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Can someone define exactly what is meant by cognitive impairment?
I posted before about an ID doc I'm currently seeing. He wants me to try IV antibiotics for a month or two.
I can think straight enough to answer questions, do some research, etc.
However, for the last couple of months, my head seems foggy and long-term concentration is VERY difficult.
Prior this the last 8-9 months, I was very mentally clear and held a great job. Life has been a lot different.
Is it safe to assume Lyme or coinfections has gotten to my central nervous system? Can oral antibiotics really help with this issue?
Posts: 7545 | From The 5th Dimension - The Twilight Zone | Registered: Mar 2008
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Frequent Contributor (5K+ posts)
Member # 15067
I forgot to mention that I do not have trouble remembering places or how to get to them.
I can handle day-to-day functions, BUT ones that require significant concentration give me more issues.
Staring at the computer screen working on spreadsheets is one thing that really is difficult. Unfortunately, that is what I do for a career.
Posts: 7545 | From The 5th Dimension - The Twilight Zone | Registered: Mar 2008
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It sounds like you and I are in a similar situation! I am not sure of the answer to your question.
However, I have been working with my concentration issues for a while. What works for me is to try to eliminate distractions, especially self-created distractions.
Distractions, e.g., email, news, dishes, "hmm... what's for dinner" etc.
So, I use my potential distractions as a reward. For example, I can check my email once I finish this particular batch of work. Works OK.
Posts: 636 | From Saratoga County, NY | Registered: Apr 2008
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"Cognitive impairment" is sort of a slippery term, as it can refer to pretty much any state in which a person's ability to process and store information is, well... impaired. The cognitive impairment one experiences as a result of a depressive disorder is nothing like the cognitive impairment one might experience as a result of, oh say... Huntington's disease, yet the same term is used to describe each. It can be somewhat problematic.
So it seems that you are experiencing some degree of "cognitive impairment." It may or may not be because the Lyme is in your central nervous system. I've heard that due to toxin release and the like, the spirochete doesn't necessarily have to be in your brain to cause concentration issues, etc. It's probably safest, though, to just assume that it is and treat accordingly.
And yes, although IV is most ideal in this situation, oral antibiotics can still help a lot, especially if you take large doses of one (or two) that penetrates the blood-brain barrier well, like the tetracyclines or cephalosporins. Doxycycline and cefuroxime axetil would be good examples of each, respectively.
Heh. I hope that wasn't too long-winded for you.
Posts: 20 | From Portland, Oregon | Registered: Feb 2008
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SUMMARY: The following items are covered: Cognitive Characteristics of Chronic Lyme Encephalopathy, Neuropsychological deficits, Possible Pathophysiologic Mechanisms of Cognitive Impairment in Lyme Disease, Clinical Impressions and Implications for Diagnosis and Treatment in Chronic Lyme Disease, Cognitive impairment in Lyme disease: specific functions and the impact or deficits.
Distinct pattern of cognitive impairment noted in study of Lyme patients by Marian Rissenberg, Ph.D. & Susan Chambers, M.D. the Lyme Times, Vol. 20, January-March 1998, pp. 29 -32
1) 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.
2) 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.
3) 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.
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 continue stimulation of production of quinolinic acid and other cytokines plays a role in the pathophysiology of Lyme encephalopathy.
4) 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 carries.
Many have been accused of hypochondriasis or malingering. As with head injury, the patient may "look fin" 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.
5) Cognitive impairment in Lyme disease: specific functions and the impact or 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 dot 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.
SUMMARY: The following items are covered: Typical time course, symptoms, cognitive and psychiatric aspects for both children and adults.
Overview of Neuropsychiatric Lyme Disease * Typical time course * Symptoms * Adults-Cognitive Aspects * Adults - Psychiatric Aspects * Neuropsychiatric Problems in Children * Children-Cognitive Aspects * Children-Psychiatric Aspects
Lyme disease may affect the brain in many ways, the most common of which is a disturbance in thinking (cognition). Other symptoms that occur frequently include headache, mood swings, irritability, depression, and marked fatigue.
This section will describe some of the typical and less typical features of neuropsychiatric Lyme disease in adults. Lyme Disease is transmitted by an Ixodes tick infected with Borrelia burgdorferi.
Borrelia burgdorferi Ixodes Scapularis Tick The spirochete which causes Lyme disease (Borrelia burgdorferi) can invade the central nervous system within days to a week of initial skin infection, as a result of dissemination through the blood stream.
The majority of patients who are treated early with antibiotics do well and incur no long term problems. Patients who are not treated until later in the illness may have a more complicated course.
While the symptoms often seen among patients with neuropsychiatric Lyme Disease are not specific to Lyme Disease and can also be found in other disorders, knowing the typical clusters of symptoms can be helpful when considering Lyme Disease as a possible diagnosis.
The more multi-systemic the symptom presentation and the more clinical features observed in a patient from the list below, the more strongly Lyme disease should be considered. Other diagnostic possibilities need to be considered in the differential diagnosis, such as mood or anxiety disorders, collagen vascular or autoimmune diseases, spinal cord compression, multiple sclerosis, metastatic diseases, endocrinological disorders, fibromyalgia, chronic fatigue syndrome, and residual damage from past brain trauma or toxin exposure.
A few points should be emphasized regarding late neuropsychiatric Lyme Disease. First, although arthritis is helpful in the diagnosis of Lyme disease, the majority of patients with cognitive troubles due to Lyme disease (Lyme Encephalopathy) do not have joint problems at the time their cognitive symptoms become manifest.
This is not widely recognized among physicians, although it is well documented in the medical literature. Second, the bedside neurologic exam does not usually disclose neurologic findings and standard office-based cognitive screening tests may not detect cognitive impairment. To detect thinking problems, the more sensitive tool of comprehensive neuropsychological testing conducted by a neuropsychologist is needed.
Third, lumbar puncture while important in the differential diagnosis should not be used to exclude neurologic Lyme disease, as roughly 20-40% of patients with confirmed neurologic Lyme Disease may test negative on routine CSF assays. Among patients who develop chronic cognitive problems, the typical time course for the manifestation of Lyme symptoms is as follows:
* Very early: Erythema migrans (a red, round, expanding rash) * 1-2 months after infection: cardiac or early neurologic involvement (meningitis, encephalitis, cranial neuropathies) with mild to marked neuropsychiatric symptoms * 6-10 months after infection: arthritis of multiple joints * 2-8 years after infection: chronic cognitive problems Typical Symptoms among patients with neuropsychiatric Lyme Disease: * Fatigue: this ranges from mild to severe, resulting at times in a need for prolonged sleep at night and additional naps during the day, much akin to chronic fatigue syndrome. * Low grade fevers * Night sweats * Migrating arthralgias (joint pains) or arthritis (joint inflammation or swelling) * Muscle pains * Sleep disturbance * Frequent and severe headaches * Cranial nerve disturbance. While facial nerve palsy or optic neuritis are not frequently seen, patients may more commonly report facial numbness and/or tingling.
* Sharp, stabbing, deep/boring, burning, or lancinating (shooting) pains * Multifocal numbness or tingling in hands or feet (signs of peripheral neuropathy) * Thinking Problems: may include problems in attention, memory, verbal fluency, thinking speed. Patients may report problems with concentration or the need to rely on lists or others because of new memory problems. For more details about typical cognitive deficits, please see cognitive aspects in adults. * Cognitive overload: Some patients experience normal environmental stimulation as being excessive, resulting in a cognitive "short-circuiting" such that the patient may start to feel confused, lose focus, stutter, or panic. It is as if the normal filtering mechanism of the brain has been rendered ineffective, leaving the patient vulnerable to a confusing array of numerous stimuli. * Brain fog: Patients with Lyme disease often use this term to describe the lack of clarity in their cognitive processes. At times, this seems similar to "depersonalization or derealization" in which a person's sense of self and place are altered. * Sensory Hyperacuities: some patients experience a heightened sensitivity to sound or to light, particularly in the early phases of neurologic Lyme Disease. In the more severe cases, patients need to wear sunglasses indoors or earplugs to diminish sensory stimulation. * Spatial or Geographic Orientation problems: For example, patients may bump into the door jambs; go to place an object on a table only to see it fall to the floor due to a misjudgement of spatial distance; get lost in a familiar place. * Problems with Speech & Fluency: stuttering, reversing words (e.g., stating "tomorrow" when one means "yesterday") * Less common neurologic syndromes: partial complex seizures, multiple-sclerosis like illness, dementia-like illness, Guillain-Barre syndrome, strokes, Tullio phenomenon. * Psychiatric symptoms in Adults: irritability, poor frustration tolerance and mood swings are common. Less commonly: panic, obsessive/compulsive behaviors, or other anxiety states. Rarely: mania, paranoia (these usually occur among patients with encephalitis). * Neuropsychiatric Problems in Children: headaches, disturbances of behavior or mood, fatigue (falling asleep in class), problems with auditory and visual attention (with some children mistakenly being diagnosed as having attention deficit disorder) * Fluctuating Symptoms: worse on some days, remarkably better on others, without clear cause.
Cognitive Aspects in Adults: * Attention Problems: Easy distractibility; difficulty handling multiple tasks at the same time; trouble sustaining attention on tasks and completing tasks; trouble following the course of conversations or the text of a book. * Memory Problems: Retrieval difficulties are common in which patients may have a hard time recalling what they know; patients may forget conversations or children may forget that they've done homework assignments. At other times, patients experience a problem with the "working memory": as if the material can't be kept on board long enough. Patients may find themselves keeping multiple lists, but then they lose track of where they put their lists. * Slower Processing Speed: Patients may find it takes them longer to respond to questions or to complete tasks. Reaction time and thinking feel sluggish. * Verbal Fluency problems: the ability to engage in normal conversations is impaired by the inability to retrieve the right word for the moment or the ability to "name" well-known people or objects. Patients may experience word substitutions or "paraphasias". A patient trying to refer to a "microwave" might, for example, say "radiator".
Or, trying to refer to "Amazon.com" the patient might say, "AOL". Or, trying to refer to "fireworks", the patient might say "skylights". Patients may also experience an impairment in speech production, such that they stutter, particularly at times of sensory overload.
Psychiatric Aspects in Adults
Irritability and moodiness are common. These tend to be most severe in neurologic Lyme disease before treatment, during the first few days or weeks of treatment, and during resurgences or relapses of active Lyme Disease.
Antibiotic therapy can be very helpful at these times. Symptoms that persist despite appropriate antibiotic therapy should be treated with psychiatric medications. It is very important for patients to take advantage of all opportunities for therapeutic benefit. These include consultation with a psychiatrist for both medication and therapy.
Psychotherapy with a psychiatrist, psychologist, or social worker can be very helpful to help the individual cope with the effects of a serious illness. Family and couples therapy can also be vitally important, particularly when family members are confused by the changed behavior or personality of the patient.
Psychiatric medication can be very helpful to combat mood and sleep disturbances, to enhance attention, to decrease central nervous system hyperacuities, to decrease excessive worry and fear, and to contribute to overall good health by countering the negative impact of neuropsychiatric disorders on the immune system.
* Mood Lability: spontaneous swings of mood; spontaneous tearfulness. At times, patients with these symptoms may appear to have a Bipolar II disorder. * Irritability: an inability to tolerate normal frustrations, with quick bursts of anger. Patients may seem to have undergone a personality change in that previously mild-mannered individuals may now become quite difficult. * Panic attacks: tachycardia, flushing, chest pain, , numbness and tingling, shortness of breath, choking feeling with the sensation of loss of control and/or of fear of death. Needs to be distinguished from tachyarrhythmias. Panic attacks unrelated to Lyme disease are usually 10-20 minutes in duration. Lyme-related panic attacks may last for an hour or more. * Less commonly: manic or psychotic episodes (during encephalitic phase), paranoia, tics, obsessive/compulsive symptoms (may trigger a milder pre- existing condition or bring on symptoms de novo)
Neuropsychiatric Problems in Children
As noted among adults, when Lyme Disease is treated early in children, few children develop long term problems. When Lyme Disease is not treated until later in the course of the illness, the clinical manifestations may be more neuropsychiatric and the response to treatment less robust.
In a large series of children with Lyme disease referred to a pediatric neurologist (Belman et al), headaches were the most commonly reported symptom. The second most common symptom were disturbances of behavior and mood. MRI abnormalities may be seen in some children following Lyme infection, located predominantly in the deep white matter, which is consistent with reports of MRI lesions seen in adults with neuroborreliosis.
These findings are similar to the MRI findings of children with parainfectious or postinfectious acute disseminated encephalomyelitis. Children in particular may appear to have "pseudo-tumor cerebri" because of an elevated opening pressure at lumbar puncture.
Complex partial seizures may also occur more commonly among children with neurologic Lyme Disease than among adults. Like adults, these children may appear to have chronic fatigue syndrome due to an extraordinary capacity for prolonged sleep at night and need for naps during the day.
Cognitive. In a study by Adams et al, children with relatively early manifestations of Lyme Disease appropriately treated with antibiotics were found to have an excellent prognosis for short-term and long-term (4 years) unimpaired cognitive functioning.
In contrast, a study by Bloom et al reported on an evaluation of 86 children for possible late manifestations of lyme disease, 12 of whom had neurocognitive symptoms thought to be related to Lyme infection. Of these 12, 5 had past or present B. burgdorferi infection in serum and CSF and had developed neurocognitive symptoms either at the time of onset of Lyme infection or months after classic manifestations of the disease.
The most prevalent neurocognitive symptoms were behavioral changes, forgetfulness, declining school performance, headache and fatigue. Two of these children had developed complex partial seizures. A comprehensive neuropsychological battery revealed that these children had normal intellectual functioning, but particular deficits related to auditory or visual sequential processing.
These deficits, as well as many other symptoms, gradually improved following ceftriaxone therapy, although two of the children continued to have auditory sequential processing deficits. A controlled study by Dr. Tager at our Lyme Disease Research Program, reported at the 1999 VIII International Lyme Disease Conference in Munich Germany, revealed that chronic Lyme Disease in children may be accompanied by cognitive and psychiatric disturbances, resulting in significant impairment in psychosocial and academic functioning.
The most prominent cognitive problems involved the domains of attention and learning specifically related to perceptual/organizational abilities, visual scanning, and sequential tracking. Psychiatric.
Two studies from different institutions found that children with Lyme Disease may develop late problems with visual and auditory attention. These children may be mistakenly diagnosed as having primary attention deficit disorder as opposed to attentional deficits secondary to a systemic infection. Other findings in children include new onset phobias (e.g., fear of the dark, separation anxiety), depression, listlessness and irritability, oppositional behavior, obsessive-compulsive behaviors, and/or Tourettes Disorder.
Posts: 873 | From WA | Registered: Dec 2005
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