All Posts Tagged With: "neuroborreliosis"

Linda’s comment:  Clinical, diagnostic and immunological characteristics of patients with possible neuroborreliosis without intrathecal Ig-synthesis against Borrelia antigen in the cerebrospinal fluid.

PCR did not reveal any Borrelia antigen in CSF. The diagnosis
and treatment of possible but not confirmed neuroborreliosis is a
clinical challenge. The clinical response to treatment may be the best
option in these cases.

Linda’s comment: The first Swiss patient with meningovasculitis due to neuroborreliosis, with recurrent multiple ischemic strokes in multiple vascular territories is evident in clinical manifestation of borreliosis. Strokes have also been found with patients with Bartonella.

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20434741&retmode=ref&cmd=prlinks

Excerpt:

The
treatment with ceftriaxone stopped the progression, but the
patient is still suffering from severe invalidating cognitive
disorders. We also comment on the pathophysiology and review the
literature of other clinical cases. Copyright (c) 2010 Elsevier
Masson SAS. All rights reserved.

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21073390&retmode=ref&cmd=prlinks

Excerpt:

Clinical Findings-Physical examination revealed that the horse was dull,
appeared depressed, was reluctant to raise its neck and head above a
horizontal plane, and had a temperature of 38.5 degrees C (101.3 degrees F).
No radiographic or scintigraphic abnormalities of the neck were found;
however, high plasma fibrinogen concentration and relative lymphopenia were
identified and the horse was seropositive for antibodies against Borrelia
burgdorferi. Analysis of CSF revealed neutrophilic inflammation, and results
of a PCR assay of CSF for B burgdorferi DNA were positive. Immunologic
testing revealed severe B-cell lymphopenia and a low serum IgM concentration
consistent with common variable immunodeficiency. 

Treatment and Outcome-The horse responded well to doxycycline treatment (10
mg/kg [4.5 mg/lb], PO, q 12 h for 60 days) and returned to normal exercise.
However, 60 days after treatment was discontinued, the horse again developed
a stiff neck and rapidly progressive neurologic deficits, including severe
ataxia and vestibular deficits. The horse’s condition deteriorated rapidly
despite IV oxytetracycline treatment, and the horse was euthanatized.
Postmortem examination revealed leptomeningitis, lymphohistiocytic
leptomeningeal vasculitis, cranial neuritis, and peripheral radiculoneuritis
with Wallerian degeneration; findings were consistent with a diagnosis of
neuroborreliosis.

Clinical Relevance-Nervous system infection with B burgdorferi should be
considered in horses with evidence of meningitis and high or equivocal serum
anti-B burgdorferi antibody titers. Evaluation of immune function is
recommended in adult horses evaluated because of primary bacterial
meningitis.

Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20805550&retmode=ref&cmd=prlinks

Excerpt:

Lyme disease is most prevalent in the northeast and upper Midwest
regions of the United States. While early symptoms may be mild
(eg, rash, flu-like symptoms, joint pain), late or persistent
infection can cause chronic neurologic impairments. Because of
this range of symptoms, physicians can have difficulty diagnosing
Lyme disease, especially in the absence of erythema chronicum
migrans. We report a case of a woman who initially presented with
severe vertigo and vomiting and later with fever, headache, and
facial droop. After more than 3 weeks of misdiagnosis, the
patient tested positive for Lyme disease and was diagnosed as
having neuroborreliosis presenting as Bell palsy and meningitis.
The authors review the history, diagnosis, and management of Lyme
disease. 

Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20842825&retmode=ref&cmd=prlinks

Excerpt:

Lyme borreliosis is a multisystem disease and when involves the
nervous system it is termed neuroborreliosis. The symptomatology
of peripheral neuroborreliosis is rich and varied. The early
symptoms are asymmetric polyradiculopathies and paralysis of the
cranial nerves (most commonly facial nerve). Thereafter, there
are multifocal mononeuropathies and
sensory-motorpolyneuropathies. Difficulties in making a correct
diagnosis can result from the long time lag between tick bite and
the occurrence of neurological symptoms. In the treatment the
most important role play antibiotics. 
CASE REPORTS: We report the cases of three patients with symptoms
of damage to various structures of the peripheral nervous system
in the course of Borrelia burgdorferi infection. In all cases,
clinical improvement was obtained after treatment with
antibiotics, which further confirms the diagnosis of
neuroborreliosis. 
CONCLUSIONS: About neuroborreliosis
as a cause of peripheral neuropathy we should always think in the
case of vague symptoms of peripheral nervous system lesions in
patients with potential exposure to tick bites. Peripheral
neuropathies may occur a long interval from the tick bite and are
not always preceded by other forms of the disease.

Full article: http://www.ncbi.nlm.nih.gov/pubmed/2795099

Excerpt:

In 1987, follow-up studies were conducted on 72 patients who had had meningoradiculitis and encephalomyelitis (8 patients) due to Borrelia burgdorferi 5-27 years previously. These patients had not been treated with antibiotics, either during the acute disease or during the interval prior to follow-up studies. The patients had exhibited the typical symptoms of Bannwarth’s syndrome during the acute phase. At the follow-up studies, 33 patients showed no, and 23 only mild, clinical residual symptoms including normal CSF findings and low-positive serum IgG borrelia antibody titres (IFT; ELISA). Three patients without sequelae exhibited persistent intrathecal secretion of oligoclonal B. burgdorferi-specific CSF IgG antibodies (Immunoblot; positive borrelia CSF IgG antibody titres). Thirteen patients exhibited mild-to-medium sequelae with persistent intrathecal formation of oligoclonal B. burgdorferi-specific CSF IgG antibodies, up to 21 years after the acute illness. This persistence can be interpreted as an “immunological scar syndrome”. Our follow-up studies appear to indicate that neurological manifestations of B. burgdorferi infections are generally (with few exceptions) of a benign nature. Most patients can be classified as having been cured without antibiotic therapy. No late manifestations of chronic progressive CNS borreliosis comparable to that of neurosyphilis have been seen following acute untreated neuroborreliosis.

Full article: http://www.biomedcentral.com/content/pdf/1471-2334-10-205.pdf

Excerpt:

Results

An informative pattern was obtained by combining two of the analysed parameters: (i), the fractions of HLA-DR-expressing CD4+ T cells and CD8+ T cells, respectively, and (ii), the level of CD40 on CD14+ CD16- monocytes. Patients infected with gram-negative bacteria or EBV showed a marked increase in monocyte CD40, while this effect was less pronounced for tuberculosis, borrelia and influenza. The bacterial agents could be distinguished from the viral agents by the T cell result; CD4+ T cells reacting in bacterial infection, and the CD8+ T cells dominating for the viruses. Patients with systemic autoimmunity also showed a increased activation, but with similar engagement of CD4+ and CD8+ T cells. Analysis of soluble TNF alpha receptors was less informative due to a large inter-individual variation.

Conclusion

Immunophenotyping including the combination of the fractions of HLA-DR expressing T cell subpopulations with the level of CD40 on monocytes produces an informative pattern, differentiating between bacterial origin, viral origin and systemic autoimmunity. Furthermore, it provides some indication of a subacute bacterial infection, such as borreliosis or tuberculosis. This flow cytometric method is suitable for clinical diagnostic laboratories, and may help in the assessment of patients with uncharacteristic inflammatory symptoms.

Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20698315&retmode=ref&cmd=prlinks

Excerpt:

The authors describe a case of Lyme disease–neuroborreliosis. In
neuroborreliosis, there are morphohistological changes:
pronounced dystrophic processes in the brain nerve cells,
spongiosis, perivascular hemorrhagic infiltrations, glial
proliferation with the formation of perivascular glial
granulomas.

Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20561635&retmode=ref&cmd=prlinks

Excerpt:

RESULTS: Eleven patients who presented with acute central nervous
system (CNS) syndrome fulfilled the diagnostic criteria for
neuroborreliosis. In the CSF studies, lymphocytic pleocytosis
with elevation of total protein and normal glucose was noted in 9
patients. The clinical syndromes were confirmed by magnetic
resonance imaging and electrophysiological studies. Ten of 11
patients were found to have brain stem or spinal cord lesions on
neuroimaging studies, and 8 patients had concomitant peripheral
nervous system involvement with electrophysiological evidence of
multiple root lesions with an acute or subacute course.
CONCLUSIONS: Lyme neuroborreliosis presenting as acute CNS
syndrome with peripheral nervous system involvement
simultaneously in the disease course, especially acute
myelopolyradiculitis, in Taiwan is different from Lyme
neuroborreliosis seen in Europe and North America. The treatment
outcome is variable and based on the severity of initial
neurological deficits, early diagnosis, and early management.
Copyright (c) 2010 Elsevier B.V. All rights reserved.

Excerpt:

We report the case of a 30-year-old man who developed severe
dysphagia owing to neuroborreliosis. He showed dysphagia,
diplopia, hiccups, and walking difficulty Neurological
examination revealed mild disturbance of consciousness, diplopia
on left lateral gaze, left-side-dominant blephaloptosis,
gaze-evoked horizontal nystagmus on left lateral gaze, mild
bilateral muscle weakness, palatoplegia, dysphagia, dysarthria,
and truncal ataxia An increased pharyngeal reflex caused
dysphagia in this patient. An EEG revealed intermittent high
amplitude slow wave activity. However, head MRI, blood count,
serum chemistry, and cerebrospinal fluid examination showed no
abnormality. Initially, brainstem encephalitis with unknown
etiology was diagnosed. The hiccups, diplopia, and ptosis were
improved by corticosteroid therapy, but other symptoms were
refractory to corticosteroid therapy and IVIg.