Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We described a 4-month-old boy with cerebral infarction due to streptococcal meningitis. He complained of cough and high fever for 2 days. On the next day he admitted to our hospital because of bad humor, drowsiness, and vomiting associated with high fever, respiratory failure and loss of consciousness. On admission, he had opisthotonic posturing, anisocoria and elevated deep tendon reflexes with left side dominance. The cerebrospinal fluid showed increased cells (564/mm3), protein (295 mg/dl), and decreased sugar (1 mg/dl). Streptococcus pneumoniae was detected in the cerebrospinal fluid. Despite intensive treatment by antibiotics, glycerol, and dexamethasone, general condition was worsened, MRI showed a high intense area along the territory of bilateral anterior cerebral arteries and left middle cerebral artery 3-D time-of-flight MRA revealed a decreased signal of these arteries, confirming cerebral infarction. Recanalization of the arteries were observed 17 days after the first MRA examination. Since complication of cerebral infarction influences the prognosis of meningitis, repetitive MRA is very beneficial in patients with bacterial meningitis in order to evaluate the vascular lesion.
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PMID:[Usefulness of MRA in an infant with cerebral infarction due to streptococcal meningitis]. 894 Aug 80

We measured soluble intercellular adhesion molecule-1 (sICAM-1) in the serum and cerebrospinal fluid (CSF) of 35 clinically active relapsing-remitting (RR) multiple sclerosis (MS) patients who underwent both lumbar puncture and gadopentetate dimeglumine (Gd-DTPA)-enhanced MRI within an interval of 1 week, and of 30 neurological controls of whom 17 had noninflammatory neurologic diseases (NIND), 8 bacterial meningitis (BM), and 5 AIDS dementia complex (ADC). Thirteen of the MS patients assumed corticosteroids at the time of the study. While sICAM-1 serum levels were highest in the BM group (p < 0.005), untreated MS patients showed levels higher (p < 0.05) than treated MS and NIND, but similar to ADC. Moreover, the untreated MS group had CSF/serum sICAM-1:CSF/serum albumin (sICAM-1 index) values higher than the treated group (p < 0.01), NIND (p < 0.005), and BM (p < 0.05); high sICAM-1 index was found also in ADC. Untreated MS patients with one or more Gd-DTPA-enhancing MRI lesions (Gd-positive) had higher mean values of CSF/serum albumin ratio (QAlbumin) and CSF mononuclear cells compared to patients without such lesions (Gd-negative). In the untreated Gd-negative patients, sICAM-1 serum levels were higher (p < 0.05) than those in Gd-positive patients. In the latter group, there were positive correlations between the number of CSF mononuclear cells and both IgG (p < 0.01) and sICAM-1 indices (p < 0.05), between QAlbumin and QsICAM-1 (p < 0.005) and between Qalbumin and the Expanded Disability Status Scale score (p = 0.05). There were no significant correlations in the Gd-negative group. These results suggest that sICAM-1 index can be a better marker of intrathecal sICAM-1 synthesis than CSF levels and provide additional insights, in vivo, into the blood-brain barrier mechanisms underlying MRI Gd-enhancement in clinically active RR MS.
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PMID:Soluble intercellular adhesion molecule-1 in serum and cerebrospinal fluid of clinically active relapsing-remitting multiple sclerosis: correlation with Gd-DTPA magnetic resonance imaging-enhancement and cerebrospinal fluid findings. 896 Jul 41

Myelopathy is an infrequently reported complication of bacterial meningitis. We report the case of a preterm neonate with group B streptococcal meningitis who developed acute transverse myelopathy with subsequent spinal cord cavitation noted by MRI. The destruction of the cerebellum and obstructive hydrocephalus resulted in a posterior fossa cyst.
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PMID:Group B streptococcal meningitis: a case of transverse myelitis with spinal cord and posterior fossa cysts. 909 37

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been
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PMID:[A 64-year-old woman with progressive gait disturbance and dementia for one year]. 978 11

A 45-year-old woman had pyrexia, headaches, collapse and hyponatraemia. Intracerebral abscess, bacterial meningitis and subarachnoid haemorrhage were excluded. She was given intravenous antibiotics and gradually recovered. One month later she was readmitted with diplopia, headache and vomiting. Serum sodium was low (107 mmol/l) and a diagnosis of inappropriate ADH secretion was made. MRI scan showed a suprasellar tumour arising from the posterior pituitary gland. A skin rash gradually faded. Serum cortisol, prolactin, gonadotrophins and thyroid hormone levels were low. A pituitary tumour was removed trans-sphenoidally, she had external pituitary radiotherapy, and replacement hydrocortisone and thyroxine. She was well for 12 months when she developed progressive weakness and numbness of both legs. Examination suggested spinal cord compression at the level of T2 where MRI scanning showed an intradural enhancing mass. This spinal tumour was removed and her neurological symptoms disappeared. Nine months after this she developed facial pain and nasal obstruction. CT scan showed tumour growth into the sphenoid sinus and nasal cavities. A right Cauldwell-Luc operation was done and residual tumour in the nasal passages was treated by fractionated external radiotherapy and Prednisolone. Histological examination of the specimens from pituitary, spinal mass, and nasal sinuses showed Rosai-Dorfman disease, a rare entity characterized by histiocytic proliferation, emperipolesis (lymphophagocytosis) and lymphadenopathy. Aged 48 she developed cranial diabetes insipidus. Although Rosai-Dorfman syndrome is rare, it is being reported with increasing frequency, and should be borne in mind as a possible cause of a pituitary tumour.
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PMID:Rosai-Dorfman disease presenting as a pituitary tumour. 1034 67

A 61-year-old male fell from a position 1 m high when building a house. An iron rod, which protruded upward from a solid base in cement, penetrated this patient's neck 15 cm to the head and was successfully extracted by himself. On admission, he complained of headache and vomiting. General examination disclosed nasal bleeding, intraoral bleeding, and L figured skin laceration in the left side of his neck at the level of the thyroid cartilage. Mild disorientation (JCS2) was noted. Otolaryngological examination disclosed hyperemia on the left side of the vocal cord as well as at the dome of the superior pharynx. Plain skull film disclosed pneumocephalus and that a piece of bone fragment of the planum sphenoidale had penetrated the brain. CT demonstrated air in the subarachnoid space, ventricular hemorrhage, intracerebral hematoma in the right frontal lobe, and subarachnoid hemorrhage in the anterior interhemispheric fissure. CAG detected neither cerebral vascular abnormalities nor cerebral aneurysm. While staying in our department, he developed mild fever and CSF rhinorrhea. The diagnosis of bacterial meningitis was made from the CSF finding and was well controlled with conservative therapy. CSF rhinorrhea stopped spontaneously with conservative treatment. Sagittal MRI continuously demonstrated contusional hematoma in the base of the right frontal lobe just above the fractured planum sphenoidale and genu of the corpus callosum following the course of the intracranially invading iron rod. The right CAG on Day 10 demonstrated vasospasm on the A1 and a 1 cm sized saccular cerebral aneurysm at the proximal right fronto-polar artery. CAG on Day 17 again showed the persistent presence of the aneurysm. For the purpose of preventing delayed rupture of the aneurysm, radical surgical treatment was planned. Microsurgical dissection disclosed that the aneurysm was located just behind the elevated fracture of the planum sphenoidale. Severe arachnoid adhesion was noted around the aneurysm. The aneurysm was successfully clipped with preservation of the parent artery without inducing new neurological deficits. From the general, otolaryngological, neuroradiological, and operative findings, this aneurysm was diagnosed as a traumatic cerebral artery aneurysm following the penetration of the skull base by the iron rod. The CAG performed at 8 months postoperatively demonstrated the patency of the parent artery and that there was no recurrence of the aneurysm. An unusual case of a traumatic cerebral artery aneurysm following the penetration of the skull base by an iron rod was thus reported.
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PMID:[A case of a traumatic anterior cerebral artery aneurysm following the penetration of the skull base by an iron rod]. 1039 43

Cavernomas fall within the group of angiographically occult lesions and may be found in up to 4 % of the population [1]. They may occur at any age, and with the advent of MRI incidental cavernomas are increasingly identified. The pathogenesis is uncertain. Familial cases are well recognised with a reported prevalence of 10-15 % [2-3]. The incidence of new lesions has been reported at 0.4 lesions per patient per year in cases with familial cavernomas [4]. Presumed cavernomas have been documented following radiation for malignancy [5-6], and stereotactic cerebral biopsy [7]. There have been no previously documented cases of de novo genesis of cavernomas following bacterial meningitis and subdural empyemas.
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PMID:De novo development of presumed cavernomas following resolution of E. Coli subdural empyemas. 1111 86

A 38-year-old man with past history of head injury at the age of 16 years was admitted to our hospital in April, 2000 because of bacterial meningitis. At the end of March 2000, he experienced massive cerebrospinal fluid (CSF) rhinorrhea when he rested in bed, and subsequently he developed high-grade fever, headache, and nuchal stiffness in 2 weeks. His symptoms and signs improved with the antibiotic therapy alone. He had no recurrence of meningitis since then. A defect of his right skull base was clarified by 3D-CT, and multiplanar reconstruction (MPR)-CT. MRI brain scan showed the dislocation of the right frontal lobe into the ipsilateral anterior ethmoidal sinus. The diagnosis of CSF rhinorrhea and bacterial meningoencephalitis were made according to his clinical manifestations and neuroradiological studies including 3D-CT, MPR-CT and MRI brain scans. These imaging modalities, which described his head anatomy precisely, helped us to clarify the cause of his illness. When CSF rhinorrhea is present, it is important to take detailed past history of head trauma, even if the event occurred more than 20 years previously.
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PMID:[A case with bacterial meningitis caused by cerebrospinal fluid rhinorrhea 22 years after head trauma]. 1180 57

Paresis or palsy of upward vertical gaze, pupillary light-near dissociation and nystagmus retractorius with convergence, were present in a boy aged 16 years and a woman aged 30 years with an obstructive hydrocephalus due to an aqueductal stenosis as a consequence of a bacterial meningitis and in a woman aged 26 years and a man aged 47 years with an outlet obstruction of the fourth ventricle after a posterior fossa operation for a tumour in the fourth ventricle. All of the patients were suspected of having a drain dysfunction. They all underwent a third-ventriculocisternostomy after which their symptoms (partially) resolved. The presenting symptoms stated are the classical triad of Parinaud's syndrome. In addition to these there are less frequent symptoms such as bilateral eyelid retraction (Collier's sign) and convergence spasms. The syndrome is rare but has a significant mortality risk and a high morbidity rate if an obstructive hydrocephalus is not diagnosed and treated. An MRI scan of the cerebrum to detect obstructive hydrocephalus with dilation of the aqueduct is the diagnostic of choice. For an obstructive hydrocephalus with dilation of the aqueduct a third-ventriculocisternostomy is the treatment of choice.
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PMID:[Parinaud's syndrome as a sign of acute obstructive hydrocephalus: recovery after acute ventriculostomy]. 1209 6

Bacterial meningitis is frequently fatal or leads to severe neurological impairment. Complications such as vasculitis, resulting in infarcts, should be anticipated and dealt with promptly. Our aim was to demonstrate the complications of meningitis by diffusion weighted imaging (DWI) in patients who deteriorated despite therapy. We studied 13 infants between the ages of 1 day and 32 months who presented with symptoms ranging from fever and vomiting to seizures, encephalopathy and coma due to bacterial meningitis, performing MRI, including DWI, 2-5 days after presentation. Multiple infarcts were found on DWI in 12 of the 13, most commonly in the frontal lobes (in 10). Global involvement was seen in four children, three of whom died; the fourth had a very poor outcome. In one case abnormalities on DWI were due to subdural empyemas. We diagnosed vasculitis in three of five patients studied with MRA. We think DWI an important part of an MRI study in infants with meningitis. Small cortical or deep white-matter infarcts due to septic vasculitis can lead to tissue damage not easily recognized on routine imaging and DWI can be used to confirm that extra-axial collections represent empyemas.
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PMID:Diffusion-weighted imaging in acute bacterial meningitis in infancy. 1290 92


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