Up to 40% of patients with Lyme disease develop neurologic involvement of either the peripheral or central nervous system. A broad range of psychiatric reactions have been associated with Lyme disease including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa, and obsessive-compulsive disorder. Depressive states among patients with late Lyme disease are fairly common, ranging across studies from 26% to 66%.
In a published study (Hajek et al, Am J Psychiatry 2002;159:297-301), one third of psychiatric patients showed signs of an infection with the Lyme spirochete, Borrelia burgdorferi. Psychiatrists who work in endemic areas need to include Lyme disease in the differential diagnosis of any atypical psychiatric disorder.
Symptoms of Neurological Lyme disease
Dissemination to the central nervous system can occur within the first few weeks after skin infection. Like syphilis, Lyme disease may have a latency period of months to years before symptoms of late infection emerge. Early signs include meningitis, encephalitis, cranial neuritis, and radiculoneuropathies.
Patients with late-stage Lyme disease may present with a variety of neurological and psychiatric problems, ranging from mild to severe: memory impairment or loss (“brain fog”), dyslexia and word-finding problems, visual/spatial processing impairment (trouble finding things, getting lost), slowed processing of information, psychosis, seizures, violent behavior, irritability, anxiety, depression, panic attacks, rapid mood swings that may mimic bipolarity (mania/depression), obsessive compulsive disorder (OCD), sleep disorders , ADD/ADHD-like syndrome, autism-like syndrome.
It’s also important to consider Lyme disease in children with behavioral changes, fatigue, school phobias, academic problems, learning disabilities, headaches, sore throats, GI complaints and/or migrating pains.
Diagnosis and Treatment
Ruling out Lyme disease as a cause of psychiatric related symptoms can be difficult because standard tests are not accurate, a third of all patients do not recall a rash or tick bite, and a long inactive period may precede the late symptoms. Delayed treatment due to an incorrect assessment of the disease process may enable an acute illness to develop into a chronic one.
Psychiatrists currently have no guidelines on how to treat these patients. While some doctors feel that psychiatric related symptoms in the context of Lyme disease are evidence of continued disseminated infection, others believe that these represent a secondary emotional response to having a serious illness.
Dr. Brian Fallon, director of the Lyme Disease Research Program at Columbia University and principal investigator of the NIH-funded study of brain imaging and persistent Lyme disease, cites five questions that suggest warning signs of Lyme encephalopathy:
- Are there markers of non-psychiatric disease such as migraines, rash, arthritis, sound or light sensitivity, tremors or twitching, cardiac palpitations, word-finding problems, short-term memory loss, cranial neuropathies, radicular or shooting pains?
- Is the psychiatric disorder atypical or unusual? For example, does a panic attack last longer than the expected 1/2 hour? Or is it a first ever panic attack at age 50?
- Is there poor or paradoxical response to psychotropic medications, or excessive side effects/sensitivity to these medications?
- Is this new-onset disease without psychological precipitants such as new stressors or secondary gain?
- Is there an absence of a personal history or family history of major psychiatric disturbances?
Negative answers to these questions do not rule out the presence of Lyme disease and co-infections. But a “yes” to most of the questions, especially in a patient with an outdoor lifestyle or a pet, demands further clinical assessment.
It has been found that even severe neuropsychiatric behavioral symptoms in infected individuals can often be reversed or ameliorated when a multi-system treatment program targeting Lyme disease is used.
When Lyme disease affects the brain, it is often referred to as Lyme neuroborreliosis or Lyme encephalopathy. Unfortunately, only a small percentage of these patients will be properly diagnosed as having Lyme disease and most continue to have relatively unsuccessful treatment with psychiatric medications. Neuroborreliosis can mimic virtually any type of encephalopathy or psychiatric disorder and is often compared to neurosyphilis. Both are caused by spirochetes, are multisystemic, and can affect a patient neurologically, producing cognitive dysfunction and organic psychiatric illness. Such symptoms may be dormant, only surfacing years later. Unlike Treponema pallidum, the cause of syphilis, the causative agent of Lyme disease, Borrelia burgdorferi, can be much more difficult to eliminate, diagnostic testing is less reliable, and interactive copathogens are major contributors in the pathophysiology.
The Lyme spirochete is slow growing and can be difficult to treat, so the patient should be treated with multi-system treatments that include appropriate antibiotics for at least two to four weeks beyond symptom resolution. Most individuals with Lyme disease respond to multi-system treatments, but the treatment course is highly patient specific.