Pain is more common in multiple sclerosis (MS) than has previously been recognised. In the present study we have investigated the occurrence of central pain (CP) in MS and defined its characteristics. Questionnaires were sent to all 429 patients with definite MS in the patient register at our neurology department. All admitting to pain were interviewed and offered an extended interview and examination. Three hundred and sixty four patients responded (86%), of whom 57.5% reported pain during the course of their disease (21% nociceptive, 2% peripheral neuropathic and 1% related to spasticity). One hundred patients (27.5%) had CP, including 18 patients (4.9%) with trigeminal neuralgia. The non-trigeminal CP was, in 87%, located in the lower and in 31% in the upper extremities. It was mostly bilateral (76%) and constant, with 88% experiencing daily pain. Only 2% had paroxysmal attacks. Aching, burning, pricking were the commonest qualities. The pain was intense with small to moderate spontaneous variation. In 5.5% of all patients (20% of the patients with CP), pain was a presenting symptom, alone or in combination with other symptoms. The most common neurological symptoms/signs besides CP were sensory abnormalities (98%, dominated by abnormal sensibility to painful stimulus and temperature). Trigeminal neuralgia in MS started later in life and after longer disease duration than non-trigeminal pain. Both types of CP existed either chronically or as a feature of relapse. Central pain is thus an important symptom in MS (around 30%) and causes much suffering.

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Different stroke sites produce different patterns of sensory deficit. The progression from painless sensory deficit to CPSP is not purely quantitative.

A series of positron emission tomography scans was made on two monkeys during a 16-month period when they received manganese(IV)oxide by subcutaneous injection. The distribution of [11C]-nomifensine uptake, indicating dopamine terminals, was followed in both monkey brains. The brain distributions of [11C]-raclopride, demonstrating D2 dopamine receptors, and [11C]-L-dopa, as a marker of dopamine turnover, were followed in one monkey each. The monkeys developed signs of poisoning namely unsteady gait and hypoactivity. The [11C]-nomifensine uptake in the striatum was reduced with time and reached a 60% reduction after 16 months exposure. This supports the suggestion that dopaminergic nerve endings degenerate during manganese intoxication. The [11C]-L-dopa decarboxylation was not significantly altered indicating a sparing of [11C]-L-dopa decarboxylation during manganese poisoning. A transient decrease of [11C]-raclopride binding occurred but at the end of the study D2-receptor binding had returned to starting values. The magnetic resonance imaging (MRI) revealed that the manganese accumulated in the globus pallidus, putamen and caudate nucleus. There were also suggestions of gliosis/edema in the posterior limb of the internal capsule. MRI might be useful to follow manganese intoxication in humans as long as the scan is made within a few months of exposure to manganese, i.e. before a reversal of the manganese accumulation.

Sixty-nine patients with traumatic knee hemarthrosis were evaluated an average of 3 days after trauma by high field (1.5T) magnetic resonance imaging (MRI) using sagittal T1, T2-weighted and coronal 3D-gradient echo images. All knees were arthroscopically examined shortly afterwards. The diagnostic validity of MRI for intraarticular pathology was determined using arthroscopy as golden standard. All patients had pathological findings on arthroscopy. The injuries were sports-related in 77% of the cases. MRI was highly sensitive (86%) and specific (92%) for diagnosis of anterior cruciate ligament tears. Diagnosis of medial meniscal tears showed a 74% sensitivity and 66% specificity. MRI detected lateral meniscal tears in 50% with an 84% specificity. As such, MRI missed 10 significant meniscus ruptures requiring surgical treatment. The sensitivity for partial or total medial collateral ligament tears was 56%, the specificity 93%. Rupture of the medial retinaculum in cases with patellar dislocation or significant damage of articular cartilage were only detected by MRI in a few cases (27% and 20% sensitivity, respectively). MRIs low diagnostic validity for intraarticular pathology with hemarthrosis may be attributed to the shifting paramagnetic properties of the blood remains and catabolic processes in meniscal and chondral tissues during the hemoglobin degradation process. Accordingly, MRI, with the technique used, could neither replace arthroscopy in the diagnosis and screening of acute knee injuries, nor select patients with need for immediate arthroscopic meniscal surgery.