Spinal cord and spinal nerve root involvement (myeloradiculopathy) in tuberculous meningitis.

Most of the information about spinal cord and nerve root involvement in tuberculous meningitis is available in the form of isolated case reports or case series. In this article, we evaluated the incidence, predictors, and prognostic impact of spinal cord and spinal nerve root involvement in tuberculous meningitis.In this prospective study, 71 consecutive patients of newly diagnosed tuberculous meningitis were enrolled. In addition to clinical evaluation, patients were subjected to magnetic resonance imaging (MRI) of brain and spine. Patients were followed up for at least 6 months.Out of 71 patients, 33 (46.4%) had symptoms/signs of spinal cord and spinal nerve root involvement, 22 (30.9%) of whom had symptoms/signs at enrolment. Eleven (15.4%) patients had paradoxical involvement. Paraparesis was present in 22 (31%) patients, which was of upper motor neuron type in 6 (8.4%) patients, lower motor neuron type in 10 (14%) patients, and mixed type in 6 (8.4%) patients. Quadriparesis was present in 3 (4.2%) patients. The most common finding on spinal MRI was meningeal enhancement, seen in 40 (56.3%) patients; in 22 (30.9%), enhancement was present in the lumbosacral region. Other MRI abnormalities included myelitis in 16 (22.5%), tuberculoma in 4 (5.6%), cerebrospinal fluid (CSF) loculations in 4 (5.6%), cord atrophy in 3 (4.2%), and syrinx in 2 (2.8%) patients. The significant predictor associated with myeloradiculopathy was raised CSF protein (>250 mg/dL). Myeloradiculopathy was significantly associated with poor outcome.In conclusion, spinal cord and spinal nerve root involvement in tuberculous meningitis is common. Markedly raised CSF protein is an important predictor. Patients with myeloradiculopathy have poor outcome.

HSV-2 DNA persistence in astrocytes of the trigeminal root entry zone: double labeling by in situ PCR and immunohistochemistry.

A previous study using an in situ polymerase chain reaction (PCR) amplification method showed persistent herpes simplex virus type 2 (HSV-2) DNA sequences in brains of experimentally infected mice, particularly in cells of the pons near the trigeminal root entry zone. The present study was undertaken to identify the CNS cell type(s) that persistently harbor HSV DNA and to define the associated pathology. Tissue sections including the trigeminal root were immunoreacted to detect cellular antigens, then an HSV sequence was amplified in situ. During acute infection, the CNS portion of the trigeminal root was focally demyelinated and contained viral antigen and HSV DNA in glial cells. Following acute infection, no infectious virus of HSV antigen was detected. Demyelinated root lesions contained cells whose nuclei were similar in size to those of astrocytes and contained HSV-2 DNA by in situ PCR. With double labeling techniques, HSV DNA-containing nuclei were often associated with glial fibrillary acidic protein immunoreactivity, but not with that of neuron-specific enolase and only rarely with galactocerebroside or transferrin immunostaining. Thus, at least some of the cells containing persistent HSV DNA are astrocytes. Since HSV DNA is detected when no infectious virus can be isolated and no HSV antigen is found, we conclude that this astrocytic infection is non-productive. While in situ hybridization methods show HSV latency-associated transcript (LAT) RNA in neuronal nuclei during latent infections in trigeminal ganglia and, occasionally, in brain, we were unable to detect HSV-2 LAT RNA in astrocytes in these lesions, which suggests that persistent HSV infection of astrocytes may differ from neuronal latency.(ABSTRACT TRUNCATED AT 250 WORDS)

The pathogenesis of pseudorabies in mice: virus replication at the inoculation site and axonal uptake.

Three-week-old mice were inoculated in the right ear pinna with pseuforabies virus. Ears were surgically removed at various times after inoculation and changes from the normal pathogenesis were observed. Virus replication in the ear tissue and cervical dorsal root ganglia was also monitored. Followed inoculation with a small dose of virus, local multiplication of the virus was necessary before the infection spread to the nerves. With larger infecting doses there was probably direct uptake of virus from the inoculum into the nerve endings. After these larger doses virus was first detected in the dorsal root ganglia 17 h agter infection, suggesting a retrograde axonal flow rate of at lease 1-7 mm/h.

Acute Lyme neuropathy presenting with polyradicular pain, abdominal protrusion, and cranial neuropathy.

A 53-year-old man developed multifocal radicular pain. The diagnosis of Lyme neuroborreliosis was delayed until bifacial paresis and right lower abdominal wall weakness developed, prompting further evaluation. Cerebrospinal fluid (CSF) examination showed aseptic meningitis. Antibodies directed against Borrelia burgdorferi were present in the serum; higher titers were present in the CSF, indicating local antibody production. Electrophysiologic studies showed both an axonal polyradiculopathy as well as demyelinative facial palsy. Ceftriaxone therapy led to marked improvement in pain and facial palsies.

Paraplegia associated with brucellosis involving the anterior lumbrosacral nerve roots.

We report the case of a 21-year-old man with paraplegia due to brucellosis involvement of lumbosacral anterior roots. Lumbosacral magnetic resonance imaging showed contrast enhancement of anterior roots and the anterior part of duramater. Conduction block was found at the level of the lumbosacral anterior roots by electrophysiological studies, including magnetic stimulation study. Wright agglutination, Rose Bengal tests and bacterial culture obtained from cerebrospinal fluid confirmed the diagnosis of neurobrucellosis. Oral administration of ceftriaxon with additional rifampin was effective, and after 3 months of treatment, laboratory data resolved and clinical signs partially improved.

Histopathologic effects of discitis on neural tissues: an experimental study.

To determine the cause of neurologic symptoms and signs seen in discitis, the neural histopathologic effects of discitis were investigated in an experimental study carried out on rats. Groups of seven rats each had their intervertebral discs inoculated with either Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, or a control solution. Histopathologic examinations of the spinal cord and nerve roots were performed after 3 weeks. On histopathologic examination, vacuolar myelopathy in the spinal cord and vacuolar neuropathy within the nerve roots near the junction with the spinal cord were found. The severity and form of vacuolar myelopathy varied according to the bacteria used for inoculation. The myelopathy and neuropathy seen in this rat model of bacterial discitis might be the result of an immunologic mechanism and could be responsible for the neurologic signs and symptoms of discitis in patients.

Neurobrucellosis and a demonstration of its involvement in spinal roots via magnetic resonance imaging.

OBJECTIVE: To present a neurobrucellosis case with spinal root involvement by means of magnetic resonance imaging (MRI). METHODS: A case of neurobrucellosis resembling Guillain-Barré syndrome is being reported. This case is unique in a way that spinal root involvement because of brucellosis was for the first time confirmed by MRI. SETTING: Spinal cord unit of a rehabilitation and care center in Ankara, Turkey. RESULTS: The correct diagnosis was made with cerebrospinal fluid culture. The patient showed a significant improvement with antimicrobial therapy and rehabilitation. CONCLUSION: Polyradiculopathy because of neurobrucellosis may mimic neurological syndromes. Rehabilitation should also be a part of its treatment.

Acute varicella-zoster virus ventriculitis and meningo-myelo-radiculitis in acquired immunodeficiency syndrome.

A 30-year-old AIDS patient with no history of cutaneous eruption, presented with rapidly progressive flaccid paraplegia, hypoesthesia, urinary retention, moderate psychomotor slowing and fever (39.8 degrees C), leading to death within 1 week. CD4 count was 290/mm3. Cerebrospinal fluid contained 210 white blood cells and 238 mg/100 ml protein. Neuropathology revealed HIV encephalitis and diffuse ventriculitis with Cowdry type A inclusions in the ependymal cells. Extensive necrotic and hemorrhagic changes with marked recrotizing vasculitis involved the entire spinal cord and spinal roots. Immunocytochemistry revealed numerous inclusion bodies positive for varicella-zoster virus (VZV) and negative for cytomegalovirus (CMV) and herpes simplex virus type 1 and 2, in ependymal cells, subpial glial cells, endothelial cells and Schwann cells. Electron microscopy confirmed herpes virus-like particles. In situ hybridization confirmed VZV genome in leptomeninges, brain, spinal cord and spinal roots. Comparable neuropathological findings and numerous VZV inclusion bodies were also found in the brain, spinal cord, and spinal roots of a 40-year-old AIDS patient who died from a fulminant ascending myeloradiculopathy previously reported as "necrotizing vasculitis of the nervous system". Direct infection of the brain by VZV, in AIDS patients, has been shown to cause leukoencephalitis and cerebral non-inflammatory vasculopathies. Our observations demonstrate that, in AIDS patients, VZV infection of the central nervous system may also be responsible for meningo-myelo-radiculitis possibly secondary to ventriculitis as in CMV infection. The role of VZV in the pathogenesis of some AIDS-related vasculitides seems also very likely.