis, and stomatitis/glossitis.
The detection of environmental toxin poisoning requires a high index of suspicion. Toxins to consider include carbon monoxide; organophosphates; and heavy metals, particularly arsenic, manganese, mercury, and thallium.
Other Conditions that Can be Similar
Dehydration
Pneumonia, COPD, and acute asthma exacerbations
Many treatable issues!
Medications:
Important offenders
Corticosteroids
Stimulants
Dopaminergic drugs (eg, L-dopa, amantadine)
Interferon
Anticholinergics
Other
Cardiovascular drugs: antiarrhythmics, digitalis
Anesthetics
Antimalarial drugs: mefloquine
Antituberculous drugs: p-cycloserine, ethambutol, isoniazid
Antibiotics: ciprofioxacin
Antivirals: HIV medications (eg, efavirenz at high plasma levels), acyclovir
Anticonvulsants (high doses)
Antineoplastics (especially ifosfamide)
Sympathomimetics (including over-the-counter preparations and ephedra-containing diet supplements)
Pain medications: opioids (especially meperidine, pentazocine), indomethacin
Miscellaneous: bacloten, caffeine, disulfiram, cyclosporine
Delusional parasitosis
We all woke up one day and said “I think I’ll be fucking nuts today.”
I think I’ll rip apart my beautiful skin.
Wait, I’m not crazy enough. I think I’ll tell someone else I see stuff in my skin.
Oh, and it burns, too.
Wait - they don’t believe me. They want proof.
I guess I’ll grab them and put them in something to show proof if needed.
After all, if you go to the ER for a spider or snake or bug bite, what are you asked?
“What kind was it? Did you happen to kill it and bring it?”
Well, I wonder why. ..
I google that I feel something biting me.
“See your physician immediately.”
It’s a weekend - go to the ER.
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