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Post by LymeEnigma on May 27, 2008 12:14:53 GMT -8
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Post by LymeEnigma on May 27, 2008 12:16:32 GMT -8
Five causes of gastroparesis:
Digestive Diseases and Sciences, Vol. 47, No. 12 (December 2002), pp. 2664–2668 (© 2002)
"In all of these cases there was a strong temporal
association between the suspected inciting event and
the onset of symptoms. When these five cases are
subjected to the criteria posed above, we believe the
criteria are reasonably well met. In all of the five cases
presented, there was no history of a viral illness
preceding the onset of symptoms, and no known
cause of gastroparesis was detected after a thorough
work-up. In all cases, there was a strong temporal
association between the suspected inciting event and
the onset of symptoms. There is good evidence to
support the development of an inflammatory neuropathy
after Lyme disease or after vaccinations, given
reports of Guillain-Barre´ syndrome, brachial neuritis,
and acute myelitis. The possibility of an inflammatory
neuropathy leading to gastroparesis does make good
biological sense, since it is well known that vagal
nerve injury can produce gastroparesis" (bold mine).
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Post by LymeEnigma on May 27, 2008 12:18:09 GMT -8
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Post by LymeEnigma on Jul 27, 2008 10:20:34 GMT -8
Idiopathic Gastroparesis Epidemiology. Idiopathic gastroparesis is at least as common as diabetic gastroparesis in most case series.[4] Patients typically are young or middle-aged and up to 90% are women. Although many individuals report an insidious clinical course with no obvious trigger, one fourth present with an acute onset of symptoms in association with acute gastroenteritis or with viral prodromal symptoms such as diarrhea, fever, myalgias, and headache.[34] Postinfectious idiopathic gastroparesis has a relatively good prognosis, with symptom resolution over several years in many cases. In most instances, the offending organism is not characterized. However, 8 of 11 children with acute-onset gastroparesis in one study tested positive for rotavirus infection.[35] Transient slowing of gastric emptying also develops after infection with parvovirus-like agents and with Lyme disease. In immunosuppressed individuals, cytomegalovirus, Epstein-Barr virus, varicella zoster virus, and herpes simplex virus may be implicated.[36,37] In one case, postinfectious gastroparesis occurred as part of a larger dysautonomic syndrome also involving cardiac conduction and bladder function.[38] Furthermore, gastroparesis has been observed after vaccination for tetanus, anthrax, and hepatitis.[39] *snip* Disorders of diffuse gastrointestinal dysfunction with associated gastroparesis. Gastroparesis frequently occurs in patients with diffuse disorders of gut motility, such as chronic intestinal pseudo-obstruction. These individuals may also present with small intestinal bacterial overgrowth, nutritional deficiencies, bowel habit abnormalities, and pneumatosis intestinalis. The prevalence of delayed emptying in scleroderma ranges from 40% to 67%, whereas rates in polymyositis-dermatomyositis and systemic lupus erythematosus are lower.[63] Gastric stasis is described in smooth muscle disorders such as myotonic dystrophy and progressive muscular dystrophy. Primary or secondary amyloidosis can cause neuropathic or myopathic intestinal pseudo-obstruction.[64-67] Gastric stasis is found in 19% to 64% of patients with chronic constipation, irritable bowel syndrome with constipation, and idiopathic megarectum.[68] Other cases of intestinal pseudo-obstruction are familial, occur after a viral prodrome, or present as a paraneoplastic phenomenon, usually with small-cell lung carcinoma.[69] Serologic markers in paraneoplastic gastroparesis or intestinal pseudo-obstruction include type 1 antineuronal nuclear antibody, anti-Purkinje cell cytoplasmic antibody, and ganglionic nicotinic acetylcholine receptor antibody.[70] Such antineuronal antibodies are also detected in some patients with idiopathic gastrointestinal dysmotility syndromes with an autoimmune basis.[71] In addition to producing an achalasia-like picture, Chagas disease may cause gastroparesis, megaduodenum, and chronic intestinal pseudo-obstruction. Other infectious agents that produce generalized gut dysmotility include varicella zoster, Epstein-Barr virus, Clostridium botulinum, and HIV.[37,72,73 www.medscape.com/viewarticle/563730_3 |
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Post by LymeEnigma on Jul 29, 2008 13:30:43 GMT -8
Meningoencephalomyeloradiculoneuritis in one case of Borrelia burgdorferi infection (Lyme disease)
Journal The Italian Journal of Neurological Sciences
Publisher Springer Milan
ISSN 0392-0461 (Print) 1126-5442 (Online)
Issue Volume 10, Number 4 / August, 1989
Category Case Reports
DOI 10.1007/BF02334954
Pages 457-461
SpringerLink Date Monday, April 10, 2006
Abstract We describe a patient having serologically confirmed Borrelia burgdorferi infection manifesting meningoencephalomyeloradiculoneuritis. The clinical and MRI features suggested a multifocal vascular nervous system involvement. EMG-ENG showed abnormalities consistent with axonal degeneration initially involving the more proximal segments of the lower limb nerves.
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Post by LymeEnigma on Jul 29, 2008 13:31:55 GMT -8
"B. burgdorferi in the CNS localized to the leptomeninges, nerve roots, and dorsal root ganglia, but not to the parenchyma. Outside of the CNS, B. burgdorferi localized to endoneurium and to connective tissues of peripheral nerves, skeletal muscle, heart, aorta, and bladder." Full article: www.nature.com/labinvest/journal/v80/n7/full/3780109a.html |
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Post by LymeEnigma on Jul 29, 2008 13:34:03 GMT -8
Isolated neuritis of the sciatic nerve in a case of Lyme disease Journal The Italian Journal of Neurological Sciences Publisher Springer Milan ISSN 0392-0461 (Print) 1126-5442 (Online) Issue Volume 19, Number 2 / April, 1998 Category Case Report DOI 10.1007/BF02427561 Pages 81-85 SpringerLink Date Wednesday, June 07, 2006 Abstract Lyme disease is an infectious disease caused by the spirocheteBorrelia burgdorferi. The course of the disease is divided into three stages, the second of which may include various types of peripheral nervous system disturbances. We report the case of a patient with persistent deficits caused by the prevalent involvement of the sciatic nerve, confirmed by electrophysiological and neuropathological findings. The most significant bioptic results were axonal degeneration and perivascular inflammation. Damage to a single peripheral nerve as the dominant clinical expression during the course of Lyme disease is an unusual finding that has been rarely described in the literature. www.springerlink.com/content/y769674318631v7q/ |
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Post by LymeEnigma on Jul 29, 2008 13:42:51 GMT -8
Spinal Cord Stimulation for the Treatment of Upper and Lower Extremity Neuropathic Pain due to Lyme Disease
Massimo Mearini, MD, Stefano Podetta, MD, Emanuela Catenacci, MD, Patrizia d'Auria, MD, Claudio Cornali, MD and Pietro Mortini, MD
Neurosurgical Clinic, Brescia University, Brescia, Italy
Address correspondence and reprint requests to: Massimo Mearini, MD, Via Lazzaretto, 32-25030 Castelmella, Brescia, ITALY. Email: mearinimax@alice.it
Background. Lyme disease is caused by Borrelia, a bacterium transmitted by the bite of a deer tick. A slow developing encephalopathy or an axonal polyneuropathy with distal paresthesia and spinal or radicular pain rarely occurs and can be hard to treat.
Materials and Methods. We report here the case of a 44-year-old woman with four-limb, intolerable, neuropathic pain as sequelae to Lyme disease, which was resistant to conservative measures and was treated successfully with concurrent, thoracic, and cervical percutaneous spinal cord stimulation (SCS).
Results. After 18 months of therapy and follow-up, this patient's analgesia, as a result of SCS, continues to be excellent, with almost complete subjective pain relief and cessation of adjuvant analgesic medication.
Conclusions. SCS may be efficacious for the treatment of neuropathic pain due to Lyme disease.
Submitted: November 29, 2005; accepted: November 29, 2006.
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Post by LymeEnigma on Jul 29, 2008 15:01:00 GMT -8
Am Fam Physician. 2007 Oct 1;76(7):997-1002.Links Bell's palsy: diagnosis and management. Tiemstra JD, Khatkhate N. Department of Family Medicine, University of Illinois at Chicago College of Medicine, Chicago, Illinois 60612, USA. jtiemstr@uic.edu Bell's palsy is a peripheral palsy of the facial nerve that results in muscle weakness on one side of the face. Affected patients develop unilateral facial paralysis over one to three days with forehead involvement and no other neurologic abnormalities. Symptoms typically peak in the first week and then gradually resolve over three weeks to three months. Bell's palsy is more common in patients with diabetes, and although it can affect persons of any age, incidence peaks in the 40s. Bell's palsy has been traditionally defined as idiopathic; however, one possible etiology is infection with herpes simplex virus type 1. Laboratory evaluation, when indicated by history or risk factors, may include testing for diabetes mellitus and Lyme disease. A common short-term complication of Bell's palsy is incomplete eyelid closure with resultant dry eye. A less common long-term complication is permanent facial weakness with muscle contractures. Approximately 70 to 80 percent of patients will recover spontaneously; however, treatment with a seven-day course of acyclovir or valacyclovir and a tapering course of prednisone, initiated within three days of the onset of symptoms, is recommended to reduce the time to full recovery and increase the likelihood of complete recuperation. PMID: 17956069 [PubMed - indexed for MEDLINE] www.ncbi.nlm.nih.gov/pubmed/17956069?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
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Post by LymeEnigma on Jul 29, 2008 15:03:50 GMT -8
Lyme disease and the peripheral nervous system John J. Halperin, MD * Department of Neurology, North Shore University Hospital, 300 Community Drive, Manhasset, New York 11030, USA email: John J. Halperin (halperin@nshs.edu) *Correspondence to John J. Halperin, Department of Neurology, North Shore University Hospital, 300 Community Drive, Manhasset, New York 11030, USA Abstract Lyme disease, the multisystem infectious disease caused by the tick-borne spirochete Borrelia burgdorferi, causes a broad variety of peripheral nerve disorders, including single or multiple cranial neuropathies, painful radiculopathies, and diffuse polyneuropathies. Virtually all appear to be varying manifestations of a mononeuropathy multiplex. Diagnosis requires that the patient should have had possible exposure to the only known vectors, Ixodes ticks, and also have either other pathognomonic clinical manifestations or laboratory evidence of exposure. Treatment with antimicrobial regimens is highly effective. The mechanism underlying these neuropathies remains unclear, although interactions between anti-Borrelia antibodies and several peripheral nerve constituent molecules raise intriguing possibilities. Muscle Nerve 28: 133-143, 2003 www.ncbi.nlm.nih.gov/pubmed/12872317?ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
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Post by itsybitsyone on Jul 30, 2008 8:50:56 GMT -8
meningoencephalomyeloradiculoneuritis? They made that up.
They took a bunch of words and stuck 'em together.
It means "My head hurts all the way down my neck and arms and no one gives a crap"
I suffer from meningoencephalomyeloradiculoneuritis. Would I admit it? NOT inproper company.
They make this disease sound more and more ridiculous every day.
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Post by LymeEnigma on Jul 30, 2008 11:16:56 GMT -8
Seriously.... I Googled it, to find the definition before I posted it, and there wasn't even a whole page of results. It is not in my medical dictionary, that's for sure.  I'm finding it interesting, however, that Lyme seems to be implicated in everything from Bell's palsy to long thoracic nerve palsy, to palsy of the vagal nerve ... being a personal victim of the latter two (long before the tick bite), I really do have to wonder, once again, if there is some kind of Lyme-like illness "running" through my family.... A lot of speculation and connecting of potentially unrelated issues, but worth some thought, just the same. *edited to fix a typo....  |
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Post by itsybitsyone on Aug 1, 2008 9:06:21 GMT -8
And when you google it, you will ONLY find it associated with Lyme disease. What happens if you search it in pubmed? I have to go see...
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Post by itsybitsyone on Aug 1, 2008 9:09:05 GMT -8
That italian one is the only thing that comes up.
So, those doctors made up a name of a set of symptoms/syndrome to describe what they saw. There was no president to call it that. They coined it, it seems, for that study.
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Post by LymeEnigma on Sept 16, 2008 17:31:33 GMT -8
Pathologic Conditions of the Lower Cranial Nerves IX, X, XI, and XII Policeni, B.A.Show author detailsEmail this author, Smoker, W.R.K.Show author details Correspondence address Department of Radiology, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242, United States Abstract The glossopharyngeal, vagus, spinal accessory, and hypoglossal cranial nerves can be affected by an acute or chronic process that has an impact on the way the patient presents clinically. Knowledge of nerve pathways and relations to surrounding structures is fundamental when evaluating patients who have lower cranial nerve symptoms. A systematic "segment-based" approach helps to narrow the differential diagnosis Pathologic conditions that cause lower cranial nerve symptoms are presented. Full article (not yet available for free): www.quosafulltext.com/sc_ddm/sc_ddm.jsp |
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