Delayed cerebral thrombosis complicating bacterial meningitis.

BACKGROUND: Delayed cerebral thrombosis has been described as a potential cause of cerebrovascular complications in patients with bacterial meningitis. We report a case of delayed cerebral thrombosis in a 63-year-old woman admitted for pneumococcal meningitis. Initially, there was a good clinical evolution under treatment with steroids and antibiotics. On day 8 after admission, she was found with a decreased level of consciousness. Her neurological condition gradually worsened. Repeated brain imaging showed extensive ischemic lesions. Despite treatment with high-dose corticosteroids, the patient died. METHODS: A literature search was conducted. Data on patient characteristics, diagnosis, treatment and outcome were collected. RESULTS: To date, 28 cases with delayed cerebral thrombosis following bacterial meningitis have been reported. Streptococcus pneumoniae was the pathogen in 89% of cases. Clinical deterioration occurred in all patients, with a duration varying from 5 to 40 days between admission and deterioration. Most common symptom was altered consciousness (83%), followed by hemiparesis (52%). Brain imaging typically shows new infarctions (96%). Fifty-six percent of patients were treated with corticosteroids after deterioration. Outcome was poor with mortality rate of 46%. CONCLUSION: Delayed cerebral thrombosis presents as a clinical deterioration, typically a sudden decline in consciousness, more than 5 days after meningitis onset. Brain imaging shows new widespread ischemic lesions. Diagnosis should be made carefully, based on clinical findings and brain imaging, after excluding endocarditis. The underlying etiology remains unknown. When delayed cerebral thrombosis is suspected, high-dose corticosteroids should be started empirically. The prognosis remains poor with high mortality rates.

MRI characteristics of trigeminal nerve involvement in patients with multiple sclerosis.

BACKGROUND: Trigeminal neuralgia and central sensory disturbances are common in patients with multiple sclerosis. The anatomic correlation to lesions in the trigeminal nuclei in the brainstem is not well studied. OBJECTIVE: We studied the anatomical characteristics of demyelinating lesions of the trigeminal complex in the brainstem on MRI in patients with MS and Clinically Isolated syndrome (CIS). MATERIALS AND METHODS: 43 Patients with MS or CIS and MRI lesions in the trigeminal complex in the brainstem were selected from a large database of patients referred for MRI because of trigeminal symptoms. RESULTS AND CONCLUSION: A linear plaque involving the intrapontine fascicular part of the trigeminal nerve and lesions of the spinal trigeminal nucleus and tract seem to be distinctive MRI findings in patients with RRMS or CIS.

Regional changes in type 1 cannabinoid receptor availability in Parkinson's disease in vivo.

The type 1 cannabinoid receptor (CB1) is a crucial modulator of synaptic transmission in brain and has been proposed as a potential therapeutic target in Parkinson's disease (PD), especially for treatment of levodopa-induced dyskinesias (LID). Our aim was to measure CB1 levels in brains of PD patients in vivo and to investigate the relation between CB1 availability and LID. We studied 12 healthy controls and 29 PD patients (9 drug-naïve patients with early PD, 10 patients with advanced PD and LID, and 10 patients with advanced PD without LID). PD patients were examined using the Unified Parkinson's Disease Rating Scale (UPDRS) and the modified Abnormal Involuntary Movement Scale (mAIMS). All subjects underwent positron emission tomography (PET) with the CB1-selective radioligand [(18)F] MK-9470 and magnetic resonance imaging (MRI). PD patients showed an absolute decrease in CB1 availability in the substantia nigra. By contrast, CB1 availability was relatively increased in nigrostriatal, mesolimbic, and mesocortical dopaminergic projection areas. CB1 availability did not differ significantly between advanced PD patients with and without LID. Within the group of PD patients with LID, there was no significant correlation between CB1 availability and LID severity. These data demonstrate regional changes in CB1 availability in PD in vivo, but do not support a role for dysregulation of CB1 levels in the pathogenesis of LID.