# Lyme Disease and DP/DR - studies, articles, links, etc.



## kcs

I know there is another thread about lyme disease from awhile back, but it is not titled as such, so is likely to be overlooked. Here is a link to the original thread for anyone who is interested. I wanted to start a thread where I could post studies and articles regarding lyme disease and some of the psychiatric problems including DP and DR specifically, as well as links to more general information about lyme disease for anyone who wants to look into it further. For a bit of background, I was recently diagnosed with lyme disease after being sick for well over 15 years, with derealization being my first and most oppressive symptom. For anyone who wants more background on me specifically and how I am doing, I started a journal of sorts in the Road to Recovery section, here is a link to that - my lyme journal.

I will be posting information and articles in this thread sporadically, depending on how I am feeling at the moment (I am pretty darn sick at this point), and what information I find or already have bookmarked. Anyone else with information is more than welcome to post as well, hopefully this will turn into a comprehensive thread on lyme disease and DP/DR.
-karen


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## kcs

http://www.angelfire.com/biz/romarkaraoke/lymeart.html

(bolding mine)
(haha, editing to add that I just noticed that it turned a bunch of the reference numbers into a cool smilie guy with sunglasses - that is pretty funny 8) )

*Lyme Disease: A Neuropsychiatric Illness*

By Brian A. Fallon, M.D., M.P.H., and Jenifer A. Nields, M.D.
Am J Psychiatry 151:11, November 1994 pp.1571-1580

Objective : Lyme disease is a multisystemic illness that can affect the central nervous system (CNS), causing neurologic and psychiatric symptoms. The goal of this article is to familiarize psychiatrists with this spirochetal illness.

Method : Relevant books, articles, and abstracts from academic conferences were perused, and additional articles were located through computerized searches and reference sections from published articles.

*Results : Up to 40% of patients with Lyme disease develop neurologic involvement of either the peripheral or central nervous system. *Dissemination to the CNS 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. Later, encephalomyelitis and encephalopathy may occur. *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%.* The microbiology of Borrelia burgdorferi sheds light on why Lyme disease can be relapsing and remitting and why it can be refractory to normal immune surveillance and standard antibiotic regimens.

Conclusions: *Psychiatrists who work in endemic areas need to include Lyme disease in the differential diagnosis of any atypical psychiatric disorder.* Further research is needed to identify better laboratory tests and to determine the appropriate manner (intravenous or oral) and length (weeks or months) of treatment among patients with neuropsychiatric involvement. (Am J Psychiatry 1994; 151:1571-1583)

Lyme Disease (Lyme borreliosis), caused by the tick-borne spirochete Borrelia burgdorferi, may progress from an initial skin infection to a disabling multisystemic illness. Now the most common vector-borne infection in the United States, Lyme disease is increasing in incidence and geographic spread (1). The disease has dermatologic, arthritic, ophthalmologic, cardiac, neurologic, and psychiatric manifestations (2). In its protean manifestations, in its spirochetal etiology, and in its course (early skin localization and rapid invasion of the central nervous system [CNS]), Lyme disease is similar to syphilis (3). Like syphilis, early recognition is important to prevent an acute, treatable illness from becoming a chronic or relapsing one. Because current diagnostic tests are not always reliable, physicians must rely on clinical presentation as the basis for diagnosis. *Because many of the symptoms of Lyme disease involve the CNS, patients with Lyme disease may be referred to psychiatrists both before and after diagnosis.*

In this article, we present an overview of Lyme disease with a particular emphasis on its neuropsychiatric features.

Transmission

Lyme disease is transmitted by an infected nymphal or adult female Ixodes tick. Smaller than the dog tick, the Ixodes tick may easily be missed on casual inspection. The bite is usually not painful. Transmission of the spirochete appears to require the tick to feed at least 12-24 hours (4). The ticks are most commonly carried by deer and by the white-footed mouse, but other carriers have been described as well.

Distribution

Lyme disease has been reported *throughout the United States and in numerous countries around the world.* The geographic spread and the incidence in the United States have been rapidly increasing. For example, during 1992, 45 states reported 9,677 cases, representing a 19-fold increase over the 492 cases reported by 11 states in 1982 (5). The State of Connecticut, which in 1992 had the highest rate of Lyme disease in the country, reported between 1991 and 1992 a threefold increase in the proportion of infected ticks in four communities and a one and a half-fold increase in reported cases throughout the state (6). The most heavily affected areas include the Northeast (New York, New Jersey, Connecticut, Massachusetts, Rhode Island, Pennsylvania), the upper Midwest (Minnesota, Wisconsin), and the Pacific coastal region (California, Oregon).
History

Although Lyme disease was first described in the United States as an arthritic illness preceded by a rash (7), early reports in Europe described a primarily neurologic illness without any arthritis (8,9). Psychiatric symptoms were described in some of these early reports.

In 1909, a Swedish physician described the classic Lyme rash, known as erythema chronicum migrans, noting that it developed at the site of an Ixodes tick bite (10). In 1922 two French doctors, Garin and Bujadoux, wrote a case entitled "Paralysis by Ticks," now thought to be the first report of Lyme meningoradiculitis (8). The patient developed erythema migrans after a tick bite, followed by radiculopathy, paralysis of a portion of one arm, anxiety, and meningitis. In 1930 Hellerstrom, of the Karolinska Institute, described a man who, 3 months after an erythema migrans rash, developed an encephalitis with psychotic symptoms, disorientation, and marked CSF abnormalities (11). In 1941 Bannwarth, a German neurologist, described the syndrome of chronic lymphocytic meningitis, which was characterized by radicular pains, lymphocytic meningitis, and peripheral nervous system involvement, especially facial palsy (9). The cases in all of these early reports, previously described as Garin-Bujadoux syndrome, Bannwarth's syndrome, and neuroborreliosis, are now considered to have been cases of Lyme disease.

In the United States, the first report of a tick-induced erythema migrans rash was in 1970 (12). In 1977 "Lyme arthritis" was described by Steere et al. (7); the article was based on an epidemiological investigation of an outbreak of presumed juvenile rheumatoid arthritis in Connecticut. In 1978 the link between Lyme arthritis and the bite of an Ixodes tick (13) was recognized. In 1982 Burgdorfer et al. isolated the etiologic agent of Lyme disease from an Ixodes tick--a spirochete now known as B. burgdorferi (14). Early in the history of Lyme disease, aspirin and nonsteroidal anti-inflammatory agents were used for symptoms that emerged after the erythema migrans rash (15). Subsequently, penicillin was shown to shorten the duration of illness, thus supporting an infectious etiology. While short courses (10 days) of oral or intravenous antibiotics were recommended at first, it is now recognized that some patients benefit from longer courses (6 weeks or longer) or repeated treatments (16-18).

Typical Clinical Manifestations of Lyme Disease

Within days or weeks after the bite of a tick infected with B. burgdorferi , a localized skin reaction may occur, consisting most typically of an erythematous annular rash (erythema migrans), which may enlarge to a size of 5 cm or greater. This early localized sign of infection may soon be followed by mild to severe flu-like symptoms.

Hematogenous dissemination may lead to early (weeks to months) heart, ophthalmologic, or nervous system involvement. Although second- or third-degree atrioventricular block is most common, rare reports of myopericarditis, left ventricle dysfunction, and cardiomegaly exist (19). Conjunctivitis can be an early manifestation of ocular involvement.

*Within the first few weeks after skin infection, B. burgdorferi may disseminate to the CNS (20-22) where it may remain quiescent for months to years before producing symptoms (23). Because approximately one-third of infected patients do not recall the tick bite or rash and because the flu-like symptoms are nonspecific and may be mild (24), patients may not realize that they are infected until long after the initial bite. Neurologic problems, which occur in 15%-40% of patients (25), may be the presenting symptom.* Early on, patients may experience headaches without any signs of inflammation in the CSF (18). Shortly thereafter, patients may develop meningitis, cranial neuritis, and motor or sensory radiculitis (26). With meningitis, symptoms may include recurrent severe headaches, stiff neck, photophobia, and, less commonly, nausea and vomiting. At this stage, objective signs are commonly present in the CSF (see the section on CNS laboratory tests). In less than half of the patients with meningitis, a mild encephalitis develops that is characterized by fluctuating disturbances of mood, concentration, memory, and sleep. Cranial neuritis, such as Bell's palsy, occurs in 5%-10% of patients with neurologic Lyme disease (27). Other signs of peripheral nerve involvement include sensory or motor radiculoneuropathies; objective abnormalities may be evident on nerve conduction studies. Symptoms of peripheral neuropathy typically include sharp shooting pains, areas of numbness, paresthesias, weakness, or fasciculations.

*Later-stage illness (months to years after infection) generally affects the joints, eyes, skin, or CNS.* Arthritic involvement begins with migratory arthralgias and, in 60% of untreated patients, develops into an inflammatory arthritis, typically affecting the large inflammatory arthritis, typically affecting the large joints, such as the knee (28). Ophthalmologic involvement may consist of localized inflammation such as uveitis, iritis, or optic neuritis (29, 30). A late dermatologic manifestation of Lyme disease, acrodermatitis chronica atrophicans, is seen almost exclusively in Europe (31).

Late neurologic involvement may be manifested by encephalomyelitis or encephalopathy (18, 23, 32). Encephalomyelitis, an uncommon late manifestation of Lyme disease, may have quite severe and diverse presentations, including spastic paraparesis, transverse myelitis, cerebellar syndromes, hemiparesis, and movement disorders (18, 32). *More common in late Lyme disease is an encephalopathy characterized by subtle to severe cognitive changes and a polyradiculoneuropathy (23).* In this stage of illness, the CSF may appear normal (18, 21) (see section on CNS laboratory tests). *Other accompanying symptoms of later infection include profound fatigue, sleep disturbance, photophobia, auditory hyperacusis, extreme irritability or emotional lability, word-finding problems, dyslexic-like errors when speaking or writing, and spatial disorientation (23, 33). Disturbances in other sensory modalities, such as taste and smell, have been reported (33, 34). These symptoms may fluctuate in intensity so that symptoms are present on some days but not others.* The profile of persistent, marked fatigue and cognitive deficits associated with late-stage Lyme disease is similar to the symptom profile of the chronic fatigue syndrome (35). Whether the late-stage symptoms of Lyme disease are due to persistent infection or to a postinfectious immune activation is an important question that requires further elucidation.

*Because patients with encephalopathy or encephalitis may experience marked mood lability, irritability, and sleep disturbance, the distinction between an organic mood disorder and a concomitant primary major depression may be quite difficult to make. *

A typical Neurologic Manifestations of Lyme Disease

Because the clinical spectrum of Lyme disease continues to expand, physicians who work in endemic areas should keep Lyme disease in the differential diagnosis of any atypical neurologic illness with multisystemic features. Case reports, for example, have linked a variety of neurologic syndromes to late Lyme disease; these include blindness (30), progressive dementias (32, 36, 37), seizure disorders (34, 38, 39), the Tullio phenomenon (40), strokes (41), extrapyramidal disorders (42), amyotrophic lateral sclerosis (43), Guillain-Barre syndrome (44), and progressive demyelinating-like syndromes mimicking multiple sclerosis (23).

Centers for Disease Control (CDC) Criteria for Diagnosis

Lyme disease surveillance by the CDC began in 1982, and in 1991 Lyme disease became nationally reportable. For epidemiologic surveillance studies (1), the CDC requires history of exposure in an endemic area and either 1) a physician-diagnosed erythema migrans rash of at least 5 cm in diameter or 2) laboratory confirmation of exposure to B. burgdorferi and at least one systemic manifestation. Systemic manifestations must be either musculoskeletal (arthritis), neurologic (lymphocytic meningitis, cranial neuritis, radiculopathy, encephalomyelitis with intrathecal antibody production), or cardiac (second- or third-degree atrioventricular conduction delays). Laboratory confirmation requires the isolation of B. burgdorferi , the demonstration of diagnostic levels of B. burgdorferi immunoglobulin (1g) M or IgG antibodies in serum or CSF, or a rising specific antibody titer on serum samples taken from acutely ill and convalescent patients.

*These criteria have been useful for epidemiologic studies, but not all patients with Lyme disease will meet this case definition. About one-third of patients do not recall the erythema migrans rash; serologic testing may be unreliable (45); and the clinical spectrum of Lyme disease continues to expand beyond the manifestations currently included in the CDC case definition. *

Laboratory Testing

Because B. burgdorferi is difficult to culture, indirect methods are used to detect the presence of the spirochete. Currently available serologic tests, such as the enzyme-linked immunosorbent assay (ELISA) and the indirect immunofluorescence assay, rely on the immune response following exposure to B. burgdorferi , but they can be unreliable, with both false positive and false negative results (45). *In a recent study, over half of the 45 laboratories studied reported falsely negative values in a known positive serum sample from a patient with Lyme disease (46).* The Western blot is also often used to examine the serum for antibodies against epitopes that are specific for B. burgdorferi (e.g., 31 kD, 34 kD, or 39 kD bands). Other laboratory tools are emerging--such as urine antigen tests (47), cell-mediated immunoassay (48), immune complex assays (49), polymerase chain reaction assays (50, 51), and borreliacidal antibody tests (52)--but these are not yet well standardized across laboratories.

Several B. burgdorferi antigens are shared by other spirochetes. For example, both B. burgdorferi and the etiologic agent of syphilis, Treponema pallidum , may cause a positive finding on the fluorescent treponemal antibody absorption tests; results of nontreponemal tests, such as the rapid plasma reagin and Venereal Disease Research Laboratory tests, are usually negative in Lyme disease (18). Patients with syphilis or periodontal disease (oral spirochetes) may have falsely positive Lyme ELISA serologies and a common 41 kD antibody to flagellar antigen evident on Western blot.

*Falsely negative test results may occur for a variety of reasons. If tested too soon after initial infection, the patient may not yet have mounted an antibody response (53). In addition, antibiotic treatment early in the infection may abrogate the humoral immune response (54). In some cases, free antibodies may not be detected because the borrelia antibodies are bound within circulating immune complexes (55). Finally, interlaboratory variability in antigenic standardization of Lyme assays may result in false negative as well as false positive results (46). 
*

CNS Laboratory Tests for Lyme Disease

The results of laboratory testing among patients with neurologic Lyme disease vary depending on the stage of the illness. In very early CNS involvement (meningismus) or late-stage infection (encephalopathy), the CSF may appear normal (18). When clinical signs of meningitis or encephalitis are present, a spinal tap may reveal a mononuclear pleocytosis, mildly increased protein, and, in some cases, an elevated IgG index or oligoclonal immunoglobulins. Intrathecal anti- B. burgdorferi antibody production is present in 70%-90% of patients with Lyme meningitis (18). Magnetic resonance imaging (MRI) studies may demonstrate punctate white matter lesions of T 2 weighted images, similar to those seen in demyelinating disorders, such as multiple sclerosis. EEG studies may show diffuse slowing or epileptic discharges, but this is uncommon.

*In patients with late Lyme encephalopathy, results of brain MRI and EEG studies are generally normal. Functional brain imaging using quantitative brain perfusion single photon emission computed tomography (SPECT), however, may reveal hypoperfusion, particularly in the cerebral white matter, even in patients with no CSF or MRI abnormalities (E.L. Logigian et al., unpublished data, 1994). Objective deficits may be seen on neuropsychological testing (23, 27, 56, 57) (table 1).* In about half of these patients, typical markers of CSF infection (pleocytosis, elevated protein, intrathecal antibody production) cannot be found (18). Current experimental research using sensitive ELISA and Western blot techniques has demonstrated the continued presence of spirochetal antigens among many patients with encephalopathy whose CSF otherwise tests normal (21). In some of these patients, results of standard antibody testing of both the serum and the CSF have been negative, but the immune complex dissociation assay revealed bound B. burgdorferi -specific antibody (58).

Given the limitations of diagnostic tests, clinicians need to consider clinical factors that would aid in the diagnosis of Lyme disease. These include a history of an erthema migrans rash or Ixodes tick bite, exposure to a Lyme endemic area, and the combination of neuropsychiatric and extraneural symptoms. Because Lyme disease is a multisystemic illness, patients whose neuropsychiatric symptoms start after a flu-like illness should be asked about a history of other symptoms of Lyme disease, including rashes, joint pains, arthritis, cardiac problems, changes in vision, and radicular pains or cranial nerve palsies.

Neuropsychological Findings

*Most studies have found that patients with Lyme encephalopathy have subtle impairments in memory, concentration, learning, and conceptual ability. Typically, the deficits suggest frontal lobe involvement, affecting short-term memory, verbal fluency, or executive cognitive functions (table 1). Logigian et al.* (23), in a study of 27 patients with chronic neurologic Lyme disease, found that 15 of the 27 had quantifiable memory deficits. In order to determine whether psychological factors might account for the memory impairment among Lyme disease patients, Kaplan et al. (56) compared 20 patients with Lyme encephalopathy with 11 fibromyalgia patients and 11 nonpsychotic depressed patients on a neuropsychological test battery. They found that the Lyme disease patients showed greater impairment on standardized memory tests than either of the comparison groups and that the impairment was independent of the number of somatic complaints and the presence of depression.

*Cognitive impairments among patients with late Lyme encephalopathy often improve with antibiotic treatment (23, 27), suggesting that active spirochetal infection causes the encephalopathy.* In Halperin et al.'s study (27) of patients with late Lyme borreliosis, serial neuropsychological testing before and after a course of intravenous antibiotics revealed marked improvement on tests of memory, attention and concentration, conceptual ability, and psychomotor and perceptual motor function. Noteworthy is that many patients with cognitive deficits did not have clinical evidence of focal CNS disease. Results of EEGs, CSF studies, and other laboratory investigations were often normal. MRI scans were abnormal in some of the patients with severe memory impairment, revealing hyperintense T 2 white matter lesions suggestive of edema or inflammation. *Some patients with late Lyme encephalopathy continue to have residual neuropsychological deficits after antibiotic treatment.*

Krupp et al. (57) compared 15 patients with Lyme disease who had complaints of persistent cognitive difficulty 6 months after antibiotic treatment to 10 healthy comparison subjects matched in age and education. Compared to the healthy subjects, the Lyme disease patients exhibited marked impairment on memory tests. In that study, the memory impairment was not correlated with serum of CSF anti- B. burgdorferi antibody titers and was not explained by MRI findings or depression. *Fatigue, however, a nonspecific marker of chronic Lyme disease, was correlated with memory impairment; this suggested to the authors that the persistent encephalopathy could be an indirect effect of systemic infection elsewhere in the body.* The authors noted that persistent neuropsychological deficits were somewhat more common among patients who had received only oral rather than intravenous therapy. In addition, of the six Lyme patients with no objective neuropsychological test deficits but subjective complaints of memory impairment, five had the highest depression scores of the entire group of 15, suggesting that depression in some Lyme patients may account for the subjective experience of cognitive dysfunction.

Psychiatric Manifestations of Lyme Disease

*A limited but ever increasing literature is beginning to suggest that psychiatric disorders may be part of the clinical profile of Lyme disease. *Before reviewing this literature, we present the following case:

Ms. A, a previously healthy 18-year-old college freshman, suddenly developed *severe and sustained anxiety, depersonalization, and panic attacks associated with insomnia and appetite loss.* She consulted the university health services. After evaluation by both a psychologist and an internist, rest was recommended, under the assumption that these symptoms represented an adjustment reaction to being away from home. As her symptoms worsened, Ms. A began to fear that she was going crazy.

Two weeks later, Ms. A returned home on a medical leave of absence. An extensive medical workup revealed no abnormalities except for a positive Lyme ELISA titer. A Western blot for B. burgdorferi also came back positive. Ms. A insisted on getting a spinal tap. Although the cell count and total protein were normal, the CSF revealed IgG antibodies to B. burgdorferi . The diagnosis of CNS Lyme disease was made. The patient was treated with a 6-week course of intravenously administered antibiotics, and over the course of the following 3 months she felt 80% better.

*Noteworthy in this case is that a diagnosis of Lyme disease was never considered by the college's counselor and internist. The private community physician also did not suspect Lyme disease, but because the patient lived in an endemic area and because Lyme disease is well-known as the "new great imitator" (59), this doctor included a Lyme test in the battery of blood tests.* After the ELISA results came back positive, the patient recalled a large annular rash several months earlier that had been followed by a brief period of moderate headaches and uncharacteristic fatigue. *Ms. A did not have any joint pain, radiculopathy, cranial nerve palsies, or cardiac symptoms. Her primary manifestation of Lyme disease was psychiatric.* Because ms. A's CSF studies demonstrated borrelial antibodies and because her psychiatric symptoms resolved so rapidly after intravenous antibiotic treatment, *active CNS infection was presumed to have been the cause of the severe anxiety and depersonalization.* *Had Ms. A's serologic Lyme test results come back falsely negative, the diagnosis of Lyme disease would have been missed.* It should be emphasized, however, that careful history taking by a clinician well-versed in the clinical spectrum of Lyme disease would have suggested the diagnosis even in the absence of positive serologic test results.

The psychiatrist's evaluation becomes complicated when psychiatric symptoms emerge after the patient has already received a standard course of antibiotic treatment. Such a situation developed with Ms. A.

One year later, *Ms. A developed a return of anxiety with panic attacks and agoraphobia. In addition, she developed rare deja vu episodes, repetitive musical hallucinations, and intrusive obsession thoughts and images.* Results of a repeat spinal tap were normal on routine testing with a nonreactive CSF ELISA for B. burgdorferi antibodies. *An EEG after sleep deprivation revealed intermittent slowing in the right and left temporal areas with rare sharp waves.* Ms. A was treated for 6 months with imipramine, with complete resolution of her panic attacks and agoraphobia. With time, the obsessional thoughts, deja vu experiences, and musical hallucinations also resolved.

Although the panic disorder and obsessive compulsive disorder may have been mere epiphenomena with the Lyme disease, the lack of a family history of these disorders and the normal premorbid history suggest that Lyme disease may have triggered these symptoms. *Severe anxiety and panic attacks have been previously described in Lyme disease (60). Obsessive-compulsive disorder has been associated with CNS infections, such as the encephalitis epidemic of 1916-1922 (61), and has also been associated with Lyme disease (62); anti-neuronal antibodies triggered by systemic infection may induce certain subtypes of obsessive-compulsive disorder (63).* Persistent infection could not be completely ruled out in Ms. A's case, given the fact that patients with late CNS Lyme disease may have no demonstrable CSF abnormalities on currently available testing. However, because of the absence of other systemic Lyme symptoms and the improvement with psychiatric medications, this patient has continued to be treated symptomatically and observed for the possible reemergence of signs of CNS infection.

Reviews

In 1990 two review articles appeared in Germany which suggested that psychiatric symptoms may be part of the picture of Lyme disease (64, 65). After an extensive review of the neurologic literature, Omasits et al. (64) concluded: *"psychiatric manifestations can at times be predominant, ranging from agitated depressive states to the clinical picture of dementia."* Kohler (65) described a staging of psychiatric symptoms, with depression occurring in early CNS disease and organic mood and psychotic disorders occurring in late-stage disease. Although Kohler's report was suggestive, there was no mention of prospectively collected data to support the staging description.

The sparse world literature on the psychiatric manifestations of Lyme borreliosis is methodologically limited. Most of the literature consists of case reports and uncontrolled small series. When standardized measures were used, they were generally self-report depression items that examined one point in time without a comparison group. Despite these marked methodological problems, the case reports and small series are provocative.

Psychiatric Case Reports

*Case reports have linked Lyme disease to a vast array of neuropsychiatric symptoms, including paranoia (37, 62, 66-68), thought disorder (66), delusions (62, 66), auditory hallucinations (62, 67), olfactory hallucinations (34), visual hallucinations (69), stereotypies (67, anorexia nervosa (70), obsessions or compulsions (62, 70), major depression (37, 58, 64), disorientation (37, 69, 70), confusion (34, 37, 70), violent outbursts (62, 70), mood lability (60, 62, 67, 70), panic attacks (60, 62), mania (60, 62), personality changes (34, 37), catatonia (67), and dementia (36, 37).* In three of these cases (66, 67, 69), it was not until the onset of a psychotic disorder that the patient was brought to medical attention. *In two of these cases, no other symptoms of systemic Lyme disease were evident at initial presentation, although a careful history revealed neck and radicular pains 4-6 months earlier.* *Four patients were hospitalized for a psychiatric illness (62, 66, 67, 70) before it was recognized that the psychiatric symptoms might be caused by CNS Lyme disease.* One patient's mania and movement disorder led to hospitalization for a neuropsychiatric evaluation, but Lyme disease was not considered and therefore not diagnosed until several months after discharge (60). *Two patients had such extensive multisystemic symptoms that somatization disorder would have been hard to rule out had these two patients not had positive results on serologic tests and a normal premorbid history (60).* Many of the patients had abnormalities noted on EEG, CSF, or structural brain imaging (34, 60, 62, 66-68, 70). In one patient (68), B. burgdorferi was successfully cultured from the CSF. In two other patients (37, 70), pathological studies of brain tissue revealed B. burgdorferi -like spirochetes.

Among the 11 well-described cases, nine patients were treated with intravenous antibiotics for presumed CNS infection (34, 60, 62, 66-68, 70). Duration of intravenous antibiotics ranged from 10 days (one course) to 29 weeks (three courses). *Although all patients responded well to antibiotic treatment, relapses occurred in several patients (37, 60, 62, 68). One 47-year-old man with seropositive Lyme disease manifested primarily by depression and memory deficits had an initial excellent response to intravenously administered antibiotics; he relapsed 5 months later, was not re-treated, was institutionalized in a state psychiatric hospital with an organic mood syndrome and progressive frontal-type dementia, and died at age 52.* The neuropathological examination revealed degeneration of the substantia ***** and thalamus, with spirochetes evident in the substantia ***** (37). *A flare-up of symptoms shortly after the initiation of antibiotics was reported in four of these patients (60, 62); in one case (62), the antibiotic treatment may have precipitated a manic episode. This treatment-initiated flare-up may reflect an inflammatory response to spirochetal lysis and antigen release, similar to the Jarisch Herxheimer reaction that occurs in the treatment of syphilis.* *In addition to worsening systemic symptoms (e.g., arthralgias, weakness, shooting pains), this reaction may include worsening neuropsychiatric symptoms, such as depression, anxiety, or photophobia (33). *

Psychiatric Series

Nine reports (23, 27, 32, 56, 57, 71-74) of larger series of Lyme patients are summarized in table 2. Irritability, mood lability, or depression were reported in seven of the nine studies, with a frequency ranging from 26% to 66% of the sample. Of the four controlled studies, three (57, 71, 73) reported that depression was greater or more frequently reported by the Lyme disease group. *Noteworthy is that all of these studies were composed of patients with disseminated Lyme disease, primarily with late neurologic symptoms consistent with encephalopathy.* The patients with Lyme encephalomyelitis (32) showed the most extreme illness, with two patients suffering from dementia-like syndromes. *The one study of children with neurologic Lyme disease (72) indicated that behavioral or mood disturbances were the second most common symptom, resulting in mood lability, decreased interest in play, or poor school performance.* Six of the 96 children in this series were thought to have psychiatric disturbances unrelated to Lyme disease.

Three of the studies relied on a clinical interview for psychiatric assessment (32, 72, 74). One used a survey based on DSM-III-R (73). Five used standardized self-report instruments (23, 27, 56, 57, 71). *In one survey of 51 seropositive patients (73), the cumulative frequency of DSM-III-R major depression since the onset of illness was three times higher among the Lyme patients than among a medically ill comparison group, even though the comparison group was both older and ill far longer.* In addition, among the Lyme patients who reported major depression, most (90%) denied a prior history of depression. It should be noted that none of the nine published series used structured psychiatric diagnostic interviews, and six of the nine studies relied solely on self-report measures. Although all of the studies in table 2 have methodological flaws (small sample size, unclear inclusion/exclusion criteria, biased samples, use of nonstandardized instruments, retrospective or cross-sectional data rather than a prospective design, reliance on patient self-report rather than a structured clinical interview conducted by an individual who was blind to the patient's diagnosis), the preponderance of evidence supports the notion that Lyme disease may be associated with marked mood changes.

In order to investigate the extent to which CNS infection with B. burgdorferi may contribute to the association between depression and Lyme disease, biological studies of depressed patients with Lyme disease, examining the CSF for evidence of direct infection or immune modulators, should be conducted. As in the investigation of depression in other medical illnesses, the multifactorial etiology of depression in Lyme disease needs to be addressed through examination of such factors as severity of illness, extent of pain, degree of disability, concomitant central neurologic symptoms or signs, psychodynamic factors, socioeconomic stressors, and family and personal history of psychiatric illness. Brain imaging studies (regional cerebral blood flow, SPECT, positron emission tomography) looking for evidence of metabolic dysfunction would also be of considerable interest.

Microbiology of B. burgdorferi

The microbiology of B. burgdorferi sheds light on why Lyme disease is an illness that at times can be relapsing and remitting and that can be refractory to normal immune surveillance and standard antibiotic regimens. *The causative agent of Lyme disease--the spirochete B. burgdorferi --has a long replication time, comparable in this respect to Mycobacterium tuberculosis . Rapidly transmitted throughout the body, B. burgdorferi is known to invade the CNS within the first few weeks after initial infection (20-22). B. burgdorferi is known to be neurotropic, leaving the CSF to adhere to glial cells or other brain tissue (75). Once in the CNS, B. burgdorferi , like T. pallidum , may remain latent, only to cause illness months to years later (23).*

Much of the genetic material in B. burgdorferi is contained in plasmids (76), resulting in the possibility of significant antigenic variability. This includes marked variability in the expression of surface antigens, with consequent alteration in immunogenicity. Such changes could lead to resistance to normal immunologic functions--for example, through a failure of the B. burgdorferi -specific antibody to induce phagocytosis--as well as to evasion of routine laboratory detection. Recent animal research (77) has found that the spirochete may undergo genetic alteration once it is sequestered in the CNS, thus resulting in a new strain of spirochete that is different from the infecting peripheral spirochete. *The remarkable strain variation of B. burgdorferi may account for the differences between the presentation of Lyme disease in Europe and in the United States (78-80). For example, in Continental Europe, arthritic involvement is less common, and most cases of neurologic Lyme disease have prominent CSF abnormalities. Late-stage neurologic Lyme disease in the United States, on the other hand, is less likely to show CSF abnormalities on routine testing (81).*

During growth, B. burgdorferi appears to shed membranous material (blebs) from its surface. These blebs coat the spirochete and have been found free in the CSF, serum, and urine (21, 82, 83). The blebs appear to interact specifically with IgM molecules. It is hypothesized that in some cases, the blebs may bind all of the free circulating B. burgdorferi -specific IgM antibodies, thereby enabling the organism itself to escape immune surveillance. In addition, the blebs possess potent, nonspecific mitogenic activity that may cause an inappropriate and ineffective stimulation of the immune system. This could initiate autoimmune disease processes (84).

*B. burgdorferi has been shown to be capable of persisting in human hosts despite extensive antibiotic treatment (17, 85-88).* Because in vitro studies demonstrate that B. burgdorferi can be recovered from antibiotic-treated fibroblast monolayers (89) and because B. burgdorferi has been shown to lodge inside human fibroblasts (89), mouse macrophages (90), and human endothelial cells (91), researchers conclude that *the intracellular location may enable the spirochete to remain inaccessible to antibiotics and normal immune surveillance. *Sequestration in other antibiotic- and immunologically privileged sites (e.g., CNS, joints, anterior chamber of the eye) may also account for persistent illness despite antibiotic treatment (20).

*Several features are known to contribute to an organism's resistance to standard lengths of antibiotic treatment. These features include an intracellular location (92), long replication time, genetic variability, and the ability to become sequestered in difficult-to-penetrate sites. B. burgdorferi appears to possess all of these characteristics. *

Pathogenesis of CNS Lyme Disease

A consistent finding in pathological studies is that the spirochete B. burgdorferi is rarely recovered from the affected organ, such as the CNS. Features consistent with a focal vasculitis, however, have been found in both the central and the peripheral nervous systems of patients with neurologic Lyme disease (93, 94). *Scientists now believe that a small number of organisms can cause significant neurologic dysfunction either through a B. burgdorferi -initiated immune response directed specifically against neural tissue or through the triggering of a nonspecific inflammatory response (93).* The immune response may remain active when spirochetal antigens are still present, as in an ongoing infection, or when a postinfectious autoimmune process has been triggered against host tissue.

Evidence exists to support the role of both specific and nonspecific immune processes in the production of CNS Lyme disease. Evidence of specific processes includes the production of B. burgdorferi -specific immune complexes and T cell responses within the CSF (95, 96), autoantibodies to neural tissue (97), and cross-reactivity of B. burgdorferi antibodies with neural tissue (98). Evidence of nonspecific processes includes an elevation of neurotoxins, such as quinolinic acid, in the CSF of Lyme patients but not normal comparison subjects (99). Of particular interest is that nonspecific products of immune activation, such as kynurenines or quinolinic acid, can be excitotoxic to neurons and have been linked to memory loss (100), anxiety and depression (101), seizures (101), and the chronic fatigue syndrome (102). In HIV-infected patients, elevations of quinolinic acid in the CSF tend to be correlated with the degree of neuropsychological deficits (100). Further investigation in this area is needed.

Lyme Disease and Syphilis

Several authors have noted similarities between Lyme disease and syphilis (3, 59, 103). Both are caused by a spirochete; syphilis by T. pallidum and Lyme disease by B. burgdorferi . Both start with skin inoculation and a localized skin reaction, followed by a desseminated multisystemic infection. Both may progress in stages. Both can cause meningitis, encephalitis, cognitive deficits, cranial neuropathy, and vasculitis. Both diseases can, in rare cases, lead to the Tullio phenomenon (40), characterized by nausea and nystagmus in response to sound stimulation. (This syndrome was previously considered pathognomonic for syphilis.) *Antibiotic treatment of both diseases may lead to an initial worsening of symptoms, including neuropsychiatric ones (33, 104).* The mechanism of injury in both infections is thought to be primarily indirect: one of immunopathogenesis, not a direct effect of the spirochete itself.

Both T. pallidum and B. burgdorferi can rapidly invade the CNS, within the first few weeks after infection. Both spirochetes can remain latent for long periods of time before the onset of disease. Both spirochetes can pass through or between endothelial cells (105, 106), thereby enabling dissemination and extensive tissue involvement. Both may persist in the host to cause a chronic infection.

Unlike T. pallidum , which is generally transmitted from host to host, the Lyme spirochete is carried by a vector. Furthermore, radiculopathy and peripheral neuropathy are features of Lyme disease that syphilis does not share.

Neurosyphilis is known to be associated with memory problems, depression, mania, psychosis, and personality changes, such as irritability, emotional lability, and apathy (107). *Recent evidence suggests that Lyme borreliosis, the "new great imitator" (59), may be associated with a similarly wide spectrum of psychiatric disorders.* What Hollos and Ferenczi (108) wrote about syphilis in 1925 bears analogy to the present state of knowledge about Lyme disease:

The psychical symptomatology of paresis is by no means only an intellectual deterioration. On the contrary, it contains almost all the mental symptoms that occur in other psychoses, very frequently the most characteristic symptoms of mania, of melancholia, of paranoia, and of dementia praecox. In many cases the diagnosis for a long time oscillates between a "functional psychosis" and paresis, and only the beginning of pupillary stiffness, a facial palsy, or the finding of a "positive Wasserman," is the determining factor.

Future Directions in Research

*There are two areas of major clinical significance in which current knowledge about Lyme disease remains incomplete: diagnosis and the optimal treatment for patients with persistent symptoms.*

*Because currently available serologic tests are not always reliable, Lyme disease remains a clinical diagnosis that is based on a constellation of typical patterns.* Diagnostic difficulty arises when patients present with symptoms that are nonspecific or atypical for Lyme disease. *If these patients test positive for B. burgdorferi , they may be told that they have falsely positive test results. If they test negative, they may be told that they clearly do not have Lyme disease.* Although the latter conclusions may be accurate in many cases, the absence of reliable laboratory tests makes such conclusions impossible to draw definitively. Although the prevalence of patients with seronegative Lyme disease is not known, such patients clearly do exist (48, 55, 109). Faced with diagnostic uncertainty, some clinicians may choose not to treat in order to avoid the risks of antibiotic therapy (110). Other clinicians who work in endemic areas may recommend an empirical trial of antibiotics because of what they judge to be a greater risk that a potentially multisystemic chronic infection may progress if untreated (17).

*Definitive treatment guidelines for Lyme disease have not been established because knowledge about this illness continues to evolve. However, because of the rapid CNS invasion, aggressive treatment is recommended as early as possible (18). General guidelines consist of 3-4 weeks of oral antibiotics for patients without evidence of central neurologic involvement or 4-6 weeks of intravenous antibiotics for patients with central neurologic involvement. In many cases, following these guidelines results in a remission of symptoms. However, in some cases, relapse occurs after antibiotics are stopped (23).*

*Because intravenous antibiotic treatment is expensive and the need for long-term treatment is not yet proven, some insurance companies are now denying reimbursement for repeated courses of intravenously administered treatment; denial of reimbursement is based on the argument that the efficacy of long-term or repeated antibiotic treatment has not been established (111). Yet clinical experience suggests that some patients with central neurologic involvement may require repeated intravenously administered treatment.* Several lines of evidence support this clinical observation. First, some patients with Lyme encephalopathy respond well to additional of antibiotics (23, 27). Second, several case reports document the persistence of the spirochete or symptoms in patients who have already had the recommended 4-6 week course of antibiotics (17, 85-88). Third, newer diagnostic techniques are able to detect the presence of B. burgdorferi antigens in some previously treated, persistently symptomatic patients (21). Fourth, as noted earlier, the microbiology of B. burgdorferi makes it clear why standard courses of antibiotics might be ineffective in some cases.

Some patients do not get better with repeated treatment. Persistent symptoms in these patients may result from permanent damage or from a postinfectious autoimmune process (112). Prospective microbiological and clinical studies are needed to identify risk factors that may predispose certain patients to develop chronic Lyme disease and to distinguish those patients who will respond to prolonged or repeated antibiotic treatment from those who will not.

Conclusions

*The neuropsychiatric effects of many infectious illnesses, bacterial (neurosyphilis, tuberculosis), parasitic neurocysticercosis, toxoplasmosis), fungal (coccidiomycoses, cryptococcosis), and viral (herpes simplex, HIV), are well known. Also well known are the prominent neuropsychiatric manifestations of illnesses, such as systemic lupus erythematosus and multiple sclerosis, that cause CNS inflammation. Early in the history of many of these illnesses, the psychiatric symptoms were thought to be functional in nature. Women suffering from multiple sclerosis were thought to be hysterical. Early depression and cognitive decline in patients with AIDS were thought to represent purely an emotional reaction to a serious illness. Later research provided objective evidence that CNS pathology caused by infection or inflammation was associated with each of these psychiatric syndromes.*

The spectrum of neuropsychiatric syndromes associated with Lyme disease is only beginning to be elucidated by clinical studies and case reports. At the same time, biological studies and brain imaging techniques suggest a physiological basis for such syndromes through one or more of the following mechanisms: direct infection in the CNS; specific, localized autoimmune reactions; or secondary but centrally active immunologic responses to systemic infection.

This article emphasizes the biological substrate of the neuropsychiatric symptoms associated with Lyme disease. The complicated secondary emotional reactions to this illness that relate to particular aspects of its symptoms, including fluctuating course, bizarreness of symptoms, cognitive disability, chronic pain, and the uncertainties surrounding its diagnosis and management, have been discussed in greater detail elsewhere (33).

*In addition to the dermatologic and arthritic manifestations, the breadth of neuropsychiatric symptoms in Lyme disease, should be recognized. The lessons painfully learned in syphilis apply here: delays in diagnosis and treatment can result in a treatable, acute illness becoming a chronic one with, in some cases, devastating consequences.*
Table 1.
Neuropsychological Test Results among Patients With Disseminated Lyme Disease

Study

N

Diagnosis

Comparison Subjects

Neuropsychological Tests a

Results

Logigian et al. (23)

27

Late neurologic Lyme disease

None

California Verbal Learning Test, Wechsler memory Scale, Wisconsin Card Sorting Test, Trail Making Test, Rey-Osterrieth Complex Figure Test, Finger Tapping Test, Hooper Visual Organization Test, Benton Face Discrimination Test, Boston Naming Test, Token Test, Oral Word Association Test

56% had memory deficit

Kaplan et al. (56)

20 b

Lyme encephalopathy

11 fibromyalgia and 11 nonpsychotic depressed patients

California Verbal Learning Test, Wechsler memory Scale, Rey-Osterrieth Complex Figure Test, MMPI, Beck Depression Inventory

Lyme disease patients were significantly more impaired on memory tests

Halperin et al. (27)

17

Neurologic Lyme disease

None

California Verbal Learning Test, Wechsler Memory Scaled, Symbol Digit Modalities, Booklet Category Test, Block Design, Purdue Pegboard

Impaired memory, attention, conceptual ability, and motor function; improvement with antibiotics

Krupp et al. (57)

15

Late Lyme disease and cognitive symptoms

10 Healthy age- and sex-matched subjects

WAIS-R c , Trail Making Test, Booklet Category Test, Oral Word Association Test, Wechsler memory Scale, Selective Reminding Test

Lyme disease patients had significantly impaired verbal fluency and memory
a Neuropsychological tests were not administered by individuals who were blind to medical diagnosis.
b A subgroup of patients from the study by Logigian et al. (23)
c Subsets of information, vocabulary, similarities, digit span, block design, object assembly, and digit symbol.

Table 2.
Psychiatric Disorders in Larger Series of Patients With Lyme Disease

Study

N

Diagnosis

Measures

Comparison Group

Results

Comments

Logigian et al. (23)

27

Late neurologic Lyme disease

MMPI (score >70 signified depression)

None

26% had extreme irritability; 33% were depressed

89% had encephalopathy

Barr et al. (71)

88

Lyme disease

Beck Depression Inventory, Spielberger anxiety scale

Seronegative patients

Significantly more depression among seropositive patients

Belman et al. (72)

96 children

Neurologic Lyme disease

Neurologic examination

None

38% had behavioral changes (irritability, lability, poor attention)

Most common system was headaches

Krupp et al. (57)

15

Late Lyme disease and cognitive symptoms

Center for Epidemiologic Studies Depression Scale neuropsychological battery

10 healthy age- and sex-matched subjects

Lyme disease patients were significantly more depressed

The most depressed patients did not have abnormal neuropsychological findings.

Fallon et al. (73)

51

Chronic, seropositive Lyme disease

Survey using DSM-III-R criteria

30 non-Lyme disease patients with arthritis

Lyme disease patients were significantly more likely to have DSM-III-R depression (66% versus 23%)

32% of Lyme disease patients reported panic attacks (versus 19% of comparison patients; n.s.)

Halperin et al. (27)

17

Neurologic Lyme disease

Beck Depression Inventory

None

Mean Beck scores did not show depression

Depressed patients may have beenn excluded from study

Kaplan et al. (56)

20 a

Lyme encephalopathy

Beck Depression Inventory, MMPI

11 fibromyalgia and 11 nonpsychotic depressed patients

Mean Beck scores were not significantly different between groups

Only 13 of the 20 patients completed the Beck inventory

Reik et al. (74)

18

Neurologic Lyme disease

Clinical interview

None

39% had mood lability and irritability; 22% had marked depression

Lyme disease diagnosed by history of erythema migrans or Lyme disease arthritis

Ackerman et al. (32)

44

Borrelia encephalomyelitis

Clinical interview

None

12 patients had mild memory and mood problems; 2 patients had dementia-like deficits

Diagnosis based on intrathecal production of Bb antibodies and clinical features.
a A subgroup of patients from the study by Logigian et al. (23).

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## kcs

This is an excellent article detailing some of the common cognitive problems with neurological lyme disease. I bolded a few that I have heard mentioned on the boards commonly, but am missing a lot I'm sure.

http://www.johndrullelymefund.org/lyme_disease_and_cognitive_impai.htm

*Lyme Disease and Cognitive Impairments*

by Robert Bransfield, M.D.

Introduction

The patient is a college graduate with Lyme encephalopathy (LE). While stopped at a traffic light, she described her thought processes as having a ?fog-like? sluggishness. When the light changes, she knows the change from red to green has significance, but at that moment cannot recall that green means go and red means stop.

This is one of many examples of cognitive impairments associated with Lyme disease. Although some cognitive symptoms are indirectly a result of other neurological or emotional impairments, others are a direct result of dysfunction of the cerebral cortex where cognitive processing occurs. Laboratory tests such as SPECT scans, MRI?s, PET scans, and psychological testing have demonstrated physiological and anatomical findings associated with dysfunction of the cerebral cortex in patients with Lyme and tick-borne diseases. The examination of human and animal brains have further supported these findings.

The cognitive impairments from Lyme disease are very different than we see in Alzheimer?s disease. Lyme disease is predominately a disease of the white matter, while Alzheimer?s is predominately a disease of the gray matter. Memory association occurs in the white matter, while memory is stored in the gray matter. White matter dysfunction is a difficulty with slowness of recall, and incorrect associations. In contrast, gray matter dysfunction is a loss of the information which has previously been stored. For example, and Alzheimer?s patient may not recall the word ?pen?, while an LE patient may have a slowness of recall or retrieval of a closely related word. Some of the symptoms I will describe are also found in encephalopathies associated with other illnesses, such as chronic fatigue syndrome, lupus stroke, AIDS, or other diseases which affect the brain. Although no single sign or symptom may be diagnostic of Lyme disease in a mental status exam, we instead look for a cluster and a pattern of signs and symptoms that are commonly associated with Lyme disease.

Everyone with LE has their own unique profile of symptoms. The assessment of these signs and symptoms is one facet of the total clinical assessment of Lyme disease. There are many ways of categorizing cognitive functioning. Let?s begin with a simple model of perception, encoding these perceptions into memory, processing what we perceive, imagery, and finally organizing and planning a response.

Simple mental functions such as flexing the index finger of the right hand, correlates with a relatively simple brain circuitry. More complex functions such as flying an airplane requires the action of a more integrated neural circuitry. The difference between these two actions is like the difference between playing middle C on a piano vs. a symphony playing an entire concert.

Attention Span

Many Lyme disease patients have acquired attention impairments which were not present before the onset of the disease. There may be difficulty sustaining attention, increased distractibility when frustrated, and a greater difficulty prioritizing which perceptions are deserving of a higher allocation of attention.

If we compare attention span to the lens of a camera, we need the flexibility to constantly shift the allocation of attention dependency upon the current life situation. For example, we shift back and forth between a wide angle and a zoom lens focus to increase or decrease acuity of attention depending on the needs of the current situation. A loss of this flexibility results in some combination of a loss of acuity (hypoacusis), and/or excessive acuity to the wrong environmental perceptions (hyperacusis). Hyperacuity can be auditory (hearing), visual, tactile (touch), and olfactory (smell).

Auditory hyperacusis is the most common. Sounds seem louder and more annoying. Sometimes there is selective auditory hyperacusis to specific types of sounds. Visual hyperacusis may be in response to bright lights or certain types of artificial lighting. Tactile hyperacusis may be in response to tight fitting or scratchy clothing, vibrations, temperature and merely being touched may be painful. Some patients prefer to wear loose fitting sweat suits and are frustrated that being touched can be painful. Olfactory hyperacusis may result in an excessive reactivity to certain smells, such as perfumes, soaps, petroleum products, etc.

Memory

Memory is the storage and retrieval of information for later use. There are several different memory deficits associated with LE. Memory is broken down into several functions ? working memory, memory encoding, memory storage and memory retrieval.

Working memory is a component of executive functioning. An example of working memory is the ability to spell the word ?world? backwards. Sometimes there are impairments of working memory as it pertains to a working spatial memory, i.e. forgetting where doors are located or where a car is parked.

Encoding is the placement of a memory into storage. We cannot retrieve a memory that was not encoded correctly into memory in the first place. One patient described being upset that someone had eaten yogurt in her kitchen during the night. Her activity during the night was not encoded into memory.

Short term (recent) memory is the ability to remember information for relatively brief periods of time. In contrast, long term memory is information from years in the past (or remote). In LE, there is first a loss of short term memory followed by a loss of long term memory very late in the illness. Patients may have slowness of recall with different types of explicit (or factual) information, such as words, numbers, names, faces or geographical/spatial cues. Not as common, there may also be slowness of recall if implicit information, such as tying shoes, or doing other procedural memory tasks.

Errors in memory retrieval include errors with letter and/or number sequences. This can include letter reversals, reversing the sequence of letters in words, spelling errors, number reversals, or word substitution errors (inserting the opposite, closely related or wrong words in a sentence.

Processing
Processing is the creation of associations which allow us to interpret complex information and to respond in an adaptive manner. Some LE patients say they feel like they acquired dyslexia or other learning disabilities, which were not present previously. Examples of processing functions that may be impaired in the presence of LE include the following:

Reading comprehension: The ability to understand what is being read.

Auditory comprehension: The ability to understand spoken language.

Sound localization: The ability to localize the source of a sound.

Visual spatial perception: Impairments result in spatial perceptual distortions. One example is microscopia, in which things seem smaller than they really are. One patient lost depth perception, and had several accidents when the car in front of her stopped. A problem associated with visual spatial processing is optic ataxia, in which there is difficulty targeting movements through space. For example, there may be a tendency to bump into doorways, difficulty driving and parking a car in tight spaces, and targeting errors when placing and reaching for objects. One patient with optic ataxia, was stopped by a policeman while driving two miles to my office because he kept swerving across the center line. Before Lyme disease he could consistently shoot 13 to 14 out of 15 free throws from the basketball foul line. Now he averages 3 of 15, and misses some shots be several feet.

Transposition of laterality: The ability to rotate something 180 degrees in your mind. For example, the ability to copy, rather than mirror, the movements of an aerobics instructor facing you.

Left-right orientation: The ability to immediately perceive the difference between left and right. Although this is a part of congenital Gertsmann?s syndrome or angular gyrus syndrome, acquired left-right confusion is the result of an encephalopathic process.

Calculation ability: The ability to perform mathematical calculations without using fingers or calculators. Many LE patients describe an increased error rate with their checkbook.

Fluency of speech: The ability of speech to flow smoothly. This function is dependent upon adequate speed of word retrieval.

Stuttering: The tendency to stutter when speech is begun with certain sounds.

Slurred speech: A slurring of words, which can give the appearance of intoxication.

Fluency of written language: The ability to express thoughts into writing.

Handwriting: The ability to write words and sentences clearly.

Imagery
Imagery is a uniquely human trait. It is the ability to create what never was within our minds. When functioning properly, it is a component of human creativity, but when impaired, it can result in psychosis. Imagery functions that can be affected by LE include:

Capacity for visual imagery: The ability to picture something, such as a map, in our head.

*Intrusive images: Images that suddenly appear which may be aggressive, horrific, sexual or otherwise.*

Hypnagogic hallucinations: The continuation of a dream, even after being fully awake.

*Vivid nightmares: A tendency towards nightmares of a vivid Technicolor nature.*

*Illusions: Auditory, visual, tactile and/or olfactory perceptions which are distorted or misperceived.*

*Hallucinations: Hearing, seeing, feeling and/or smelling something that is not present. In LE, sometimes this takes the form of hearing music or a radio station in the background. Unlike schizophrenic hallucinations, these are accompanied by a clear sensorium, and the patient is aware hallucinations are present.*

*Depersonalization: A loss of a sense of physical existence.

Derealization: A loss of a sense that the environment is real.
*
Organizing and Planning
Organizing and planning a response is the most complex mental function, and is dependent upon all the functions already described. These functions, along with attention span and working memory, are referred to as executive functioning. Organizing and planning functions that can be
affected by LE include:

Concentration: The ability to focus thought and maintain mental tracking while performing problem solving tasks.

*?Brain fog?: Described by many LE patients. Although difficult to describe in objective, scientific terms: it is best described as a slowness, weakness, and inaccuracy of thought processes. Prioritizing, organizing, and implementing multiple tasks with effective time management.*

Simultasking: The ability to concentrate and be effective while performing multiple simultaneous tasks.

*Initiative: The ability to initiate spontaneous thoughts, ideas and actions rather than being apathetic or merely responding to environmental cues.*

Abstract reasoning: The capacity for complex problem solving.

*Obsessive thoughts: May interfere with productive thought.

Racing thoughts: May interfere with productive thought.*

An assessment of each of these areas of functioning is a critical component in the clinical assessment of LE. The cognitive assessment is only a part of the assessment of LE. Other components include the psychiatric assessment, the neurological assessment, a review of somatic symptoms, epidemiological considerations and laboratory testing when indicated. I have gradually developed a structured cognitive assessment which focuses upon the areas mentioned after examining many patients with late stage neuropsychiatric Lyme disease. I have also incorporated concepts from others that have made major contributions in this area, such as Drs. Rissenberg, Nields, Fallon, Freundlich and Bleiwiss. It is difficult to explain exactly how Lyme disease causes cognitive impairments. The variability of these symptoms suggests an episodic
release of a endotoxin or cytokine which may contribute to the cognitive dysfunction. This is an area where considerable research is needed, and is beyond the scope of this article.

*The symptoms described are often very difficult for patients to describe, and are difficult for many physicians to understand. As a result, patients with these impairments are sometimes erroneously viewed as being hypochondriachal, psychosomatic, depression, or malingering.
These symptoms are real and must be explained: that cannot be discounted as being imaginary.*

There are many treatment strategies. Antibiotics and a number of different psychotropics are helpful to many. I have found Aricept to be helpful in the treatment of ?brain fog? and problems with slowness of retrieval.

To those of you who have LE, be realistic about your limitations and the validity of these limitations. Use strong areas to compensate for areas of weakness. Avoid excessive stress which compounds the problem. Be aware that certain tasks challenge many higher level attributes. Maintain hope and retain an effective working relationship with your family, support system and treatment team.


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## kcs

Here are a few more articles. This first one has pictures, so I won't bother cutting and pasting which would lose the images:
Overview of Neuropsychiatric Lyme Disease

And here is a Symptom List from Canadian Lyme Disease Foundation
Symptoms of Lyme Disease

* The Tick Bite (fewer than 50% recall a tick bite or get/see the rash)

1. Rash at site of bite
2. Rashes on other parts of your body
3. Rash basically circular and spreading out (or generalized)
4. Raised rash, disappearing and recurring

* Head, Face, Neck

5. Unexplained hair loss
6. Headache, mild or severe, Seizures
7. Pressure in Head, White Matter Lesions in Head (MRI)
8. Twitching of facial or other muscles
9. Facial paralysis (Bell's Palsy)
10. Tingling of nose, (tip of) tongue, cheek or facial flushing
11. Stiff or painful neck
12. Jaw pain or stiffness
13. Dental problems (unexplained)
14. Sore throat, clearing throat a lot, phlegm ( flem ), hoarseness, runny nose

* Eyes/Vision

15. Double or blurry vision
16. Increased floating spots
17. Pain in eyes, or swelling around eyes
18. Oversensitivity to light
19. Flashing lights/Peripheral waves/phantom images in corner of eyes

* Ears/Hearing

20. Decreased hearing in one or both ears, plugged ears
21. Buzzing in ears
22. Pain in ears, oversensitivity to sounds
23. Ringing in one or both ears

* Digestive and Excretory Systems

24. Diarrhea
25. Constipation
26. Irritable bladder (trouble starting, stopping) or Interstitial cystitis
27. Upset stomach (nausea or pain) or GERD (gastroesophageal reflux disease)

* Musculoskeletal System

28. Bone pain, joint pain or swelling, carpal tunnel syndrome
29. Stiffness of joints, back, neck, tennis elbow
30. Muscle pain or cramps, (Fibromyalgia)

* Respiratory and Circulatory Systems

31. Shortness of breath, can't get full/satisfying breath, cough
32. Chest pain or rib soreness
33. Night sweats or unexplained chills
34. Heart palpitations or extra beats
35. Endocarditis, Heart blockage

* Neurologic System

36. Tremors or unexplained shaking
37. Burning or stabbing sensations in the body
38. Fatigue, Chronic Fatigue Syndrome, Weakness, peripheral neuropathy or partial paralysis
39. Pressure in the head
40. Numbness in body, tingling, pinpricks
41. Poor balance, dizziness, difficulty walking
42. Increased motion sickness
43. Lightheadedness, wooziness

* Psychological well-being

44. Mood swings, irritability, bi-polar disorder
45. Unusual depression
46. Disorientation (getting or feeling lost)
47. Feeling as if you are losing your mind
48. Over-emotional reactions, crying easily
49. Too much sleep, or insomnia
50. Difficulty falling or staying asleep
51. Narcolepsy, sleep apnea
52. Panic attacks, anxiety

* Mental Capability

53. Memory loss (short or long term)
54. Confusion, difficulty in thinking
55. Difficulty with concentration or reading
56. Going to the wrong place
57. Speech difficulty (slurred or slow)
58. Stammering speech
59. Forgetting how to perform simple tasks

* Reproduction and Sexuality

60. Loss of sex drive
61. Sexual dysfunction
62. Unexplained menstral pain, irregularity
63. Unexplained breast pain, discharge
64. Testicular or pelvic pain

* General Well-being

65. Unexplained weight gain, loss
66. Extreme fatigue
67. Swollen glands/lymph nodes
68. Unexplained fevers (high or low grade)
 69. Continual infections (sinus, kidney, eye, etc.)
70. Symptoms seem to change, come and go
71. Pain migrates (moves) to different body parts
72. Early on, experienced a "flu-like" illness, after which you have not since felt well.
73. Low body temperature
74. Allergies/Chemical sensitivities
75. Increased effect from alcohol and possible worse hangover


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## kcs

This image isn't displaying right for me, but I think it is a problem with my computer - let me know if you can't see it, I think I may have a copy of it saved if so. This is from the Lyme Disease Association website at http://www.lymediseaseassociation.org/ Many doctors still will tell you that there is no lyme disease in "x" state - this map (of CDC cases) shows otherwise.










Here is a similar map for your furry friends - shows incidence of lyme in dogs state by state - http://www.dogsandticks.com/US-map-lyme-disease-dogs/index.html


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## kcs

EDIT - I'm removing the Wikipedia link on the Lyme Disease Controversy, because it has become the target of an editing war between the sides, so the information on there is no longer accurate. If anyone wants some really good information on the controversy, I would instead refer you to the new book, Cure Unknown by Pamela Weintraub. It is an excellent and informative read.

If you got through that and are curious about whether or not your congresspeople are signed on to the lyme bills currently in congress, here is a good link for more info - http://www.lymediseaseassociation.org/HR741/HR741.html - if these bills pass, it will go a long way toward better diagnosis and treatment for lyme.

Ok, I'm tired now, so that is enough for today.
-karen


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## kcs

Ok, just one more for tonight - http://www.10news.com/video/14795018/index.html
This is a video of musician Daryl Hall discussing his battle with Lyme Disease. Not specific to neurocognitive lyme, but a good video nonetheless.
-k


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## kcs

http://www.cumc.columbia.edu/dept/nyspi/flatp/terms.html

*Key Terms*

*Encephalopathy:* disturbance or disease of the brain. In Lyme disease, this term usually refers to the patient who has developed cognitive problems later in the course of Lyme Disease.

*Meningitis:* inflammation of the meninges surrounding the brain. Patients may experience headache, light sensitivity, pain when moving the head, nausea and vomiting. Patients with Lyme Disease typically develop this as an early neurologic reaction to infection with the agent of Lyme disease.
*
Encephalitis: *inflammation of the brain. Patients may experience confusion, irritability, spontaneous tearfulness, geographic disorientation, sleep disturbance, and impaired memory, attention, and/or verbal fluency.

*Encephalomyelitis:* inflammation of the brain and spinal cord. Patients may experience symptoms affecting the brain such as confusion, headache, word-finding problems as well as signs of spinal cord involvement such as weakness, sensory loss in the legs, urinary problems. The cerebrospinal fluid may show abnormalities such as increased white blood cells. Encephalomyelitis may be triggered or perpetuated by viral or other infections such as spirochetal infection with Borrelia burgdorferi. Lyme encephalomyelitis may be mistakenly diagnosed as multiple sclerosis.

*Radiculopathy: *a disturbance in the nerve that may cause shooting pain, numbness or tingling in the distribution of a nerve root. Emanates from the spinal cord. "Sciatica" is a good example of radicular pain in that it starts from the spinal cord and shoots down the leg.

*Erythema Migrans:* an expanding rash that is pathognomonic for Lyme Disease, occurring shortly after the tick bite in many but not all patients. Satellite rashes may occur at later points in the illness. The typical appearance is of a "bull's eye" - a red rash with central clearing that gradually enlarges. The "EM" rash however may have a wide variety of other appearances as well.

*Vasculitis:* inflammation of the blood vessels. Many diseases can cause a vasculitis, such as Lupus, syphilis, cocaine abuse, Lyme disease, and primary angiitis of the central nervous system.

*Herxheimer Reaction: *This typically refers to an exacerbation of symptoms or new onset of symptoms shortly after starting antibiotic therapy. This is thought to be due to a flare of the immune system in response to the killing of the spirochetes. Because of this reaction, it is often the case that a physician will tell the patient: "You feel worse? Terrific! That's a sign you're getting better."

*Seronegativity *This refers to the situation in which blood tests for Lyme disease do not indicate past or current infection. Some patients may in fact test negative because they are being tested too soon after the tick bite or because they have been treated with antibiotics that diminish the immune response.

*PCR (Polymerase chain reaction).* This refers to one of the tests used to help detect the genetic material (DNA or RNA) of the spirochete that causes Lyme Disease. Unlike the ELISA and Western blot which only tell you that a person's immune system has generated antibodies to the spirochete, the PCR actually tells you that pieces of the genetic material of the organism are present. This test is considered to be a stronger indication that the organism that causes Lyme disease is actually present in the body.

*Neuropsychological Testing: *This is not the same as neuropsychiatric testing. Neuropsychiatric testing is not a precise term, but it usually refers to an interview conducted by a psychiatrist who asks about mood, medical status, and cognition (sometimes performing a small set of tests of memory and attention in the office). Neuropsychological Testing refers to a formal battery of tests of brain functions, such as auditory and visual memory, auditory and visual attention, visual motor performance, intelligence, speed of mental processing, verbal fluency, mental flexibility. A comprehensive battery, usually performed by a neuropsychologist, may take 4-8 hours or more.


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## Guest

Dyslexic's wetdream... :roll: :lol:


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## kcs

This link has a lot of information about diagnosis and treatment - http://www2.lymenet.org/domino/file.nsf/UID/guidelines

Good informative link on laboratory testing, and explanation of why tests can be inaccurate in some situations (we need more research!) - Laboratory Testing for Lyme Disease Also has a very in-depth section on Herheimer reaction, here is a quote from it, but the whole section is very interesting:


> In our clinic, prior to starting any antimicrobial therapy, especially if our patient is na?ve to treatment, we emphasize to the patient that they may notice certain significant clinical events while on therapy. In the occasional patient in whom we have no firm diagnosis but where we are suspicious enough to offer short-term empiric oral therapy, we are intentionally a bit vague about providing information to the patient about the Herxheimer effect, as we do not wish to influence a response by suggestion. We have found the Herxheimer response in LD to be as myriad as the course of persistent LD itself. It is na?ve for one to expect to witness simply a flu-like syndrome, although this certainly happens. Instead, generally one sees an intensification of pre-existing symptoms, e.g. increased brain fog or muscle/joint pain, where these symptoms were reported prior to therapy. On the other hand, it is equally common to take reports of new symptoms, e.g. headache in a patient who previously reported symptoms other than headache. In general, the Herxheimer reaction is worse in our most seriously ill patients and most violent at the onset of therapy. The Herxheimer response typically occurs within 3 to 5 days, but may take up to 2 weeks to appear. These symptoms may persist for days or weeks and often become a major management concern as our patient may suffer considerably in the process of treatment. Eventually, as therapy progresses, we tend to witness a dampening of the intensity of the Herxheimer response, as well as some reports of positive clinical gains. Introduction of new therapy, as we cycle antibiotics through our treatment schedule (see treatment program to follow), invariably leads to intensification or new symptoms, all of which are unpleasant. In fact, if we do not observe a new response when therapy is added or substituted, we question the efficacy of our program. Later in this report, we refer to dermal or neurologic Herxheimer phenomena, which we feel reflect local manifestations of pyrogenic cytokines in response to treatment.


-k


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## kcs

http://www.canlyme.com/links.html
This is a very good listing of online support groups and other links by region - there are a number of groups listed for Canada, Europe and Australia too.

There are Yahoo groups set up for every state - if you can't find yours, let me know and I will track it down for you.
-karen


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## kcs

***Sign the petition***
http://www.lymediseaseassociation.org/referral/Petitions/Petition.php?id=1



> Lyme Disease Association, Inc.
> 
> PO Box 1438, Jackson, New Jersey 08527
> 888-366-6611 [email protected] 732-938-7215 (Fax)
> LymeDiseaseAssociation.org
> 
> Petition
> 
> We, the undersigned, are gravely concerned by the new Infectious Disease Society?s (IDSA) guidelines on Lyme disease. These guidelines call for absolute reliance upon either the presentation of an Erythema migrans rash or positive serologic blood tests to diagnose Lyme disease and recommend severely limited courses of antibiotic treatment when either a rash or a positive test are present. They take the place of a longstanding policy of deference to the clinical discretion of the treating physician in both diagnosing and treating the disease. We find it most troubling that the new IDSA guidelines fail to explain the scientific justifications for their absolute reliance upon the rash and current blood testing to diagnose the disease in light of the numerous studies and medical opinions concluding that the rash is either not discovered by or present in many infected persons and that the serologic testing methods recommended by the IDSA are inherently unreliable because they do not even remotely approach a dispositive level of accuracy. Widespread adoption of these guidelines by practitioners, insurers, and government entities will, therefore, cause real and egregious harm to many patients by inhibiting physicians who otherwise would be free to clinically diagnose and treat this disease.
> 
> These guidelines fail to meaningfully address the needs of patients with chronic Lyme disease, who are now relegated to the pile of diseases with unknown etiology, like CFS and FMS, and who are provided with only symptomatic relief, while the underlying infectious disease is allow to progress unabated. Studies have shown that patients with chronic Lyme disease suffer a degree of debility equal to that of patients with congestive heart failure. Failure to address the underlying infectious disease etiology keeps these patients sick, which is inhumane and immoral. There are no chronic Lyme disease patient studies supporting symptomatic therapies, which presumably would be necessary for life at considerable cost to insurers and society. Moreover, the IDSA rejected out-of-hand the requests by patients and their treating physicians to participate in the guideline development process. No medical society should be able to dictate patient healthcare through exclusionary guidelines that ignore considerable scientific evidence and fail to meet the basic goal of medicine-to improve the quality of life of the patient.


http://www.lymediseaseassociation.org/referral/Petitions/Petition.php?id=1


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## kcs

*Has your congressperson signed on to the lyme research bills in congress?* For anyone with lyme, with a family member with lyme, anyone who lives in an endemic area, or anyone who has concerns about the lack of funding for lyme research, be sure that your congresspeople have signed on as co-sponsors of this bill, and if they haven't, then be sure to write to them to urge them to do so.

Here is a list of current co-sponsors of Senate Bill 1708:
http://thomas.loc.gov/cgi-bin/bdquery/z?d110:SN01708:@@@P

And here is a list of current co-sponsors of House Bill 741 (the bills are identical):
http://thomas.loc.gov/cgi-bin/bdquery/z?d110:HR00741:@@@P

http://thomas.loc.gov/cgi-bin/bdquery/z?d110:SN01708:


> S.1708
> Title: A bill to provide for the expansion of Federal efforts concerning the prevention, education, treatment, and research activities related to Lyme and other tick-borne diseases, including the establishment of a Tick-Borne Diseases Advisory Committee.
> Sponsor: Sen Dodd, Christopher J. [CT] (introduced 6/27/2007) Cosponsors (14)
> Related Bills: H.R.741
> Latest Major Action: 6/27/2007 Referred to Senate committee. Status: Read twice and referred to the Committee on Health, Education, Labor, and Pensions.SUMMARY AS OF:
> 6/27/2007--Introduced.
> 
> Lyme and Tick-borne Disease Prevention, Education, and Research Act of 2007 - Requires the Secretary of Health and Human Services to establish the Tick-Borne Diseases Advisory Committee. Requires the Committee to advise the Secretary and the Assistant Secretary for Health regarding how officials can: (1) ensure interagency coordination and communication and minimize overlap regarding efforts to address tick-borne diseases; (2) identify opportunities to coordinate efforts with other federal agencies and private organizations addressing such diseases; (3) ensure interagency coordination and communication with constituency groups; *(4) ensure that a broad spectrum of scientific viewpoints is represented in public heath policy decisions and that information disseminated to the public and physicians is balanced;* and (5) advise relevant federal agencies on priorities related to Lyme and tick-borne diseases.
> 
> Requires the Secretary, acting through the appropriate federal officials, to provide for the coordination of all federal programs and activities related to Lyme and other tick-borne diseases, including: (1) developing sensitive and accurate diagnostic tools and tests, (2) improving the efficient utilization of diagnostic testing currently available; (3) accurately determining the prevalence of such diseases; (4) evaluating the feasibility of creating a national uniform reporting system; (5) providing and promoting access to a clearinghouse of information on such diseases; (6) increasing public education related to such diseases; (7) creating a physician education program; (8) establishing epidemiological research objectives to determine the long term course of illness for Lyme disease; and (9) determining the effectiveness of different treatment modalities by establishing treatment outcome objectives


This link has a lot of additional information, as well as sample letters:
http://www.lymediseaseassociation.org/HR741/HR741.html
-karen


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## kcs

the Lyme Disease Association runs a referral database - http://www.lymediseaseassociation.org/Doctor_Referrals.html - you have to sign up, but it is easy, and worth it to get a referral to an ILADS LLMD.
-k


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## scaredstupid

If you don't mind me asking, about how much does a Lyme test cost. I really want to get tested because I really think it's possible that I have Lyme's, but I'm as broke as a joke.  Would insurance cover this?


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## kcs

It is usually a couple hundred, give or take depending on how many tests they run - if you run a full panel including the co-infections it is a lot more, but that may not be necessary to start with. The most important is the Western Blot. There might be pricing on their website - http://www.igenex.com, not sure. Insurance sometimes covers some of it, but you can't always depend on it. Definitely worth it though, even if you have to scrimp on some other things for awhile, IMHO.
-karen


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## Surfingisfun001

Ya forsure worth it. Scaredstupid you might want to read this guy's story, it's pretty interesting. His DP was induced by marijuana but his actual problem was that he had lyme. Took 10 years to figure out...might be worth it to get tested ASAP.

http://abchomeopathy.com/forum2.php/49698/


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## kcs

I apologize if this is a duplication, I posted this in the other thread and can't remember if I posted it here....

Lyme Disease, Comorbid Tick-Borne Diseases, and Neuropsychiatric Disorders
-k


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## kcs

New study that demonstrates persisting infection after antibiotic treatment, and also demonstrates that Lyme is present even when cultures are negative. This supports what ILADS has been saying all along and proves that the IDSA standard treatment of 3-4 weeks of antibiotics are not enough to get rid of the lyme spirochetes, as well as that lyme tests can be negative when a patient is actually infected with lyme. One more blow to the IDSA viewpoint, the world of veterinary medicine is worlds ahead of human medicine in the diagnosis and treatment of lyme disease.

http://aac.asm.org/cgi/content/abstract/AAC.01050-07v1



> *Persistence of Borrelia burgdorferi Following Antibiotic Treatment in Mice*
> Emir Hodzic, Sunlian Feng, Kevin Holden, Kimberly J. Freet, and Stephen W. Barthold*
> 
> Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California at Davis, One Shields Avenue, Davis, CA 95616
> 
> * To whom correspondence should be addressed. Email: [email protected].
> 
> Abstract
> 
> The effectiveness of antibiotic treatment was examined in a mouse model of Lyme borreliosis. Mice were treated with ceftriaxone or saline for one month, commencing during the early (3 weeks) or chronic (4 months) stages of infection with Borrelia burgdorferi. Tissues from mice were tested for infection by culture, polymerase chain reaction (PCR), xenodiagnosis, and transplantation of allografts at 1 and 3 months after completion of treatment. In addition, tissues were examined for spirochetes by immunohistochemistry. In contrast to saline-treated mice, mice treated with antibiotic were consistently culture-negative, but tissues from some of the mice remained PCR-positive, and spirochetes could be visualized in collagen-rich tissues. Furthermore, when some of the antibiotic treated mice were fed upon by Ixodes scapularis ticks (xenodiagnosis), spirochetes were acquired by the ticks, based upon PCR, and ticks from those cohorts transmitted spirochetes to na?ve SCID mice, which became PCR-positive, but culture-negative. Results indicated that following antibiotic treatment, mice remained infected with non-dividing but infectious spirochetes, particularly when antibiotic treatment was commenced during the chronic stage of infection.


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## kcs

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18097481

*The Pathogenesis of Lyme Neuroborreliosis: From Infection to Inflammation*

Abstract
This review describes the current knowledge of the pathogenesis of acute Lyme neuroborreliosis (LNB), from invasion to inflammation of the central nervous system. Borrelia burgdorferi (B.b.) enters the host through a tick bite on the skin and may disseminate from there to secondary organs, including the central nervous system. To achieve this, B.b. first has to evade the hostile immune system. In a second step, the borrelia have to reach the central nervous system and cross the blood?brain barrier. Once in the cerebrospinal fluid (CSF), the spirochetes elicit an inflammatory response. We describe current knowledge about the infiltration of leukocytes into the CSF in LNB. In the final section, we discuss the mechanisms by which the spirochetal infection leads to the observed neural dysfunction. To conclude, we construct a stringent concept of the pathogenesis of LNB.


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## kcs

I just wanted to post some information about the recent IDSA settlement with CT Attorney General Blumenthal in the antitrust lawsuit, as it really highlights what is going on politically with this mess, and why people are having so much trouble getting a diagnosis. It also really shows how important it is to see an ILADS doctor as opposed to an infectious disease doc, since most infectious disease docs follow the flawed IDSA guidelines. If you have read news reports about this, you are likely missing a lot of the story. Ok, here's the official press release from Blumenthal, definitely worth reading, and will probably shock the crap outta ya:
http://www.ct.gov/ag/cwp/view.asp?a=2795&q=414284



> Connecticut Attorney General's Office
> 
> Press Release
> 
> Attorney General's Investigation Reveals Flawed Lyme Disease Guideline Process, IDSA Agrees To Reassess Guidelines, Install Independent Arbiter
> 
> May 1, 2008
> Attorney General Richard Blumenthal today announced that his antitrust investigation has uncovered serious flaws in the Infectious Diseases Society of America's (IDSA) process for writing its 2006 Lyme disease guidelines and the IDSA has agreed to reassess them with the assistance of an outside arbiter.
> 
> The IDSA guidelines have sweeping and significant impacts on Lyme disease medical care. They are commonly applied by insurance companies in restricting coverage for long-term antibiotic treatment or other medical care and also strongly influence physician treatment decisions.
> 
> Insurance companies have denied coverage for long-term antibiotic treatment relying on these guidelines as justification. The guidelines are also widely cited for conclusions that chronic Lyme disease is nonexistent.
> 
> "This agreement vindicates my investigation -- finding undisclosed financial interests and forcing a reassessment of IDSA guidelines," Blumenthal said. "My office uncovered undisclosed financial interests held by several of the most powerful IDSA panelists. The IDSA's guideline panel improperly ignored or minimized consideration of alternative medical opinion and evidence regarding chronic Lyme disease, potentially raising serious questions about whether the recommendations reflected all relevant science.
> 
> "The IDSA's Lyme guideline process lacked important procedural safeguards requiring complete reevaluation of the 2006 Lyme disease guidelines -- in effect a comprehensive reassessment through a new panel. The new panel will accept and analyze all evidence, including divergent opinion. An independent neutral ombudsman -- expert in medical ethics and conflicts of interest, selected by both the IDSA and my office -- will assess the new panel for conflicts of interests and ensure its integrity."
> 
> Blumenthal's findings include the following:
> 
> * The IDSA failed to conduct a conflicts of interest review for any of the panelists prior to their appointment to the 2006 Lyme disease guideline panel;
> 
> * Subsequent disclosures demonstrate that several of the 2006 Lyme disease panelists had conflicts of interest;
> 
> * The IDSA failed to follow its own procedures for appointing the 2006 panel chairman and members, enabling the chairman, who held a bias regarding the existence of chronic Lyme, to handpick a likeminded panel without scrutiny by or formal approval of the IDSA's oversight committee;
> 
> * The IDSA's 2000 and 2006 Lyme disease panels refused to accept or meaningfully consider information regarding the existence of chronic Lyme disease, once removing a panelist from the 2000 panel who dissented from the group's position on chronic Lyme disease to achieve "consensus";
> 
> * The IDSA blocked appointment of scientists and physicians with divergent views on chronic Lyme who sought to serve on the 2006 guidelines panel by informing them that the panel was fully staffed, even though it was later expanded;
> 
> * The IDSA portrayed another medical association's Lyme disease guidelines as corroborating its own when it knew that the two panels shared several authors, including the chairmen of both groups, and were working on guidelines at the same time. In allowing its panelists to serve on both groups at the same time, IDSA violated its own conflicts of interest policy.
> 
> IDSA has reached an agreement with Blumenthal's office calling for creation of a review panel to thoroughly scrutinize the 2006 Lyme disease guidelines and update or revise them if necessary. The panel -- comprised of individuals without conflicts of interest -- will comprehensively review medical and scientific evidence and hold a scientific hearing to provide a forum for additional evidence. It will then determine whether each recommendation in the 2006 Lyme disease guidelines is justified by the evidence or needs revision or updating.
> 
> Blumenthal added, "The IDSA's 2006 Lyme disease guideline panel undercut its credibility by allowing individuals with financial interests -- in drug companies, Lyme disease diagnostic tests, patents and consulting arrangements with insurance companies -- to exclude divergent medical evidence and opinion. In today's healthcare system, clinical practice guidelines have tremendous influence on the marketing of medical services and products, insurance reimbursements and treatment decisions. As a result, medical societies that publish such guidelines have a legal and moral duty to use exacting safeguards and scientific standards.
> 
> "Our investigation was always about the IDSA's guidelines process -- not the science. IDSA should be recognized for its cooperation and agreement to address the serious concerns raised by my office. Our agreement with IDSA ensures that a new, conflicts-free panel will collect and review all pertinent information, reassess each recommendation and make necessary changes.
> 
> "This Action Plan -- incorporating a conflicts screen by an independent neutral expert and a public hearing to receive additional evidence -- can serve as a model for all medical organizations and societies that publish medical guidelines. This review should strengthen the public's confidence in such critical standards."
> 
> THE GUIDELINE REVIEW PROCESS
> 
> Under its agreement with the Attorney General's Office, the IDSA will create a review panel of eight to 12 members, none of whom served on the 2006 IDSA guideline panel. The IDSA must conduct an open application process and consider all applicants.
> 
> The agreement calls for the ombudsman selected by Blumenthal's office and the IDSA to ensure that the review panel and its chairperson are free of conflicts of interest.
> 
> Blumenthal and IDSA agreed to appoint Dr. Howard A. Brody as the ombudsman. Dr. Brody is a recognized expert and author on medical ethics and conflicts of interest and the director of the Institute for Medical Humanities at the University of Texas Medical Branch. Brody authored the book, "Hooked: Ethics, the Medical Profession and the Pharmaceutical Industry."
> 
> To assure that the review panel obtains divergent information, the panel will conduct an open scientific hearing at which it will hear scientific and medical presentations from interested parties. The agreement requires the hearing to be broadcast live to the public on the Internet via the IDSA's website. The Attorney General's Office, Dr. Brody and the review panel will together finalize the list of presenters at the hearing.
> 
> Once it has collected information from its review and open hearing, the panel will assess the information and determine whether the data and evidence supports each of the recommendations in the 2006 Lyme disease guidelines.
> 
> The panel will then vote on each recommendation in the IDSA's 2006 Lyme disease guidelines on whether it is supported by the scientific evidence. At least 75 percent of panel members must vote to sustain each recommendation or it will be revised.
> 
> Once the panel has acted on each recommendation, it will have three options: make no changes, modify the guidelines in part or replace them entirely.
> 
> The panel's final report will be published on the IDSA's website.
> 
> ADDITIONAL FINDINGS OF BLUMENTHAL'S INVESTIGATION
> 
> IDSA convened panels in 2000 and 2006 to research and publish guidelines for the diagnosis and treatment of Lyme disease. Blumenthal's office found that the IDSA disregarded a 2000 panel member who argued that chronic and persistent Lyme disease exists. The 2000 panel pressured the panelist to conform to the group consensus and removed him as an author when he refused.
> 
> IDSA sought to portray a second set of Lyme disease guidelines issued by the American Academy of Neurology (AAN) as independently corroborating its findings. In fact, IDSA knew that the two panels shared key members, including the respective panel chairmen and were working on both sets of guidelines a the same time -- a violation of IDSA's conflicts of interest policy.
> 
> The resulting IDSA and AAN guidelines not only reached the same conclusions regarding the non-existence of chronic Lyme disease, their reasoning at times used strikingly similar language. Both entities, for example, dubbed symptoms persisting after treatment "Post-Lyme Syndrome" and defined it the same way.
> 
> When IDSA learned of the improper links between its panel and the AAN's panel, instead of enforcing its conflict of interest policy, it aggressively sought the AAN's endorsement to "strengthen" its guidelines' impact. The AAN panel -- particularly members who also served on the IDSA panel -- worked equally hard to win AAN's backing of IDSA's conclusions.
> 
> The two entities sought to portray each other's guidelines as separate and independent when the facts call into question that contention.
> 
> The IDSA subsequently cited AAN's supposed independent corroboration of its findings as part of its attempts to defeat federal legislation to create a Lyme disease advisory committee and state legislation supporting antibiotic therapy for chronic Lyme disease.
> 
> In a step that the British Medical Journal deemed "unusual," the IDSA included in its Lyme guidelines a statement calling them "voluntary" with "the ultimate determination of their application to be made by the physician in light of each patient's individual circumstances." In fact, United Healthcare, Health Net, Blue Cross of California, Kaiser Foundation Health Plan and other insurers have used the guidelines as justification to deny reimbursement for long-term antibiotic treatment.
> 
> Blumenthal thanked members his office who worked on the investigation -- Assistant Attorney General Thomas Ryan, former Assistant Attorney General Steven Rutstein and Paralegal Lorraine Measer under the direction of Assistant Attorney General Michael Cole, Chief of the Attorney General's Antitrust Department.


Here is the text of the actual settlement: http://www.ct.gov/ag/lib/ag/health/idsaagreement.pdf

Now with this information in mind, go and reread the Wiki page on the lyme disease controvery: http://en.wikipedia.org/wiki/Lyme_disease_controversy
-k


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## kcs

And also wanted to post some information about current media...

The film Under Our Skin recently opened at the Tribeca Film Festival, and is currently doing the film festival route - they are still figuring out how it will be released, TV or theatres, but there are some screenings happening in some areas of the country: http://www.openeyepictures.com/underourskin/index.html

The book Cure Unknown by Pamela Weintraub will be released on June 10 - it is supposed to be an excellent and comprehensive look at lyme disease, and the controversy surrounding it, Weintraub is a writer for Discover magazine, so you know it will be well written - http://www.amazon.com/exec/obidos/t...t_shr?_encoding=UTF8&m=ATVPDKIKX0DER&v=glance

There are also two magazine articles currently, Psychology Today has an excerpt from Pamela Weintraub's book in the June issue, and also, the June issue of Self Magazine has an article by one of the editors about her bout with neurological lyme disease. Both articles are definitely worth reading.

And lastly, CALDA, the California Lyme Disease Association, has just finished their new website which is very comprehensive, and worth checking out, even for those who are not in California - http://www.lymedisease.org/
-k


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## kcs

http://www.lymeneteurope.org/


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## kcs

I posted this info in my journal, but wanted to post it here as well...

This weekend I saw the movie Under Our Skin, awesome movie, I can't recommend it enough to anyone wanting to learn more about lyme disease, and the controversy surrounding it. Amazing movie, artfully shot, comprehensive, and really gets the point across about what is going on currently with the lyme wars. They are currently working on securing distribution for it, it is doing the film festival rounds right now, and there are a few community screenings planned which are listed on the website. You can also get a prerelease version (movie only, no extras) here, that is how I was able to see it - you want the home version, which is about $34.

Also, the book Cure Unknown by Pamela Weintraub just came out yesterday, and is getting rave reviews - she is an editor/writer at Discover Magazine, so her approach to science writing is very sound. I picked up a copy at Barnes and Noble, they had it already at the one I went to luckily, it will probably take me awhile to get through it though, since my reading abilities have really suffered due to the lyme. She goes into great detail about the controversy as well, and has some amazing insights into what is going on. Amazon link

-k


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## kcs

Finished reading Cure Unknown - if you have any interest in what is going on at all, you owe it to yourself to read this book, it is very well written, and will piss you off when you understand what has been happening and why. Check out the website at http://www.cureunknown.com/, you can read the first few chapters there....
-karen


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## kcs

> Distinct Pattern of Cognitive Impairment Noted in Study of Lyme Patients
> 
> Marian Rissenberg PhD & Susan Chambers MD, The Lyme Times, Vol. 20, Jan-Mar 1998, pp. 29-32
> I. Cognitive Characteristics of Chronic Lyme Encephalopathy
> 
> On the basis of both a formal neuropsychological study of 49 patients (APA 5/96) and on clinical observation and comprehensive neuropsychological examination of well over 100 patients, a distinct pattern of cognitive impairment occurring chronic Lyme disease can be described. These patients consistently demonstrate deficits in directed, sustained and divided attention, planning and organization of responses, temporal ordering, verbal fluency, abstract reasoning, speed of processing, and motor programming. The overall pattern of intellectual impairment is not unlike that seen with diffuse brain injury, and it most often results in some degree of work-related disability.
> 
> Although performance is impaired on measures of cognitive functions associated with specific brain regions -- receptive and expressive language, visuospatial problem solving and memory -- the quality of performance is not suggestive of focal lesions in these areas. Rather, deficits are secondary to impairment of higher level integrative functions, likely mediated by complex neuronal systems. Specifically, the receptive language deficit is secondary to impaired auditory tracking and slowing of mental processing. The expressive language deficit is secondary to impaired word retrieval and response planning, The visuospatial problem solving deficit is secondary to impairment of mental flexibility, conceptualization and the ability to compare and contrast necessary in decision making. Finally, deficits on test of memory function are most often secondary to impairment of the encoding or initial processing of information, which depends on attention, and the retrieval of stored information. The storage of new information, or memory per se, is rarely impaired.
> 
> This pattern suggests that cognitive dysfunction in chronic Lyme, while expressed variably across individual patients, results from a common factor -- the breakdown of diffusely represented processes involving both integration and activation, and impacting primarily on attention and reasoning. The fluctuation of impairment over short periods of time suggest that a physiologic rather than a structural mechanism is responsible.
> 
> II. Neuropsychological deficits in chronic Lyme disease
> (A study presented at the annual meeting of The American Psychiatric Association , May 1996)
> 
> The neuro-psychological characteristics of 49 patients with Lyme disease were examined. The study set out to answer three questions:
> 
> 1) Do all patients with subjectively perceived cognitive dysfunction have measurable intellectual impairment on objective testing?
> 
> 2) In those without measurable impairment, does depression account for the perception of cognitive dysfunction?
> 
> 3) What is the nature of the cognitive impairment in Lyme disease when it does occur?
> 
> Subjects were patients seen consecutively between 1990 and 1994 in a private neuropsycological practice with complaints of cognitive dysfunction and a symptom complex consistent with Lyme disease. Diagnosis was based on former CDC criteria. Mean duration of illness, defined as the time from the onset of general symptoms to the neuro-psychological exam, was 4.7 years (range: 3.3 to 14 years). Mean age was 39.9 years (range: 21 to 58 years) from 18 to 60 years. Mean level of education was 15.3 years (range 12 to 20 years).
> 
> Subjects were interviewed and administered a comprehensive battery of tests, including the complete WAIS-R and WMS-R, and additional test of language, attention, reasoning, visuospatial processing and complex motor function. They also completed the Beck Depression Inventory and a symptom checklist. Tests were divided into seven groups based on the cognitive functions they are presumed to measure: Attention, Memory, Language, Visuospatial Processing, Reasoning, Verbal Fluency and Motor programming.
> 
> Subjects were grouped into three levels of impairment based on their neuropsychological performance: Intact (N=11; 22%), with no functions impaired, Moderate (N=31; 63%) with two functions impaired, and Severe (N=7; 14%) with three or more functions impaired. Subjects in the Severe group met diagnostic criteria for dementia. The correlation between depression and cognitive impairment was nonsignificant, but the trend was positive, rather that negative. Anxiety by self report was significantly greater in the impaired groups that the Intact group. Duration of illness was greater in the Severe group (nonsignificant).
> 
> Of the 38 subjects with cognitive impairment, deficits of attention were most common, occurring in 26 subjects (68%) Deficits of memory storage were least common, occurring in 8 subjects (21%), Motor, Verbal Fluency, Visuospatial, Language and Reasoning deficits occurred in 24, 26, 29, 36 and 36% of the subjects respectively.
> 
> III. Possible Pathophysiologic Mechanisms of Cognitive Impairment in Lyme Disease
> 
> Based on these findings and on patients' reports, two characteristics of Lyme Encephalopathy arise which provide insight as to possible neurophysiologic mechanisms:
> 
> One, the nonfocal nature of the cognitive functions affected, and
> 
> Two, the subtle fluctuations and reportedly abrupt and global shifts in cognitive function from one day to another in a given patient.
> 
> Four broad categories of possible neurophysiologic mechanisms might be compatible with this pattern:
> 
> 1) Diffuse cerebral diffusion abnormalities -- Single photon emission computerized tomography (SPECT) scans of the brain in Lyme disease often display a diffuse pattern consistent with heterogeneous areas of hyperfusion and/or diminished neuronal metabolism. While vasodilators are often capable of reversing these abnormal patterns on SPECT scan, this reversal does not consistently correlate with a symptomatic improvement in cognitive function.
> 
> 2) Alterations in cellular metabolism at the cortical level -- Evidence of alterations in neurotransmitter function is suggested by clinical evidence of cognitive improvement following treatment with selective serotonin reuptake inhibitors (SSRI's) which appears to be independent of their antidepressant effect. Systematic studies of the impact of SSRI's on cognitive function, as well as the role of other transmitters, are required.
> 
> 3) Neuro transmitter abnormalities (imbalances of synthesis and/or receptor activity) -- Neurotoxic substances may well play a role in Lyme Encephalopathy, given the neurotropic nature to Treponema pallidim, and the close parallel between syphilis and Lyme disease, it is possible that Borrelia burgdorferi could produce intracellular or extracellular neurotoxins which we have yet to identify.
> 
> 4) Neurotoxic substances produced endogenously or possibly exogenously -- Endogenous neurotoxins have been identified as by-products of the humoral immune response. Among these is quinolinic acid, a product of the interleukin cascade system, which accumulates as a result of the humoral response to acute infectious agents and functions as a neuronal excitotoxin. As there are many similarities between Lyme Encephalopathy and the nonspecific mental dysfunction of acute systemic infections, such as influenza, it is quite possible that continued stimulation of production of quinolinic acid and other cytokines plays a role in the pathophysiology of Lyme encephalopathy.
> 
> IV. Clinical Impressions and Implications for Diagnosis and Treatment in Chronic Lyme Disease
> 
> This study demonstrates that for the majority of chronic Lyme patients with cognitive complaints, there is in fact a measurable and significant decline in intellectual acuity. The nature and severity of the cognitive impairment is such that it interferes with all aspects of normal functioning: employment, home, marriage, social interactions, and general emotional well-being. Rather than the cognitive complaints being secondary to anxiety or depression, as is sometimes suspected, depression and anxiety increase with, and are apparently secondary to, cognitive impairment and the emotional and practical impact of a loss of competence. Thus, while patients with chronic Lyme disease can present a confusing and "psychiatric" picture to the clinician, it is important that their concerns be properly investigated and addressed.
> 
> Patients with Lyme encephalopathy complain of problems with memory and concentration, word retrieval, confusion, problems with thinking, "mental fogginess", a decline in job performance, difficulty with calculations, directions, and judgment. Decreased initiative, manifest as difficulty getting started with or following through with projects is often noted. Mood disturbance is common with complaints of irritability, explosiveness or "a short fuse," sadness, hopelessness or guilt, increased anxiety or mood swings. Sleep disturbance is also common, and can present as initial, middle or terminal insomnia or some combination of these. Fatigue is universal. Headache is common, and of course joint and muscle pain. Increased sensitivity to light and noise, visual disturbance, and tingling in the extremities are also common.
> 
> On interview, patients with Lyme encephalopathy tend to be vague and disorganized in the presentation of the history of their illness. This is despite their close attention to their symptoms and having recounted them many times before. Although in most cases memory of discreet events - tests, dates, diagnoses, responses to medications - is intact, the patient is unable to recall them spontaneously or organize them in temporal order. They may be unclear as to their chief complaint. They may completely lose track of what they were saying, sometimes repeatedly, or of what the question was. They may get off on a tangent and have trouble re-orienting themselves. Frequent prompting and refocusing will be necessary; beginning the interview with an open-ended question like "Tell me what the problem is" will allow these qualities to become clear.
> 
> Often patients with chronic Lyme disease will seem overly focused on their illness, or overly concerned with convincing the clinician that they are ill. The clinician may be tempted to interpret this as evidence of a primary psychiatric disorder. It is important to understand that the frustration many of these patients experience is real, and results from the general attitude of doubt toward Lyme disease as a serious and chronic illness, the invisibility of their symptoms, the difficulty in getting a definitive diagnosis and getting approval for extended treatment from insurance carriers. Many have been accused of hypochondriasis or malingering. As with head injury, the patient may "look fine" though they are having difficulty with very basic work, social and day to day functioning.
> 
> The cognitive deficits in chronic Lyme disease involve primarily attention and arousal mechanisms. Patients have difficulty keeping track of external and internal events, retrieval of information from memory and with planning and sequencing, as occurs in attention deficit disorder. However their experience is different from that of ADD, in that rather than having the experience that there are many thoughts competing for attention, the Lyme patient has difficulty bringing any thought into clear focus. They experience difficulty thinking. One patient described it as the universe ending six inches from his face. He can't process information that is not immediately apparent, immediately experienced. Another said that when he tries to think about something, or figure something out, all he can do is repeat the question -- he can't get to the meaning. This is like the idea of "surface" versus "deep" processing in cognitive psychology. Reading a passage for typing errors would be surface processing, while reading for meaning is deep processing. One patient, a physician, described it as a "mental intention tremor" -- the more she tries to focus on something the more out of focus it becomes.
> 
> The clinician should proceed with empathy and reason. Specific cognitive complaints in previously high functioning individuals are unusual and indicative of serious illness, either psychiatric or neurologic. Comprehensive neuropsychological evaluation will most often differentiate the two.
> 
> Where the neuropsychological exam is normal or there is a significant psychiatric component, a psychiatric evaluation is advised. Psychiatric symptomatology is not uncommon in Lyme and the presence of depression, anxiety, obsessive compulsive symptoms, flat affect and so on may cloud the issue of significant cognitive decline. Both the cognitive and psychiatric symptoms would be expected to improve with antibiotic treatment in Lyme encephalopathy. However sometimes concurrent treatment with psychotropic medication is necessary.
> 
> Unfortunately for some patients, significant cognitive impairment persists even after years of antibiotic treatment. These patients may never be able to return to their premorbid level of employment, or be gainfully employed at all. Cognitive remediation can help them learn strategies for improving memory and concentration and relieving stress. Support and advice in regard to living with a chronic condition is equally important. Strategies include reducing work hours when possible, taking regular rest periods during the day, limiting the number of outings in a week, and using a calendar to stay organized and structure their time.
> 
> V. Cognitive impairment in Lyme disease: specific functions and the impact of deficits
> 
> 1. Attention and mental tracking. Includes directed and sustained attention: the ability to direct and maintain one's focus on a particular event or idea, whether in the environment or internally; and divided attention: the ability to simultaneously attend to two events, or do two or more things at a time, or to retain awareness of one thing while doing another.
> 
> Impact: difficulty functioning effectively in many situations, remembering what one was doing before a distraction, keeping track of conversation, taking notes while someone is speaking, remembering that someone is on hold, or what you were about to say.
> 
> 2. Memory: Retaining new information.
> 
> Impact: secondary to impaired attention, slowing of processing and the retrieval of stored information, but not storage per se; a tendency to lose or forget things; miss appointments; repeat oneself.
> 
> 3. Receptive language: understanding spoken or written language
> 
> Impact: secondary to impaired attention and speed of processing; difficulty participating in meetings or social conversation; difficulty with reading comprehension.
> 
> 4. Expressive language: Using spoken or written language to express ideas
> 
> Impact: difficulty finding the right word; using the wrong word and not noticing; not being able to express oneself or communicate.
> 
> 5. Visuospatial Processing: Efficient scanning of the visual field, making sense of how things are related in space; visuospatial conceptualization and problem solving.
> 
> Impact: a tendency to get lost; difficulty with reading comprehension.
> 
> 6. Abstract reasoning: The ability to generalize from the particular; to identify the common factor between related concepts; to compare and contrast two things or ideas; to see the "big picture"; to identify the critical factor in a situation; to anticipate consequences and make inferences regarding cause and effect.
> 
> Impact: difficulty with decision making, planning, and problem solving.
> 
> 7. Speed of mental and motor processing: The ability to think and respond quickly; critical to understanding speech which occurs at a fairly constant rate.
> 
> Impact: difficulty understanding or keeping up a conversation; functioning in a timely manner in day to day situations; meeting deadlines.


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## BusyBee

kcs said:


> I know there is another thread about lyme disease from awhile back, but it is not titled as such, so is likely to be overlooked. Here is a link to the original thread for anyone who is interested. I wanted to start a thread where I could post studies and articles regarding lyme disease and some of the psychiatric problems including DP and DR specifically, as well as links to more general information about lyme disease for anyone who wants to look into it further. For a bit of background, I was recently diagnosed with lyme disease after being sick for well over 15 years, with derealization being my first and most oppressive symptom. For anyone who wants more background on me specifically and how I am doing, I started a journal of sorts in the Road to Recovery section, here is a link to that - my lyme journal.
> 
> I will be posting information and articles in this thread sporadically, depending on how I am feeling at the moment (I am pretty darn sick at this point), and what information I find or already have bookmarked. Anyone else with information is more than welcome to post as well, hopefully this will turn into a comprehensive thread on lyme disease and DP/DR.
> 
> -karen


Hi, im wondering if you can help me. My doctors sent me away after testing for the obvious; anemia, thyroid, blood disorders, auto immunes, brain scan, ECG.
TWO MONTHS into feeling so ill and depersonalised Dr Bee had an idea.. Lyme desease. I went to the Doctors the next day and suggested it to him. He said, 'well done' and ordered a blood test immidiatly.
Results came back negative. I know that Lyme is difficult to detect on blood samples alone when in the early stages.. do you think there is a chance that i could still have it?


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## cbeck

kcs said:


> Finished reading Cure Unknown - if you have any interest in what is going on at all, you owe it to yourself to read this book, it is very well written, and will piss you off when you understand what has been happening and why. Check out the website at http://www.cureunknown.com/, you can read the first few chapters there....
> -karen


Hey Karen, here we are so many years later. I went down the road of cfids to eventually find out that I had Lyme disease. I was treated aggresively by a LLMD and my dr was way worse, after 6-7 months of hard IV drips i just gave up. Little did I know that I came out of dr and was so involved in life thatI barely thought about it. Scared to even come back here. Now I am back, I have relapsed. I have an appt. the 27th with my Lyme Doc. in the Bay area. Just wierd that you ended up on the same road. I became ill in 1999. Had 4 great years of no dr. Let me know how you are doing or shoot me an email @ [email protected]
Clay


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