Neurological Complications of Lyme Disease

Medical topics with questions, information and discussion related to Lyme disease and other tick-borne diseases.
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ChronicLyme19
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Re: Neurological Complications of Lyme Disease

Post by ChronicLyme19 » Wed 3 Dec 2014 0:25

Update: Went back to a neurologist. Explained the symptoms again, notes from PT and chiropractor better, did not prompt the doctor....result....damage to the 11th cranial nerve! Now for a battery of tests to find the specific spot on the CN11. Woot!

This guy also told me a story about another lymee who had some other weird "atypical" nerve damage.
Half of what you are taught is incorrect, but which half? What if there's another half missing?

RitaA
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Re: Neurological Complications of Lyme Disease

Post by RitaA » Wed 3 Dec 2014 9:55

Your persistence in getting answers certainly seems to be paying off. Here's hoping that identifying the exact location will translate into effective treatment for you. You are definitely one step closer, and this is great news!

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ChronicLyme19
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Re: Neurological Complications of Lyme Disease

Post by ChronicLyme19 » Wed 3 Dec 2014 18:53

All thanks to your post RitaA :)

It's just such a hard symptom to describe/pin point. You don't lose sensory function, but you lose some motor function. When they do the push and pull muscle tests they don't see great abnormalities because there are so many other support muscles in the area. The slight drooping of the shoulder can be lost in a baggy shirt. It was my trainer who kept telling my my right shoulder was always lower and the one who finally helped me describe it as a control/stability issue not a total loss of function.

Three years later...finally an answer.
Half of what you are taught is incorrect, but which half? What if there's another half missing?

RitaA
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Re: Neurological Complications of Lyme Disease

Post by RitaA » Thu 4 Dec 2014 20:10

I wish I could take even some of the credit for this breakthrough of yours, but I really cannot. Even if I posted a thing or two about cranial nerves (mostly because I was also interested in the topic), you had the patience and took the time to sift through them, and then do further research that enabled you to connect the dots.

Yes, I can certainly relate to the feeling of having answers several years later because most of my doctors simply gave up even trying to figure out the reason(s) for my long list of health issues. My breakthrough moment came many years after being too unwell to work, and only because my neurologist became aware of an atypical ALS patient who tested positive for Lyme disease -- thanks only to the suggestion of a very astute nurse on the team at a well-respected neuromuscular clinic. That's the primary reason my neurologist finally decided to refer me to the same Infectious Diseases specialist who had diagnosed and treated the patient whose ALS diagnosis was changed to Lyme disease. The expression "Better late than never" certainly applies in both of our cases, and I remain grateful every single day for my much-improved health.

Even though Cranial Nerve VII is the one most often mentioned in connection with Lyme disease, it seems that any cranial nerve(s) could potentially be involved. While the following is written for the benefit of medical professionals, I thought I'd include it here for reference purposes:

http://meded.ucsd.edu/clinicalmed/neuro2.htm
CN11 (Spinal Accessory): CN 11 innervates the muscles which permit shrugging of the shoulders (Trapezius) and turning the head laterally (Sternocleidomastoid).


Good luck, and please do keep us posted.


Edited to add:

While it may not happen very often, the change in my fellow Lyme disease patient's diagnosis from ALS to a treatable infection has occurred in the past:

http://europepmc.org/abstract/MED/7610670
ALS-like sequelae in chronic neuroborreliosis
(PMID:7610670)

Hänsel Y, Ackerl M, Stanek G

Neurologischen Abteilung des Kaiser-Franz-Josef-Spitals, Wien.
Wiener Medizinische Wochenschrift (1946) [1995, 145(7-8):186-188]
1995/01
Type: Journal Article, Case Reports, English Abstract (lang: ger)


Abstract

CSF investigation in a 61-year old female patient with clinical picture of motoneuron disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.

RitaA
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Re: Neurological Complications of Lyme Disease

Post by RitaA » Fri 5 Dec 2014 7:31

ChronicLyme19,

Just in case you haven't come across this yet, you may want to have a look:

http://www.ncbi.nlm.nih.gov/books/NBK387/
Clinical Methods: The History, Physical, and Laboratory Examinations
3rd Edition

Chapter 64 Cranial Nerve XI: The Spinal Accessory Nerve

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ChronicLyme19
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Re: Neurological Complications of Lyme Disease

Post by ChronicLyme19 » Fri 5 Dec 2014 19:44

RitaA, you did it again! More clues that fit!! This makes sense with the CN11 involvement. I had some TMJ like symptoms after going on the rifampin this month...
The eleventh nerve has two parts. The smaller cranial part arises from cells in the nucleus ambiguus and ultimately is distributed with the vagus nerve. This portion innervates the pharyngeal muscles.
Half of what you are taught is incorrect, but which half? What if there's another half missing?

velvetmagnetta
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Re: Neurological Complications of Lyme Disease

Post by velvetmagnetta » Fri 5 Dec 2014 23:33

I just wanted to tell you two, ChronicLyme19 and RitaA, that I am so appreciative of your posts on this thread. Thank you, and please keep posting whatever you learn!

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ChronicLyme19
Posts: 564
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Re: Neurological Complications of Lyme Disease

Post by ChronicLyme19 » Mon 8 Dec 2014 0:50

I sporadically have had trouble with pills getting stuck in the top of my throat. I just thought I wasn't drinking enough water with them. But even after two cups they'd be stuck. This could be why. Cervical MRI tomorrow with contrast, but this makes me think its higher up. I can't quite tell if this part would be in or outside the skull, and if the cervical MRI would go up high enough. I had a brain MRI in Aug, but it was without contrast. Probably need to call the neuro back and let him know this. I didn't think the swallowing issue was related, but now I do...
Half of what you are taught is incorrect, but which half? What if there's another half missing?

fastuno
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Re: Neurological Complications of Lyme Disease

Post by fastuno » Fri 23 Jun 2017 13:12

SEARCH: pseudotumor cerebri lyme
https://www.ncbi.nlm.nih.gov/pubmed/?te ... rebri+lyme
_____________________________________
Ugeskr Laeger. 1995 Feb 13;157(7):901.
Ellermann A1, Hjelt K.
[Pseudotumor cerebri caused by Lyme borreliosis].
"Abstract

Lyme borreliosis may cause a wide range of clinical symptoms. The two previously described paediatric cases of Lyme borreliosis with symptoms of pseudotumor cerebri were associated with characteristic cutaneous symptoms. A case of seven year-old girl with six weeks of headache, vomiting nausea and fatigue as the only symptoms was shown to suffer from pseudotumor cerebri with papilloedema and increased intracranial pressure caused Borrelia burgdorferi. Specific treatment with intravenous penicillin and later intravenous ceftriaxone (due to development of penicillin allergy) for a total of ten days caused the symptoms to gradually disappear over following three to four weeks. Hence, even if pseudotumor cerebri is the only symptom, it is recommended that testing for Lyme borreliosis should be carried out."

https://www.ncbi.nlm.nih.gov/pubmed/7701654

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J Neurol. 2016 Mar;263(3):500-7. doi: 10.1007/s00415-015-8007-x. Epub 2016 Jan 6.
Lyme disease-related intracranial hypertension in children: clinical and imaging findings.
Ramgopal S1, Obeid R2, Zuccoli G3, Cleves-Bayon C2, Nowalk A4.
"Abstract

Lyme disease (LD) is a tick-borne infection that is endemic to multiple areas of the United States. Patients with LD may present with sign and symptoms of intracranial hypertension (IH). The objective of this study is to evaluate the history, clinical findings, CSF analysis, and brain imaging results in pediatric patients with increased intracranial pressure secondary to LD. A retrospective database search was performed using the International Classification of Diseases (ICD) 9/10 codes to identify patients diagnosed with LD and IH between 2004 and 2014 at a tertiary referral pediatric hospital. Clinical, laboratory and neuroimaging data for each patient were reviewed. Seven patients met inclusion criteria; mean age was 9.6 years (standard deviation 4.0 years); 4/7 patients were male. Average body mass index was 18.8 kg/m2 (standard deviation 3.0 kg/m2). Fever was present in four patients. Four had a history of LD related erythema migrans. All had elevated CSF opening pressure with leukocytosis and lymphocytic predominance. MRI obtained in six patients showed contrast enhancement of various cranial nerves. Tentorial enhancement was noted in all patients. In addition, patients had widening of the optic nerve sheath (ONS), optic nerve protrusion, and flattening of the posterior globe consistent with increased intracranial pressure. All patients had resolution of their symptoms after initiation of antibiotic therapy. In endemic areas, LD should be included in the differential of IH. MRI can help distinguish IH due to LD from its idiopathic form due to the presence of tentorial and cranial nerve enhancement in the former in addition to abnormal CSF showing leukocytosis with lymphocyte predominance."
https://www.ncbi.nlm.nih.gov/pubmed/?te ... g+findings

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DOI: http://dx.doi.org/10.1016/j.amjmed.2008.02.032
Pseudotumor Cerebri: Early Manifestation of Adult Lyme Disease
John E. Castaldo, MD Correspondence information about the author MD John E. Castaldo Email the author MD John E. Castaldo ,Erin Griffith, MS ,Daniel H. Monkowski, MD
"To the Editor:

Neuroborreliosis is an infection of the nervous system by Borrelia burgdorferi. Symptoms of central nervous system (CNS) Lyme disease typically include headache, nuchal rigidity, fatigue, nausea, vomiting, cranial neuropathy, and radiculoneuritis. In a minority of patients with Lyme disease, encephalitis can result.1, 2

We describe a patient who initially presented with symptoms of increased intracranial pressure, papilledema, and serum testing positive for Lyme disease. Pseudotumor cerebri has been reported as a complication in pediatric patients with Lyme disease.3, 4, 5 In addition, a recent report described a case of pseudotumor cerebri as a late complication of Lyme disease in an adult.6 We report the first case of pseudotumor cerebri documented as the initial presentation of CNS Lyme disease in an adult."

http://www.amjmed.com/article/S0002-934 ... 0/fulltext

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DOI: http://dx.doi.org/10.4065/75.3.315
Lyme Disease and Pseudotumor
Lawrence Zemel, MD Connecticut Children's Medical Center Hartford

"To the Editor. I was surprised, after reading the November 1999 Residents’ Clinic,1 that Lyme disease was not included in the differential diagnosis of increased intracranial pressure, especially since Minnesota is an endemic area for this tick-borne illness. Lyme disease may have protean neurologic manifestations, including pseudotumor; this association was first described in 1985.2 Since then, I have treated 4 children, between 8 and 14 years old, with increased intracranial pressure secondary to Lyme disease. All children were seropositive by both enzyme-linked immunosorbent assay and Western blot assay at the time of their headache. Only 1 of the 4 children had previous erythema migrans. Two of the 4 had a mild lymphocytic pleocytosis (0.055, and 0.022 × 109L). Cerebrospinal fluid (CSF) opening pressures ranged from 300 to 550 mm H2O. All cranial computed tomographic scans were normal. Polymerase chain reaction (PCR) assays on the CSF were negative for Barrelia DNA in all samples, but selective intrathecal antibody production was documented in 2 of the 4 children.

These 4 children with Lyme-associated pseudotumor cerebri all responded to a combination of intravenous ceftriaxone and oral acetazolamide, with resolution of their symptoms and papilledema. Certainly in Connecticut I would want to rule out this potentially treatable cause of pseudotumor."

http://www.mayoclinicproceedings.org/ar ... 6/fulltext
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Pediatr Infect Dis J. 2006 Jan;25(1):91-2.
Neuroborreliosis with progression from pseudotumor cerebri to aseptic meningitis.
Steenhoff AP1, Smith MJ, Shah SS, Coffin SE.
"Abstract
We report a patient with an initial diagnosis of Lyme-associated pseudotumor cerebri who developed cerebrospinal fluid pleocytosis consistent with Lyme meningitis. The case illustrates the importance of considering neuroborreliosis in the differential diagnosis of pseudotumor cerebri and describes the evolution of cerebrospinal fluid findings in this condition."
https://www.ncbi.nlm.nih.gov/pubmed/16395117
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Clin Infect Dis. 2003 Jul 15;37(2):e25-6. Epub 2003 Jul 9.
Lyme disease complicated with pseudotumor cerebri.
Nord JA1, Karter D.
Yea, OK the "first" ...but my IIH was caused by Lyme Disease & I have spoken to others who developed IIH with Lyme too... none of us were in such studies & no one cared to report anything!!! I see this goes on a lot in medicine & with many other conditions too.
"Abstract
To our knowledge, pseudotumor cerebri as a complication of Lyme disease has been described only in children. We report the first case of an adult with pseudotumor cerebri due to Lyme disease and the use of serial lumbar punctures as the sole therapy."
https://www.ncbi.nlm.nih.gov/pubmed/12856231

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[Pseudotumour cerebri in a patient with Lyme disease and hypothyroidism].
[Article in Spanish]
García-Moreno JM1, Borobio-Enciso MV, Angulo-Fraile S, Izquierdo G.
" Abstract
INTRODUCTION:
Lyme disease is a complex infectious disease affecting multiple organic systems. The most frequent complications are of a dermatological, rheumatological, ophthalmological, cardiac and neurological nature. Among the neurological complications, pseudotumour cerebri is considered to be a rare manifestation of the disease. Hypothyroidism, however, is known to be only infrequently associated to pseudotumour cerebri. Paparone recently reported a case in which Lyme disease and primary hypothyroidism were concurrent, and Becker and Trock described the case of three patients with concurrent thyrotoxicosis and Lyme disease.
CASE REPORT:
We present the case of a 19 year old female with pseudotumour cerebri and hypothyroidism secondary to autoimmune thyroiditis, which improved after treating her for concomitant Lyme.
CONCLUSIONS:
We suggest there is a common aetiopathogenic connection between the three processes through autoimmune thyroiditis triggered by Borrelia burgdorferi. Thus, in this patient, the pseudotumour cerebri could be due to either a direct mechanism, triggered by B. burgdorferi, or indirectly, through hypothyroidism secondary to thyroiditis induced by B. burgdorferi, or perhaps to both mechanisms. It might be wise to consider infection by B. burgdorferi in patients with pseudotumour cerebri or thyroiditis coming from areas in which Lyme disease is endemic"
https://www.ncbi.nlm.nih.gov/pubmed/12717650
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Dev Med Child Neurol. 2002 Sep;44(9):641-2.
Intracranial hypertension in neuroborreliosis.
Härtel C1, Schilling S, Neppert B, Tiemer B, Sperner J.
"Abstract
Neuroborreliosis is an infection of the nervous system caused by the spirochete Borrelia burgdorferi, from which patients most commonly develop lymphocytic meningitis, radiculoneuritis, or cranial neuropathy. In this report a 9-year-old male with an unusual neurological complication of neuroborreliosis--benign intracranial hypertension (BIH)--is described. Clinical symptoms of BIH, which consist of increased CSF pressure in the absence of an intracranial mass or obstruction to the circulation of CSF, resolved completely after antibiotic therapy with ceftriaxone."
https://www.ncbi.nlm.nih.gov/pubmed/12227619
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June 2002
A Child With Venous Sinus Thrombosis With Initial Examination Findings of Pseudotumor Syndrome
Irfan Ansari, MD; Brian Crichlow, MD; Kammi B. Gunton, MD; et al Gary R. Diamond, MD; Joseph Melvin, MD
Arch Ophthalmol. 2002;120(6):867-869. doi:
" A child with venous sinus thrombosis whose initial clinical findings were consistent with an isolated pseudotumor syndrome without any predisposing factors is described.
Report of a Case
A 6-year-old white girl was seen at the emergency department of a children's hospital with complaints of headaches for 3 weeks and diplopia for 2 days. Three weeks prior to examination, she had 2 episodes of emesis. Findings from systemic review were negative for fever, neck stiffness, ear pain, or upper respiratory symptoms. There was no history of tick bites, skin rashes, or recent travel. She lived in an urban community in Pennsylvania. The remainder of her medical history was unremarkable.
On examination she was afebrile with normal vital signs, alert, and cooperative. Visual acuity was 20/20 OU, and color plate test results from Ishihara plates was normal in each eye. Ocular motility revealed 10% bilateral abduction deficits. Anterior segment examination results were normal. Fundus examination findings revealed mild bilateral disc edema. The remainder of her general and neurologic examination was unremarkable; specifically, no other cranial nerve deficits were present.
Magnetic resonance imaging scans of the head were normal. Lumbar puncture disclosed an opening pressure of 450 cm H2O. Cerebrospinal fluid composition showed a red blood cell count of 2 cells/µL; white blood cell count, 20 cells/µL (85% lymphocytes, 13% monocytes); and normal protein and glucose levels. An initial diagnosis of a pseudotumor syndrome was entertained. However, magnetic resonance venous imaging showed complete occlusion of right and partial occlusion of left transverse sinus (Figure 1) revealing the diagnosis of venous sinus thrombosis."
" erum Lyme titers were positive for IgG and IgM at 4.1 mg/dL (<0.9 mg/dL, negative; >1.1 mg/dL, positive). Cerebrospinal fluid polymerase chain reaction and Western immunoblot were positive for Borrelia burgdorferi."
http://jamanetwork.com/journals/jamaoph ... cle/270833
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Cephalalgia. 1993 Jun;13(3):207-9.
Headache resembling tension-type headache as the single manifestation of Lyme neuroborreliosis.
Brinck T1, Hansen K, Olesen J.
"Abstract
We present two patients with monosymptomatic headache resembling chronic tension-type headache as the first manifestation of Lyme neuroborreliosis. The headache developed over a few days in both cases and lasted for three months in the first case and for two and a half years in the second case before the diagnosis of Lyme neuroborreliosis was made. Neuroimaging and many laboratory investigations did not lead to the diagnosis, which was only established after lumbar puncture. The CSF in both cases showed high protein, lymphocytic pleocytosis and Borrelia burgdorferi-specific intrathecal antibody synthesis. The headache disappeared completely after treatment with penicillin G. In patients suffering from daily headaches which have developed subacutely, Lyme neuroborreliosis should be considered even in the absence of signs of meningeal irritation. A lumbar puncture should be performed more often than is presently customary and the CSF should be examined for pleocytosis as well as Borrelia burgdorferi-specific intrathecal antibody synthesis."

https://www.ncbi.nlm.nih.gov/pubmed/8358780
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Pediatrics. 2003 Dec;112(6 Pt 1):e477-9.
Lyme disease presenting with persistent headache.
Moses JM1, Riseberg RS, Mansbach JM.
"Abstract
Increased intracranial pressure in patients with Lyme disease is an uncommon but reported finding. We discuss 2 patients from Lyme endemic areas who initially presented with headache, nausea, and vomiting and were eventually found to have increased intracranial pressure, a mild cerebrospinal fluid pleocytosis, and positive Lyme titers. It has been shown that increased intracranial pressure in association with neuroborreliosis can lead to blindness. In endemic areas, it is important for practitioners to consider Lyme disease when patients present with persistent headache, especially in those who have evidence of increased intracranial pressure."
https://www.ncbi.nlm.nih.gov/pubmed/14654649
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Spinal Fluid and Brain Tests
"a. Spinal Fluid
Patients with neurologic symptoms suggestive of central nervous system involvement should have a lumbar puncture with determination of opening pressure. When the CSF is examined, the fluid should be sent for routine studies such as cell count, and protein and glucose levels. In addition, the CSF should be sent for Bb PCR assay and paired serum and CSF should be sent for calculation of the intrathecal index. Please note that the serum should be drawn on the same day as the spinal fluid for an optimal study. The index refers to the ratio of Bb antibodies in the CSF compared to the serum, corrected for immunoglobulin levels in each of those fluid compartments. When the index is positive, that indicates that there is a preferential production of antibodies against Bb in the CSF – a finding strongly suggestive of central nervous system invasion by the agent of Lyme disease. It is believed that the index may remain positive long after the initial infection has been treated due to immunologic memory. If the CSF is being examined as part of the differential diagnosis with multiple sclerosis, the neurologist is also likely to order other tests, such as an assay for oligoclonal bands. Unfortunately, patients may have neurologic Lyme disease but test negative on the Lyme index. When positive however, the clinician can be confident that this particular individual has or has had central nervous system Lyme disease."
http://www.columbia-lyme.org/patients/l ... fluid.html

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Headache. 1995 Mar;35(3):125-30.
Headache characteristics in hospitalized patients with Lyme disease.
Scelsa SN1, Lipton RB, Sander H, Herskovitz S.
"Abstract
We reviewed 49 patients consecutively hospitalized for neurologic Lyme disease to determine the frequency and characteristics of recent onset headaches in this group. All patients had positive serum Lyme ELISAs and other neurologic illness excluded. Recent-onset headache occurred in 26 of 49 patients (53%). Patients with headaches more commonly had central nervous system involvement (54% vs 19%, P < .05) and flu-like illness (58% vs 19%, P < .0005). Eight of 26 (31%) met criteria for meningitis or encephalitis with abnormal CSF examinations. All 8 had focal findings (6), cognitive dysfunction (1), or both (1). The remaining 18 patients had recent-onset headaches resembling migraine (9), tension-type headache (5), or neither (4). Antibiotic treatment resulted in complete headache resolution in 11 of 14 patients with available follow-up data. Based on these findings, we conclude that recent-onset headaches are common in patients hospitalized with Lyme disease. Of those with meningitis or encephalitis requiring intravenous antibiotics, all had focal neurologic findings or cognitive abnormalities, not just headaches"
https://www.ncbi.nlm.nih.gov/pubmed/7721571
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Common and uncommon neurological manifestations of neuroborreliosis leading to hospitalization
Philipp Schwenkenbecher, Refik Pul, Ulrich Wurster, Josef Conzen, Kaweh Pars, Hans Hartmann, Kurt-Wolfram Sühs, Ludwig Sedlacek, Martin Stangel
, Corinna Trebst, and Thomas Skripuletz

"In patients with a combination of deficits, back pain was the first symptom,
followed by headache, and finally by cranial nerve palsy. Indeed, signs of meningitis were often found in patients with neuroborreliosis, but usually did not cause admission to a hospital. Unusual cases included patients with
sudden onset paresis that were initially misdiagnosed as stroke and one patient with acute delirium. Cerebrospinal fluid (CSF) analysis revealed typical changes including elevated CSF cell count in all but one patient, a blood-CSF barrier dysfunction (87%), CSF oligoclonal bands (90%), and quantitative intrathecal synthesis of immunoglobulins (IgM in 74%, IgG in 47%, and IgA in 32% patients)"

" Pseudotumor cerebri presents another disease which might be related to neuroborreliosis. In several reports typical symptoms of pseudotumor cerebri such as headache and papilledema and an elevated CSF opening pressure have been described predominantly affecting children [4960]. In these patients antibiotic treatment led to normalization of symptoms and CSF pressure."

http://download.springer.com/static/pdf ... 5517e2c261
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Biomed Pharmacother. 1989;43(6):397-400.
Lyme disease.
Bourke SJ1.
"Abstract
Neurological problems form an important part of the clinical spectrum of Lyme disease. A triad of aseptic meningoencephalitis, cranial neuritis and peripheral neuritis is unique to the disease. However, the list of neurological manifestations described includes pseudotumour cerebri, hemiparesis, demyelinating disorders, optic atrophy, recurrent laryngeal nerve palsy and purulent meningitis so that Lyme disease must now be considered in the differential diagnosis of a wide range of neurological disorders."
https://www.ncbi.nlm.nih.gov/pubmed/2686764
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Pseudotumor cerebri and Lyme disease: A new association†
M.D. Harold S. Raucher, M.D. David M. Kaufman , M.D. Johanna Goldfarb Correspondence information about the author M.D. Johanna Goldfarb M.D. Ronald I. Jacobson, M.D. Bruce Roseman, , M.D. Robert R. Wolff
http://www.jpeds.com/article/S0022-3476 ... 1/abstract
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Pediatr Neurol. 1998 May;18(5):439-41.
Pseudotumor cerebri in Lyme disease: a case report and literature review.
Kan L1, Sood SK, Maytal J.
" Abstract
Pseudotumor cerebri is an unusual presentation of Lyme disease. The case of an 8-year-old girl with pseudotumor cerebri secondary to acute neuroborreliosis is reported. She presented with acute onset of headache, papilledema, sixth nerve palsy, increased intracranial pressure, and cerebrospinal fluid pleocytosis. Serum and cerebrospinal fluid Lyme antibodies were positive. Twelve reported cases that mostly presented with systemic findings and signs of Lyme disease before development of pseudotumor cerebri were reviewed. We conclude that acute neuroborreliosis can present with pseudotumor cerebri as an initial manifestation. It is important to include Lyme disease in the differential diagnosis of pseudotumor cerebri in an area endemic for Lyme disease."
https://www.ncbi.nlm.nih.gov/pubmed/965 ... t=Abstract
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J N J Dent Assoc. 1998 Winter;69(1):19, 21, 62-3 passim.
Lyme disease awareness for the New Jersey dentist. A survey of orofacial and headache complaints associated with Lyme disease.
Heir GM1, Fein LA.
"Abstract
The incidence of Lyme disease is increasing in New Jersey. In 1996, 2,190 cases were reported, representing an increase of 487 cases from the 1,703 reported in 1995 [Table 1]. Symptoms associated with Lyme disease include headache and facial pain that often mimics dental pathology and temporomandibular disorders. Patients with complaints of vague, non-specific dental, facial or head pain, who present with a multisystemic, multi-treatment history, are suspect. This article discusses Lyme disease in New Jersey and the clinical presentation of Lyme disease that the dental practitioner may encounter. A summary of data is provided which was collected from 120 patients diagnosed with laboratory confirmed Lyme disease. The most common orofacial, head and dental complaints seen in the Lyme disease patient are reviewed. This information will hopefully aid in establishing a diagnosis and appropriate referral where indicated."
"The headaches were bilateral, pressure-like or throbbing with a temporo-parieto-occipital distribution, being stronger in the occipital region. The pain would reach a ten-point intensity on a ten-point verbal pain scale with dizziness. Attacks were accompanied by nausea and intense osmophobia, "
https://www.ncbi.nlm.nih.gov/pubmed/9584762

Full article here:
http://www.scielo.br/pdf/anp/v71n7/0004 ... 07-470.pdf
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Pediatr Emerg Care. 1998 Oct;14(5):356-61.
Emergency department presentations of Lyme disease in children.
Bachman DT1, Srivastava G.

"Abstract
OBJECTIVE:
To review the clinical characteristics and diagnostic evaluation of children with Lyme disease evaluated in an emergency department (ED) in an endemic area.

DESIGN:
A retrospective review of the demographic, historical, clinical, and laboratory data of pediatric patients with a final diagnosis of Lyme disease.

SETTING:
The pediatric ED of an urban university hospital.

PARTICIPANTS:
Children with Lyme disease evaluated during the three-year period from 1992 to 1994.

RESULTS:
Twenty-nine children ranging in age from three to 19 years who were diagnosed with Lyme disease subsequent to a visit to a pediatric ED were identified. Four patients had early localized disease with erythema migrans and varying degrees of systemic symptoms. Ten had early disseminated Lyme disease, with multiple erythema migrans, neurologic involvement (including three patients with pseudotumor cerebri), or carditis. Fifteen cases of late Lyme disease with arthritis were identified. Recognition of Lyme arthritis proved particularly difficult; seven children were initially diagnosed as having septic arthritis, six of whom underwent arthrotomy. Marked elevations of the erythrocyte sedimentation rate and synovial fluid white blood cell counts were observed in these patients, making it difficult to distinguish Lyme disease from septic arthritis on the basis of laboratory findings.

CONCLUSION:
Lyme disease is an infrequent, often difficult, diagnosis in children who present to an ED. Early disseminated and late disease predominate; classic erythema migrans is uncommon in the ED in comparison with other ambulatory venues. Diagnosis of Lyme arthritis may be difficult; exposure in an endemic area and clinical findings may help distinguish it from septic arthritis. Overall, underdiagnosis of Lyme disease may actually be more of a problem than overdiagnosis in the ED setting. Recognition of Lyme disease by emergency medicine practitioners requires familiarity with its epidemiology and its multiple manifestations."

https://www.ncbi.nlm.nih.gov/pubmed/9814407

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