Herpes simplex encephalitis
Herpes simplex virus is thought to be one of the most common single causes of severe sporadic encephalitis. Herpes simplex virus has a predilection for the temporolimbic areas. With herpes simplex encephalitis, a prodrome of 1 to 7 days of upper respiratory tract infection is followed by headache, fever, seizures, bizarre behavior, psychosis, and fluctuating mental status. Identification is crucial and early treatment is vital.
Accumulating evidence suggests that the nervous system is affected in the early stage of HIV infection. This may lead to presentation of a patient with cognitive and behavioral symptoms even before any physical manifestations of the disease become evident.
The patient may present with attention/concentration deficits, memory problems, apathy, social withdrawal, and psychomotor slowing,5 a picture that can often be mistaken for depression. Therefore, HIV infection should be suspected in patients presenting with these symptoms who have not had a previous psychiatric history and who are part of a high-risk population. Even in patients with an established diagnosis of HIV/AIDS, any new onset of behavioral and psychiatric disturbance could be secondary to other opportunistic infections, such as with Toxoplasma gondii, or to neoplasms. Antiretroviral medications can cause a wide range of neuropsychiatric adverse effects as well.
This category of dementia is not as uncommon as once thought. Onset is usually between the ages of 45 and 70 years. The most common manifestation is dysfunction of social and personal conduct (frontal lobe signs). Patients usually present with disinhibited behavior, impulsivity, and neglect of personal hygiene, which may lead to inappropriate social behavior such as swearing in public, inappropriate sexual behavior, shoplifting, or impulsive buying. In addition, patients may engage in overeating. Utilization behavior is also common, leading to a tendency to touch things and use objects without a purpose. Profound lack of insight is usually the rule rather than the exception. A combination of these symptoms can easily mislead a clinician into diagnosing a functional psychiatric disorder.6
Onset of Huntington disease usually starts in the 40s or 50s. Psychiatric symptoms may be present for years before neurological symptoms become apparent. Change in personality, paranoia, ideas of reference, depression, and anxiety are common.1 A family history is often present. Laboratory genetic studies can confirm the presence and number of CAG repeats on chromosome 4.
Various endocrine disorders can initially present with psychiatric symptoms.1 Hypothyroidism can lead to a clinical presentation similar to that of depression, including apathy, psychomotor slowing, memory problems, and anxiety.
Hyperthyroidism can present with significant anxiety, insomnia, agitation, hyperactivity and, in rare cases, psychosis. Adrenal as well as para- thyroid disorders can present with a variety of psychiatric and behavioral symptoms. Depression can often be the sole manifestation of pancreatic tumors. Consider pancreatic cancer in elderly patients with back pain and new-onset depression.
Systemic lupus erythematosus
In patients with systemic lupus erythematosus, neuropsychiatric manifestations can occasionally present in the early stage of the disease, before the involvement of other systems. Neuropsychiatric symptoms can also coincide with relapses and remissions of the disease itself. Confusion, depression, psychosis, and anxiety have all been described as neuropsychiatric symptoms.
Acute intermittent porphyria
This autosomal dominant disorder should be suspected when a young person, usually in the third decade of life, presents with acute onset of psychiatric symptoms along with medical symptoms characterized by acute abdominal pain, nausea, vomiting, constipation, headaches, and seizures; peripheral neuropathy is also common. Psychiatric symptoms are present in 25% to 75% of cases and range from acute anxiety and depression to severe emotional lability and even psychosis. Some of the precipitants of an acute crisis are inadequate nutrition, endocrine factors, alcohol(Drug information on alcohol) use, infections, and adverse effects of some medications.1
Wernicke encephalopathy caused by thiamine(Drug information on thiamine) (vitamin B1) deficiency should be suspected in a patient with chronic alcoholism who presents with acute onset of confusion along with the neurological triad of nystagmus, ataxia, and ophthalmoplegia, although all patients may not present with the complete triad. This syndrome may persist as Korsakoff syndrome with amnesia.
Vitamin B12 deficiency often presents with depression, psychosis, dementia, and occasional delirium, even before the diagnosis of megaloblastic anemia or other neurological symptoms such as neuropathy. Vitamin D levels should be checked in a patient with a diagnosis of somatoform disorder and diffuse aches and pains, especially bone pain.
Adverse effects of pharmacotherapy
In this era of multiple medication use, the role of medication adverse effects in mental status changes should obviously be suspected. The key is taking a very careful and detailed medical history and obtaining collateral information. The list of medications that can cause mental status changes is extensive and widely available in the medical literature. The effects of over-the-counter medications or herbal remedies, which may contribute to mental status changes are often ignored. There have been clinical cases of ephedra-induced mania and psychosis, dextromethorphan(Drug information on dextromethorphan)-induced psychosis, and delirium induced by chronic salicylate use.
This article illustrates some general concepts that may help a clinician differentiate secondary psychiatric manifestations of underlying neurological and medical disorders from primary psychiatric disorders, using specific clinical disorders as examples. The clinician is encouraged to "think outside the box" when presented with perplexing cases, keeping in mind that A and B can coexist, A can lead to B, and B can be caused by a yet unidentified C. Taking a detailed medical history, paying close attention to the clinical course of the disease, performing appropriate neurological and medical examinations, and consulting other physicians may significantly reduce the number of diagnostic errors in these challenging clinical situations.