All Posts Tagged With: "CSF"

Cerebrospinal fluid in adults with Lyme

Excerpt:

In acute LNB, all
patients had elevated cerebrospinal fluid (CSF) leukocyte counts. In
contrast to infections by other bacteria, CSF lactate was lower than 3.5
mmol/l in all but 5 patients. The CSF findings did not differ between
polyradiculoneuritis, facial palsy, and meningitis. The CSF in LNB
patients strongly differed from CSF in VM patients with respect to
protein concentration and the CSF/serum albumin quotient.

Meningoradiculitis and encephalomyelitis due to Borrelia burgdorferi

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.

Tick-borne encephalitis (TBE) in a 6 week old infant

Full article: https://www.thieme-connect.com/ejournals/abstract/neuropediatrics/doi/10.1055/s-2004-819478

Excerpt:

Case report: A 6-week-old girl developed fever, irritability, meningeal signs with bulging fontanelle and a partial, secondary-generalized seizure. CSF yielded pleocytosis (172 lymphocytes, 81 mono-cytes/ul) and elevated protein (0,83g/l), cranial MRI showed encephalitic signs in both frontal and parietal lobes. Because of a tick bite in an endemic area 10 days before admission, ELISA-IgG and IgM to TBE-virus were sought and found in serum, whereas Borrelia burgdorferi serology, Herpes-simplex virus PCR and bacterial CSF-culture were negative. Phenobarbitone was administered because of repetitive seizures, while the EEG showed series of sharp waves in the right parieto-temporal region. She consecutively became seizure free. At first follow-up after 6 weeks she demonstrated pathologic neurological signs with increased muscular tone, hyperreflexia, fidgety movements, and EEG showed slow waves in the right parieto-temporal region.

Clinical manifestations and neuroimaging in neuroborreliosis

Full article: https://www.thieme-connect.com/ejournals/abstract/neuropediatrics/doi/10.1055/s-2006-974121

Excerpt:

Neuroborreliosis often presents with cranial nerve palsy, aseptic meningitis or meningoencephalitis. Cerebral arteriopathy has rarely been reported as single cases. Here we present a retrospective analysis from 1997 to 2005 in the Berlin area. In this period neuroborreliosis was confirmed in 47 children through the finding of specific antibodies against Borrelia burgdorferi in CSF.

22 (47%) suffered from facial palsy as a presenting symptome, in one of them the palsy was bilateral. Four children (9%) had palsies of other cranial nerves, and four patients (9%) presented with paresis of an arm, hemiparesis, or spastic paraparesis. 16 children (34%) reported headache on admission, 15 (32%) presented with myalgia and/or arthralgia. Two patients (4%) had paraesthesia, another two (4%) were atactic. Ten (21%) had unspecific symptoms such as fever, fatigue, loss of appetite, or nausea. Other symptoms included general slowdown, sensoric or motoric aphasia, agitation, confusion, incomplete Horner’s syndrome, and mucosa haemorrhage, each in one patient.

In 19 patients (40%) cerebral imaging was performed. 13 (68%) were found to be normal, or rather revealed typical lesions in a patient with an underlying neurofribromatosis type 1. In one child with hemiparesis, and in one with multiple cranial nerve palsies, arterial subtraction angiography (DAS) confirmed multifocal vasculitis and dissection of the left Aa. vertebralis and basilaris, respectively. In one girl with hemiplegia, MRI revealed an infarction of the according internal capsule. Although angiography was not done this finding is suspicious of focal arteriopathy. The girl also had a homozygous mutation of factor V Leiden.

Neuroborreliosis – an epidemiological, clinical and health economical s

Neuroborreliosis – an epidemiological, clinical and health economical study from an endemic area in the south-east of Sweden.

Excerpt:

Department of Infectious Diseases, Ryhov County Hospital, Jönköping, Sweden.

We studied retrospectively the medical records of all patients diagnosed with neuroborreliosis (NB) by cerebrospinal fluid (CSF) analysis in Jönköping County, Sweden, during 2000-2005 (n=150). The number of NB cases increased from 5 to 10/100,000 inhabitants/year. In 17% of the patients, Borrelia-antibodies were found in CSF but not in serum at the time of diagnosis. Facial palsy, headache and fever were frequent manifestations in children, whereas unspecific muscle and joint pain were the most commonly reported symptoms in older patients.

Lyme Encephalopathy

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists. First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

Is the diagnosis correct?
Are there comorbid psychiatric disorders that could be treated better? Does the patient have a psychogenic medical illness? What was the patient’s response to prior antibiotics?
Was previous treatment adequate? How long was the course, and what was the route of administration? Was there a subsequent relapse Continued

Lyme Encepalopathy

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists.
First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

Is the diagnosis correct?
Are there comorbid psychiatric disorders that could be treated better? Does the patient have a psychogenic medical illness? What was the patient’s response to prior antibiotics?
Was previous treatment adequate? How long was the course, and what was the route of administration? Was there a subsequent relapse Continued