Early disseminated infection (1 to 4 months)
Stage 2 symptoms include headache, stiff neck, facial paralysis, tingling or numbness in extremities, abnormal pulse, sore throat and fever. Approximately 50 percent of untreated patients suffer from stage 2 symptom.If Lyme disease isn’t found and treated while early symptoms are present, or if you don’t have early symptoms that trigger the need for treatment, the infection may affect the skin, joints, nervous system, and heart within weeks to months after the initial infection.
Additional Symptoms may include:
- An expanding, circular rash at the site of the bite. More rashes may appear on other parts of your body as the infection spreads.
- Pain, weakness, or numbness in the arms or legs.
- Not being able to use the muscles of the face.
- Headaches or fainting that continues to happen.
- Poor memory and reduced ability to concentrate.
- Conjunctivitis (pinkeye) or sometimes damage to deep tissue in the eyes.
- Brief episodes of pain, redness, and swelling in one or more large joints—most often the knee. Joint problems are common.
- Occasional rapid heartbeats (palpitations) or, in rare cases, serious heart problems.
Lyme Disease and the Heart
Lyme carditis occurs when Lyme bacteria that have disseminated in the blood establish infection in heart tissue.3,4 Lyme carditis usually occurs in association with joint or nervous system manifestations, although the heart may be the only site of clinically apparent disease. Early studies revealed that carditis occurred in ≈4% to 10% of untreated Lyme disease patients, with a higher rate if asymptomatic carditis was included.3 Because of the use of antibiotic therapy early in infection, Lyme carditis is now considered an uncommon manifestation of Lyme disease in adults and a rare manifestation in children.4 Most cases of Lyme carditis occur between June and December, 4 days to as long as 7 months (median 21 days) after initial illness. There is a slight male predominance and two age peaks of 5 to 14 years and 44 to 59 years. It is unclear whether patients with underlying heart disease have an increased risk of cardiac involvement or complications from Lyme disease compared with the general population. Lyme carditis is much less common in Europe than in the United States, which may be because of differences in strains of Lyme disease bacteria in Europe and North America.
The Lyme bacterium can infect all parts of the heart, including the conduction system around the atrioventricular node, the outer or inner membranes of the heart, the cardiac muscle, and more rarely, cardiac blood vessels or heart valves.3,4 Tissue damage results primarily from inflammation that occurs as the host immune cells respond to bacteria that enter the tissue. The predominant cardiac manifestation is partial heart block caused by impairment of the electric signal that controls contraction of the upper and lower chambers of the heart. Heart block usually is mild, with complete resolution within 6 weeks after onset. The most common symptoms are light-headedness, fainting, shortness of breath, palpitations, and/or chest pain. Heart block occasionally is complete and permanent, requiring insertion of a pacemaker. Myocarditis or pericarditis may occur. Death has been reported in a few cases.
References Bockenstedt LK. Lyme disease. In: Firestein GS, Budd RC, Gabriel SE, O’Dell JR, McInnes IB., eds. Kelley’s Textbook of Rheumatology, 9th ed. Philadelphia, PA: Elsevier; 2013:1815–1828. Google Scholar
The second stage of Lyme disease can affect the heart, causing inflammation of the heart muscle. This can result in abnormal heart rhythms and
How does the heart work?
The heart is a two-stage electric pump whose job it is to circulate blood through the body. The initial electrical impulse that begins the process of a heartbeat is generated by a group of cells located in the upper chamber of the heart, the atrium. These cells act as an automatic pacemaker, starting the electric signal that spreads along the “wiring” within the heart muscle, allowing a coordinated squeeze so that the pump can function.
The heart has four chambers. The upper chambers are the right and left atria (singular = atrium) while the lower chambers are the right and left ventricles. The right side of the heart pumps blood to the lungs while the left side pumps it to the rest of the body.
Blood from the body depleted of oxygen and containing carbon dioxide is collected in the right atrium and then pushed into the right ventricle with a small beat of the upper chamber of the heart. The right ventricle pumps the blood to the lungs to pick up oxygen and release the carbon dioxide. The oxygen-rich blood returns to the left atrium where the small atrial beat pushes it to the left ventricle. The left ventricle is much thicker than the right because it needs to be strong enough to send blood to the entire body.
There are special cells in the right atrium called the sinoatrial node (SA node) that generate the first electrical impulse, allowing the heart to beat in a coordinated way. The SA node is considered the “natural pacemaker” of the heart. This pacemaker function begins the electrical impulse which follows pathways in the atrial walls, almost like wiring, to a junction box between the atrium and ventricle called the atrioventricular node (AV node). This electric signal causes muscle cells in both atria to contract at once. At the AV node, the electric signal waits for a very short time, usually one- to two-tenths of a second, to allow blood pumped from the atria to fill up the ventricles. The signal then passes through electric bundles in the ventricle walls to allow these chambers to contract, again in a coordinated way, and pump blood to the lungs and body.
The SA node generates an electric beat about 60 to 80 times a minute, and each should result in a heartbeat. That beat can be felt as an external pulse. After a heartbeat, the muscle cells of the heart need a split second to get ready to beat again, and the electrical system allows a pause for this to happen.
Stage 3 Lyme Disease Signs
Stage 3 Lyme Disease is called late disseminated Lyme disease. The bacteria have spread throughout the body.
Stage 3 Lyme Disease Signs involves symptoms in various organs. Symptoms include arthritis of one or two large joints; disabling disorders such as confusion; short-term memory loss; inflammation of the heart and tissue surrounding the brain; and numbness in the hands, legs and feet. For some patients, symptoms persist for months or even years.
Stage 3 Lyme Disease Signs :
Within a few weeks to 2 years after the start of the infection, about 60% of people develop arthritis, with joint pain and swelling. The knee is the joint most often affected. In stage 3 you may have temporary bouts of arthritis or you may feel the arthritis all the time. You may have ongoing nervous system problems, but this is less likely.
Symptoms of nervous system problems during stage 3 may include:
- Numbness or tingling in your hands and feet
- Trouble concentrating
- Weakness in your arms or legs
Courtesy Of: http://www.cumc.columbia.edu
Lyme Disease and How it can affect the brain and nervous system.
Patients with neurologic symptoms suggestive of central nervous system involvement should have a lumbar puncture with determination of opening pressure. When the CSF is examined, the fluid should be sent for routine studies such as cell count, and protein and glucose levels. In addition, the CSF should be sent for Bb PCR assay and paired serum and CSF should be sent for calculation of the intrathecal index. Please note that the serum should be drawn on the same day as the spinal fluid for an optimal study. The index refers to the ratio of Bb antibodies in the CSF compared to the serum, corrected for immunoglobulin levels in each of those fluid compartments. When the index is positive, that indicates that there is a preferential production of antibodies against Bb in the CSF – a finding strongly suggestive of central nervous system invasion by the agent of Lyme disease. It is believed that the index may remain positive long after the initial infection has been treated due to immunologic memory. If the CSF is being examined as part of the differential diagnosis with multiple sclerosis, the neurologist is also likely to order other tests, such as an assay for oligoclonal bands. Unfortunately, patients may have neurologic Lyme disease but test negative on the Lyme index. When positive however, the clinician can be confident that this particular individual has or has had central nervous system Lyme disease.
Unlike SPECT and PET images which assess brain function, MRI captures the physical structure of the brain. Inflammatory abnormalities in the brain are also assessed with MRI scans. In children with neurologic Lyme disease, the MRI may reveal white matter hyperintensities suggestive of inflammation or areas of demyelination. Up to 40% of adults with Lyme disease may also have small white matter hyperintensities, but it should be noted that the number of hyperintensities increase with age – even among patients who do not have Lyme disease. In addition, certain factors such as ischemic disease or a history of smoking may result in an increased number of hyperintense areas.The white matter hyperintensities are sometimes called UBOs or “unidentified bright objects”. In some patients, antibiotic treatment results in a diminution or disappearance of these hyperintensities. Certain MRI sequences, such as FLAIR, are best able to detect hyperintensities. These MRI images in Lyme Disease may appear similar to the demyelinated areas seen in the “white matter” of the brain MRI of patients with multiple sclerosis. The brain MRI of the young patient at the left revealed MS-like lesions in this individual with a fully positive IgG Lyme Western blot indicating immune reactivity against the agent of Lyme disease. Because an MRI scan uses a very powerful magnet, patients with pacemakers or other metallic implants should not get an MRI.
Comprehensive cognitive assessments are valuable for several reasons. First, they provide an objective measure of the person’s cognitive functioning at a specific point in time. Second, by providing fully quantitative results, the testing is a very useful way to monitor change in response to treatment for patients with cognitive deficits. Third, neuropsychological tests may help to differentiate between organic or neurologic and psychiatric causes of cognitive problems. Fourth, an understanding of static deficits may help to guide the individual in the construction of alternate strategies to cope with cognitive deficits; for example, a person with auditory attention problems may do best with visually presented information.
Since subjective reports of cognitive difficulties, such as memory problems, do not always correlate with objective data, we cannot rely only on self-reported cognitive problems. A comprehensive selection of tests is administered, including measures of general intellectual functioning as well as specific areas of functioning such as verbal and visual memory and learning, attention/concentration, verbal fluency, processing speed, fine and gross motor functioning, and executive functioning is administered. The sensitivity of neuropsychological tests in identifying brain dysfunction is high, though the test deficits are not specific to Lyme Disease. Measures of psychopathology, particularly depression and anxiety are administered as well since affective states may affect cognitive performance.
Impairments in memory, working memory, attention and mental activation, language conceptual ability, and motor function have been documented in adults with LD. The most consistently identified deficits in adults with Lyme disease have been problems with verbal memory, verbal fluency and mental processing speed. Verbal memory is typically assessed by a list-learning task such as the Buschke Selective Reminding Test or the California Verbal Learning Test. Verbal fluency is often assessed through the Controlled Oral Word Association Test or through Category fluency tests. Speed of processing is assessed through any of the timed tests, such as digit symbol.
Studies by Keilp, Kaplan, Krupp and others support the hypothesis that cognitive impairments are caused by CNS dysfunction and not secondary to a psychological response to chronic illness. Subjective memory impairments may however be higher in LD patients with comorbid depression, a finding which strengthens our recommendation that patients with depression should be monitored closely by a psychopharmacologist.