The Lyme Basket
  • Home
  • How to Remove a Tick
  • What is Lyme Disease
  • Symptoms of Lyme
  • Diagnosing Lyme
  • Treatment
  • Tick-Borne Illnesses
  • Our Lyme Story
  • Topic Blog
  • Videos
  • Support Groups
  • Lyme and Suicide
  • Lyme Journal
  • Fun Stuff
  • Links
  • Contact Us
  • Disclaimer

This is a very important two part article that I just could not hide in a link. If you read only one complete article this is one of my very top picks. Lyme is a hidden disease, one that is misunderstood by the medical community as well as the general public. Because those with Lyme may not "look sick" they often do not receive the support they need to successfully battle this devastating disease. I have highlighted in bold some of the ideas in this article that I thought were especially useful to me when we were first diagnosed. The first section of this article deals with Lyme, depression, and suicide the second section addresses many of the issues and difficulties facing Lyme Disease patients trying to get proper, effective treatment.

It is vital that you understand that
you must seek out the knowledge and the help needed
to win your battle with Lyme Disease.

Lyme, Depression, and Suicide   By Robert C. Bransfield, MD
In the late 1970’s, I treated a depressed patient who appeared to have more than just depression. Her weight increased from 120 to 360 pounds, she was suicidal, had papilledema, arthritis, cognitive impairments, and anxiety. This patient became disabled, went bankrupt, and had marital problems. Like many whose symptoms could not be explained, she was referred to a psychiatrist. However, I was never comfortable labeling her condition as just another depression. At the time, I did not consider her illness could be connected to other diagnostic entities, such as neuroborreliosis, erythema migrans disease, erythema chronicum migrans, Bannwoth’s syndrome, Garin-Bujadoux syndrome, Montauk knee, or an ar–thritis outbreak in Connecticut. With time, the connection between Borrelia burgdorferi infections and mental illnesses such as depression became increasingly apparent. In my database, depression is the most common psychiatric syndrome associated with late stage Lyme disease.

Although depression is common in any chronic illness, it is more prevalent with Lyme patients than in most other chronic illnesses. There appears to be multiple causes, including a number of psychological and physical factors.
From a psychological standpoint, many Lyme patients are psychologically overwhelmed by the large multitude of symptoms associated with this disease. Most medical conditions primarily affect only one part of the body, or only one organ system. As a result, patients singularly afflicted can do activities which allow them to take a vacation from their disease. In contrast, multi-system diseases such as Lyme, depression, chronic Lyme disease can penetrate into multiple aspects of a person’s life. It is difficult to escape for periodic recovery. In many cases, this results in a vicious cycle of disappointment, grief; chronic stress, and demoralization.

It should be noted that depression is not only caused by psychological factors. Physical dysfunction can directly cause depression. Endocrine disorders such as hypothyroidism, which cause depression, are sometimes associated with Lyme disease and further strengthen the link between Lyme disease and depression.
The most complex link is the association between Lyme disease and central nervous system functioning. Lyme encephalopathy results in the dysfunction of a number of different mental functions. This in turn results in cognitive, emotional, vegetative, and/or neurological pathology.

 Although all Lyme disease patients demonstrate many similar symptoms, no two patients present with the exact same symptom profile.
Other mental syndromes associated with late state Lyme disease, such as attention deficit disorder, panic disorder, obsessive-compulsive disorder, etc., may also contribute to the development of depression. Dysfunction of other specific pathways may more directly cause depression. The link between encephalopathy and depression has been more thoroughly studied in other illnesses, such as stroke. The neural injury from a stroke causes neural dysfunction that causes depression. Injury to specific brain regions has different statistical correlation with the development of depression.

Once depression or other psychiatric syndromes occur with Lyme disease, treating them effectively improves other Lyme disease symptoms as well and prevents the development of more severe consequences, such as suicide.
Suicidal tendencies are common in neuropsychiatric Lyme patients. There have been a number of completed suicides in Lyme disease patients and one published account of a combined homicide/suicide. Suicide accounts for a significant number of the fatalities associated with Lyme disease.

In my database, suicidal tendencies occur in approximately 1/3 of Lyme encephalopathy patients. Homicidal tendencies are less common, and occurred in about 15% of these patients. Most of the Lyme patients displaying homicidal tendencies also showed suicidal tendencies. In contrast, the incident of suicidal tendencies is comparatively lower in individuals suffering from other chronic illnesses, such as cancer, cardiac disease, and diabetes.


To better understand the link between Lyme disease and suicide, let’s first look at an overview of suicide. Chronic suicide risk is particularly associated with an inability to appreciate the pleasure of life (anhedonia). People tolerate pain without becoming suicidal, but an inability to appreciate the pleasure of life highly correlates with chronic suicidal risk. Of course, there are many other factors that also contribute to chronic risk. For example, one study demonstrated that 50% of patients with low levels of a serotonin metabolite (5HIAA) in the cerebrospinal fluid committed suicide within two years. Apart from factors which contribute to chronic suicidal risk, there are also factors which trigger an actual attempt, i.e.; a recent loss, acute intoxication, unemployment, recent rejection, or failure.

There is much impairment from Lyme disease which increases suicidal risk factors. However, suicidal tendencies associated with Lyme disease follow a somewhat different pattern than is seen in other suicidal patients. In Lyme patients, suicide is difficult to predict. Attempts are sometimes associated with intrusive, aggressive, horrific images. Some attempts are very determined and serious. Although a few attempts may be planned in advance, most are of an impulsive nature. Both suicidal and homicidal tendencies can be part of a Jarish-Herxheimer reaction.


I cannot emphasize enough the behavioral significance of the Jarish-Herxheimer reaction. As part of this reaction, I have seen and heard numerous patients describe becoming suddenly aggressive without warning. I can appreciate skepticism regarding this statement. How can this be explained? Like many other symptoms seen in Lyme disease, it challenges our medical capabilities. In view of this observation, I advise that antibiotic doses be increased very gradually when suicidal or homicidal tendencies are part of the illness.
Although I have discussed the significance of depression and suicide associated with Lyme disease, I would like to say  treatment does help. Combined treatment which addresses both the mental and somatic components of the illness significantly improves the overall prognosis.

 
This is supported by clinical observation and laboratory research showing antidepressant treatment improves immunocompetence. It has been demonstrated in vitro that antidepressants which act on the serotonin 1A receptor (most antidepressants) increase natural killer cell activity. In addition, there are undoubtedly other indirect effects on the immune system through other neural or neuroendurocrine and autonomic pathways. To state this more concisely - antidepressants can result in antibiotic effects, and antibiotics can have antidepressant effects.
Most depression and suicidal tendencies often respond to treatment.

Suicide is a permanent response to a temporary problem. Many people who survive very serious attempts go on to lead productive and gratifying lives. Suffering can be reduced. The joy of life can be restored. Needless death can be prevented. Don’t give up hope. There are answers, solutions, and assistance. There is life after Lyme.

*************************************************************************************************
False negative test results have been widely reported in both early and late disease.
Many Lyme patients were firstly diagnosed with other illnesses such as Juvenile Arthritis, Rheumatoid Arthritis, Reactive Arthritis, Psoriatic Arthritis, Infectious Arthritis, Osteoarthritis, Fibromyalgia, Raynaud's Syndrome, Chronic Fatigue Syndrome, Interstitial Cystis, Gastroesophageal Reflux Disease, Fifth's Fisease, Multiple Sclerosis, scleroderma, lupus, early ALS, early Alzheimers Disease, crohn's disease, ménières syndrome, reynaud's syndrome, sjogren's syndrome, irritable bowel syndrome, colitis, prostatitis, psychiatric disorders (bipolar, depression, etc.), encephalitis, sleep disorders, thyroid disease and various other illnesses.

The minimum time a tick needs to be attached to humans in order for the Lyme bacteria to be transmitted is estimated to be 24 to 48 hours, HOWEVER this applies only to the laboratory setting. In real life as a person moves, scratches, brushes up against things, sleeps and rolls over, the tick can be compressed causing its stomach contents to expel into the victim at any time. Recent incomplete attachment to an infected host could also cause tick saliva to be infective.

Early onset symptoms are fever, malaise (a vague feeling of bodily discomfort or unwellness, possibly nausea), fatigue, headache, muscle aches (myalgia), and joint aches (arthralgia). Many do not get these early symptoms and their first signs may be tingling/numbness, weakness in muscle control, tremors/tics, optic disturbances, memory deficiency (usually short term memory) psychiatric presentations, periods of unexplained anger/rage, headache, neck pain, spinal tenderness, lower back pain, neurologic defined pain/sensations such as hot/cold, either surface or deep, or other such neurologic disorders which then progress to or are
combined with disturbances of other other systems in the body such as cardiac, musco-skeletal, sinus, jaw/teeth (TMJ).  Coinfections may bring a mix of their own symptoms and testing issues.
 
Time and again this office receives phone calls from patients who have a rash, and in some cases had had a tick attached at the site, only to be told by their physician to come back a month later for a test. It is imperative that clinicians understand that the presence of a homogenous or "bull's eye" rash caused by a tick-bite is indicative of infection, and treatment should be started immediately. Do not look at this as simply an allergic reaction to the bite. Err on the side of caution. Most blood tests do not work until 4-6 weeks after infection has occurred, and any delay may cause complications at a later date.

Remember also to advise the patient of the likelihood of a Jarisch-Herxheimer (Herx) reaction upon initiation of treatment. This is common in spirochaetal disease treatment and is caused as a result of toxins released as the die off of the spirochetes takes place. The bull's-eye rash (erythema migrans) may occur in some cases (30%+) but is often missed or unrecognized and does not rule out Lyme Disease in its absence. It is not always a bull's eye and can be more generalized in appearance.
The incubation period from infection to onset of erythema migrans is typically 7 to 14 days but may be as short as 3 days and as long as years.

As reported by RICHARD SADOVSKY, M.D., American Academy of Family Physicians, "The diagnosis of Lyme disease is clinical. Early infection is often accompanied by false-negative serologic tests, although this can occur late in the disease. The positive predictive value of serologic testing is low in patients with vague symptoms unaccompanied by any objective signs."
Some infected individuals have dormant illness (asymptomatic infection has been determined by serological testing) later manifesting from trauma or immuno-suppression, or manifest only non-specific symptoms such as fever, malaise, tingling/numbness sensations, meningitis, encephalitis, headache, fatigue, or myalgia.

The patient may in many cases not recall a tick bite. Ticks, especially in the nymph stage may feed undetected and fall off leaving behind only a sinister calling card...borrelia burgdorferi (Lyme disease) and possible co-infections (echlirosis, babesiosis, bartonella).
Lyme disease spirochetes disseminate from the site of the tick bite by cutaneous, lymphatic and blood borne routes. The signs of early 'disseminated' infection can occur within days to weeks.

Symptoms may also slowly reveal themselves over a long period of time with patients showing up at their doctors with vague, varied symptoms and no knowledge of a tick bite nor rash.
In addition to possible multiple (secondary) erythema migrans lesions, early disseminated infection may be manifest as disease of the nervous system in varying degrees (ie. muscle twitches, tics, numbness/tingling, lower back/neck pain), the musculoskeletal system, or the heart. Early neurologic manifestations include aseptic meningitis (infection in the cerebrospinal fluid also called lymphocytic meningitis), cranial neuropathy (changes in nerve sensation of the skull , face/jaw region, especially facial full/partial nerve palsy), and radiculoneuritis (nerve root involvment). Musculoskeletal manifestations may include migratory joint and muscle pains with or without objective signs of joint swelling. Cardiac manifestations may include rapid/fluctuating heart rate (tachycardia), slowing of the heart rate below 60 bpm (bradycardia), myocarditis (inflammation of the muscular walls of the heart) and transient atrioventricular blocks [the inappropriate delay (or complete inability) of an electrical impulse, generated in the atria, to reach the ventricles (via the atrioventricular node)].B. burgdorferi (Lyme) infection in the untreated or inadequately treated patient may progress to late disseminated disease weeks to years after infection.

Manifestations of late disseminated Lyme disease are intermittent swelling and/or pain of one or a few joints (asymetrically), chronic axonal polyneuropathy, or encephalopathy, the latter usually manifested by cognitive disorders, eye disturbances, sleep disturbance, fatigue, memory and personality changes (including depression, bi-polar disorder and psychiatric manifestations). More frequently, Lyme disease morbidity may be severe, chronic, and disabling.

An ill-defined post-Lyme disease syndrome is said to occur in some persons following treatment for Lyme disease. But this is clearly an 'active' not 'post' lyme infection and further treatment must continue if resolution is to be gained.
Fatalities are recorded ranging from heart problems to suicide.