Biomedical subjects
F Vingerhoets
Publications and source records attributed to F Vingerhoets.
Manganese intoxication in the rhesus monkey: a clinical, imaging, pathologic, and biochemical study.
We gave three adult rhesus monkeys seven IV injections of manganese chloride at approximately 1-week intervals. We evaluated neurologic status by serial clinical examinations and performed a levodopa test if the animal developed features of basal ganglia dysfunction. After the animals were killed, we performed neuropathologic, neurochemical, and laser microprobe mass analysis (LAMMA) studies. Two of three animals developed a parkinsonian syndrome characterized by bradykinesia, rigidity, and facial grimacing suggestive of dystonia but not tremor. Neither animal responded to levodopa. Autopsy demonstrated gliosis primarily confined to the globus pallidus (GP) and the substantia nigra pars reticularis (SNr). We detected focal mineral deposits throughout the GP and SNr, particularly in a perivascular distribution. LAMMA studies noted that mineral deposits were primarily comprised of iron and aluminum. The severity of pathologic change correlated with the degree of clinical dysfunction. These studies demonstrate that, in contrast to Parkinson's disease (PD) and MPTP-induced parkinsonism, manganese primarily damages the GP and SNr and relatively spares the nigrostriatal dopaminergic system. Further, the results suggest that Mn-induced parkinsonism can be differentiated from PD and MPTP-induced parkinsonism by the clinical syndrome and response to levodopa. The accumulation of iron and aluminum suggests that iron/aluminum-induced oxidant stress may contribute to the damage associated with Mn toxicity.
Chronic relapsing neuropathy associated with Castleman's disease (angiofollicular lymph node hyperplasia).
We report a 17-year-old patient who presented a chronic relapsing sensorimotor demyelinating neuropathy with 6 relapses over a 7-year period, preceding by 4 years the diagnosis of a multicentric angiofollicular lymph node hyperplasia. A role for Epstein-Barr virus (EBV) as a trigger of the neuropathy may be suggested by the presence of EBV DNA in the biopsied abdominal abdominal adenopathies. This unusual reported association seems to have a better prognosis than the known chronic progressive form of neuropathy associated with Castleman's disease and the Crow-Fukase syndrome.
Respiratory dysfunction in stroke.
Respiratory function depends on numerous neurologic structures, the organization of which extends from the cerebral cortex to the medulla. The study of patients who have had strokes has allowed deductions about this organization, and various neurologic pathways have been increasingly recognized. The voluntary pathway travels with the corticospinal motor tract. It is typically damaged in the "locked-in" syndrome and leads to normal automatic breathing that cannot be voluntarily altered. The automatic pathway takes its origin in the lower brainstem and is damaged mainly in lateral medullary strokes. Even a unilateral lesion here may lead to complete failure of respiration and result in death during sleep (Ondine's curse). The preservation of the limbically induced fluctuations of respiration in automatic breathing suggests a third pathway that may share its distal extent with the automatic pathway. Respiratory dysfunctions may also provide useful information regarding the cause and prognosis of stroke.
Atrial fibrillation after acute stroke.
BACKGROUND AND PURPOSE: Atrial fibrillation (AF) is a risk factor for stroke, although it may not always be directly responsible for the stroke. On the other hand, cardiac arrhythmias and electrocardiographic changes have been reported after ischemic stroke and numerous other intracranial pathologies. We tested the hypothesis that some patients with acute stroke may develop transient AF as a consequence of the stroke. METHODS: This study was based on 1,661 patients with first-ever stroke consecutively hospitalized and prospectively included into the Lausanne Stroke Registry. "Recent AF" was defined as AF discovered at or after ("after-admission" AF) admission in patients without any previous history of AF. Populations with recent AF and after-admission AF were compared for AF evolution, risk factors, and lesion type and distribution with patients with previous history of AF (known AF) and with patients with another recognized cardiac source of embolism (cardioembolic). RESULTS: Twenty-four patients had recent AF on admission, and 17 developed it a few hours to 3 days after stroke. AF disappeared after a few days in 26 (63%; 94% of after-admission AF) patients. Stroke was a primary hematoma in 9.8% of patients with recent AF, 2.8% of patients with known AF, and 0.9% (p < 0.001) of patients with cardiac source of embolism. Parietoinsular (32%) and brain stem (11%) involvement were more common in recent AF than in cardioembolic stroke in general (16.7% and 6.7%, respectively; p < 0.05). CONCLUSIONS: AF discovered after an acute stroke lasted no more than a few days, suggesting that it may have occurred as a consequence of the stroke. This possibility is emphasized by the significant predominance in patients with recent AF of primary hematoma, which cannot be caused by AF, and of parietoinsular and brain stem involvement, which are experimentally known as arrhythmogenic. This hypothesis should be considered in patients with acute stroke and previously unknown AF before therapeutic decisions are made.
Hyponatremia hypo-osmolarity in neurosurgical patients. "Appropriate secretion of ADH" and "cerebral salt wasting syndrome".
This prospective study is based on 256 patients with severe brain injury. Six patients (2.3%) developed the clinical picture of inappropriate secretion of antidiuretic hormone (SIADH): 3 in the first 3 days following the injury, 3 after more than a week. Their ADH plasmatic level were measured by radio-immunoassay. In the former, many factors, largely iatrogenic, can explain the increased secretion of ADH we found and which is then definitely "appropriate". It should be prevented by fluid restriction. In the latter, we found adequately low ADH levels, when the hypo-osmolarity is taken into account. Here, the aetiology seems to be a renal salt loss, eventually in relation to a natriuric factor (e.g. atrial natriuretic factor), justifying the term: "Cerebral salt wasting syndrome". With the resistance to fluid restriction, the treatment still remains a problem.