Biomedical subjects
Publications and source records attributed to F Regli.
The intellectual impairment appearing during the Parkinson's disease has been analysed and compared with the severity of the motor deficit respectively with the presence of the cerebral atrophy determined by computed tomography. The organic mental syndrome was more frequently observed in males and well correlated with the degree of cortical and subcortical atrophy.
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Two patients received intravenous heparin shortly after carotid transient ischemic attacks (TIAs), and developed a cerebral hemorrhage in the same area with 24 hours. CT scan performed before starting anticoagulation was normal, blood pressure was not too high when the hemorrhage developed, although the patients suffered (treated) chronic hypertension, and the Partial Thromboplastin Time did not exceed 90 seconds. No definitive explanation can be provided for this severe complication but recent studies suggest that in some TIAs, significant local ischemic changes may persist after the resolution of clinical symptoms. This risk, although very low, should be considered in cases with chronic arterial hypertension (even treated), because of disturbances of cerebrovascular regulation. In the near future, nuclear magnetic resonance scanning might allow detection of the cases with TIAs, in which focal metabolic alterations persist after disappearance of clinical symptoms.
A woman had difficulties in word finding since age 59, this became a Broca's aphasia then a global aphasia. The only possible expression was written and agrammatic with many semantic errors. Calculation was preserved as well as constructional praxis. Ideomotor praxis was slightly impaired. Visual recognition and somatagnosia were normal. Neurological examination showed neither motor nor sensitive impairment. Visual fields were normal. CT scan at onset was normal. Later a slight cortical atrophy appeared predominating on the sylvian fissures, slightly more severe on the left side. Reviewing the literature the authors draw attention on the possible occurrence of an evolutive aphasia being the first evidence of a dementia. The impairment of the other cognitive functions would only appear after several years.
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During a 5-year period, 85 patients with TIAs, 65 patients with embolic brain ischemia of cardiac source and 50 patients with progressing stroke received intravenous heparin within 96 h. Twelve (6%) developed an early bleeding in the area involved by ischemia. In the 2 cases with transient ischemic attacks (TIAs) (2.3%), major functional sequelae persisted and the 2 cases with emboli from heart (3.2%) died, whereas among the 8 cases with progressing stroke (16%), only 3 worsened from anticoagulant-induced bleeding. Intracerebral bleeding was not associated with excessive anticoagulation or high blood pressure and was related to a large infarction only in the cases with emboli from the heart. Among the 108 patients who were placed on acenocoumarol during 3-12 months after heparin therapy, only one (0.9%) suffered a hemorrhagic infarct from a probable recurrent embolization. The risk of anticoagulant-induced intracerebral bleeding is quite different between the varieties of preceding ischemic events, with different subsequent impact on prognosis.
Monoclonal gammopathies are diseases characterized by proliferation of a single B-cell clone, and include MGUS, multiple myeloma and Waldenström's macroglobulinemia. We have studied 8 patients with monoclonal gammopathy (2 "monoclonal gammopathies of undetermined significance" [MGUS], 2 multiple myeloma and 4 Waldenström's macroglobulinemia) and associated neurological complications (polyneuropathy, encephalopathy, noncompressive myelopathy). Of the two cases with MGUS, one is associated with polyneuropathy and the other with myelopathy. Three of the patients with Waldenström's disease have polyneuropathy and one myelopathy. Both patients with multiple myeloma had encephalopathy. At present there is no specific therapy for the neurological complications of monoclonal gammopathy; the best approach is treatment of the underlying hemopathy.
During a follow-up study (40 months) of 80 patients with proven uni- or bilateral occlusion of internal carotid artery (ICA), delayed cerebroretinal ischemic events occurred in 46% of the cases (distal to the occluded ICA in 40%). Ischemia in the area ipsilateral to the ICA occlusion most often corresponded to microemboli following the external carotid collateral pathways, less often to hemodynamic hypoperfusion, and exceptionally to microemboli from stenosis of the contralateral ICA or of the vertebrobasilar system. Ischemia in the contralateral ICA area was due to microemboli from stenosis of the corresponding ICA. Vertebrobasilar ischemia was usually hemodynamic, and foreshadowed a poor outcome. A variety of medical or surgical treatments may be indicated according to the mechanisms of these delayed episodes.
Four cases are described in which asterixis was the main symptom of a focal brain lesion: controlateral asterixis from thalamic hemorrhage or infarction, and bilateral asterixis from posterior parietal hematoma or glioblastoma. The features of this symptom and the localization of the causal lesions make it possible to consider asterixis as a focal and transitory afferent motor dysfunction.
A neuropsychological evaluation of 41 patients with multiple sclerosis was carried out. The investigation included language and memory tests, a visual reproduction task, and one test sensitive to frontal lobe damage. The results show that most of the patients have neuropsychological defects mainly concerning memory. However, only one case of global deterioration was found. The result also suggest that men are more impaired than women, without correlation with age or length of illness. These findings are discussed in the light of the literature.
We described a patient with occlusion of an internal carotid artery in whom delayed transient ischemic attacks distal to the occlusion alternated with vertebrobasilar attacks. Microembolization through the vertebrobasilar system was emphasized because the middle cerebral artery was filled by the basilar artery through the posterior communicating artery, and one vertebral artery showed important atheromatous emboligenic changes. Other mechanisms appeared improbable because of the type of collateral circulation and absence of other associated emboligenic changes and hemodynamic phenomena.
Right hemiparesis with right-sided pain and ataxia developed in a 68-year-old man. Sensation, neuropsychological function, and somatosensory evoked potentials were normal. Computed tomography showed an isolated fresh infarct in the left part of the thalamus. The pain and ataxic disturbances were related to involvement of the thalamus itself, but the hemiparesis with hyperactive tendon reflexes and Babinski's sign was probably due to associated dysfunction in the adjacent internal capsule from compression or edema. In the available clinicopathological reports of cases with hemiparesis and thalamic infarction, contiguous involvement of the internal capsule or no associated lesion has been reported. Because of the occurrence of pain, which is not present in pontine, mesencephalic, or capsular ataxic hemiparesis, we suggest that the syndrome seen in our patient be called "painful ataxic hemiparesis."
A patient with an infarct limited to the paramedian thalamus and upper mesencephalon on the right side suffered a conjugate upgaze palsy associated with a monocular paresis of downward gaze in the ipsilateral eye (vertical "one-and-a-half" syndrome). This paresis involved tonic and phasic components. Vertical oculocephalic movements and conjugate horizontal gaze were normal. It is suggested that the unilateral lesion destroyed the fibres of the posterior commissure and the descending fibres to the ipsilateral subnucleus of the inferior rectus and contralateral subnucleus of the superior oblique just after they decussate, probably above the level of the third nerve nucleus. A complex disturbance of vertical gaze may be due to a unilateral thalamo-mesencephalic lesion.
We studied two patients with large cerebellar haemorrhages, who were conscious on admission and did not deteriorate during the following days. Surgical decompression was not performed and the patients regained their former level of activity, except for moderate persisting ataxia. We suggest that cerebellar haemorrhage may have a benign spontaneous outcome, more often than previously assumed from autopsy series. The main selection criteria for surgery is an impaired state of consciousness and evidence of neurological worsening. Taken alone, the size of the haemorrhage on computerized tomography is not a reliable criterion for surgery.
Five patients with "locked-in" syndrome and dysconjugate palsy of horizontal gaze were studied. In all cases internuclear ophthalmoplegia due to dysfunction or destruction of the median longitudinal fasciculus was combined with an ipsilateral gaze palsy, producing the "one-and-a-half" syndrome. Clinical and electro-oculographic examination suggested involvement of the paramedian pontine reticular formation when all ipsilateral saccades were abolished, when exotropia of the contralateral eye was present, and when vestibular stimulation showed full conjugate deviation to the damaged side. Involvement of the abducens nucleus was suggested when the palsy of ipsilateral gaze was not dissociated on vestibular stimulation. In three cases these clinical deductions were confirmed by the pathological study, which showed a corresponding destruction of the median longitudinal fasciculus, paramedian pontine reticular formation and abducens nucleus. In one case the one-and-a-half syndrome evolved into a total horizontal gaze palsy, which corresponded to involvement of the abducens nucleus contralateral to the initially destroyed paramedian pontine reticular formation. Vertical oculocephalic response disappeared, because of destruction of the median longitudinal fasciculus on both sides (bilateral internuclear ophthalmoplegia). Patients with the locked-in syndrome provide a unique situation in which complex pontine oculomotor disturbances may be studied, because consciousness is preserved. In these patients, dissociated and dysconjugate oculomotor palsy may have been underestimated.