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Biomedical subjects

F Regli

Publications and source records attributed to F Regli.

394 records · Page 22Linked to original sources
PubMedDate not supplied

Transient ischemic attacks and external carotid artery. A retrospective study of 23 patients with an occlusion of the internal carotid artery.

Twenty-three patients with occlusion of an internal carotid artery have been followed 5 to 50 months after angiography. None had a later permanent stroke. Eight had delayed TIAs in the occluded internal carotid area, never in another area. In these TIAs the role of the homolateral external carotid artery is emphasized, because in the 8 cases this artery was the main collateral to the occluded internal carotid, and angiography had shown atheromatous stenosis of homolateral external/common carotid arteries or an irregular stump at the site of the occlusion. Hemodynamic and embolic mechanisms are discussed, especially the latter, because of the absence of severe stenosis and evidence of emboligenic plaques.

Adult↗
PubMedDate not supplied

Delayed TIAs distal to bilateral occlusion of carotid arteries -- evidence for embolic and hemodynamic mechanisms.

We studied 4 patients with bilateral carotid artery occlusion who suffered delayed TIAs in one of the occluded internal carotid or common carotid areas. Hemodynamic mechanisms were prominent in two patients, in head turning and orthostatic hypotension. In the other two cases, embolic phenomena through the homolateral external carotid collateral pathways were probable, because this artery (or the common carotid artery) showed atheromatous stenosis and major collateral supply to the brain and retina. Different mechanisms may be responsible for further ischemia after bilateral occlusion of carotid arteries.

Aged↗
PubMedDate not supplied

Cerebral infarction with transient signs (CITS): do TIAs correspond to small deep infarcts in internal carotid artery occlusion?

Among 75 patients in whom internal carotid artery (ICA) occlusion was discovered on angiography, 5 presented with transient ischemic attacks (TIAs) without suffering a stroke. Although neurological examination was normal, all had evidence for one (in one instance two) hypodense lesion suggesting infarction contralateral to the neurological dysfunction on computed tomography (CT). These infarcts were small and deeply located, being indistinguishable from lacunes in most cases. We suggest that cerebral infarction with transient signs ( CITS ) may be a usual finding in patients with ICA occlusion who suffer isolated TIAs. In these cases, CITS may correspond to incomplete cerebral necrosis related to a well-developed collateral supply, or to recurrent ischemia in the region of an old "silent" infarct. CITS should be differentiated from TIAs, which may be diagnosed only in absence of visible structural lesion.

Aged↗
PubMedDate not supplied

Isolation of speech area from focal brain ischemia.

A patient with atrial fibrillation and internal carotid artery occlusion developed mixed transcortical aphasia. The CT scan showed two recent distinct infarcts in the dominant hemisphere, one in the precentral artery area (pial artery infarct) and one in the borderzone area between the posterior and middle cerebral arteries territories (watershed infarct). The perisylvian speech areas were spared, but probably disconnected from other areas by the infarcts. The syndrome of isolation of speech area may be caused by vascular conditions which are able to produce simultaneous pial artery and watershed infarcts, and is not necessarily related to more extensive processes of the brain.

Aged↗
PubMedDate not supplied

The syndrome of unilateral tuberothalamic artery territory infarction.

The study of 3 personal cases and 5 published cases of unilateral infarct limited to the territory of the tuberothalamic artery suggests that this syndrome should be differentiated from the other thalamic syndromes. The onset is usually sudden, with moderate contralateral weakness. Sensory changes may be present but remain mild. The patients are apathetic, show perseveration and may be disoriented. In left-sided infarcts, transcortical aphasia, verbal and visual memory impairment and sometimes acalculia are found. In right-sided infarcts, hemispatial neglect, visual memory impairment and disturbed visuospatial processing are common. A decreased level of consciousness, disturbed ocular movements, severe motor weakness and delayed abnormal movements do not occur. Involvement of the ventral lateral and dorsomedial nucleus with sparing of the intralaminar nuclei, posterolateral formation and upper midbrain may explain this picture. The fact that the tuberothalamic artery arises from the posterior communicating artery, which often receives its supply from the carotid system, further justifies considering unilateral tuberothalamic infarcts as a syndrome.

Acute Disease↗
PubMedDate not supplied

Leukoencephalopathy in patients with ischemic stroke.

Thirty-one (16 women, 15 men; mean age 68 years) of 1,000 consecutive patients with an ischemic stroke investigated systematically with computed tomography (CT), Doppler, electrocardiography (ECG), and biological tests had a diffuse hypodensity of the cerebral hemispheric white matter on CT, a sign indicative of leukoencephalopathy. In 25 of the 31 patients, the acute infarct was deep. Leukoencephalopathy was more frequent in patients with a deep infarct (8%) than in patients in whom the cortex was involved (0.8%) (p less than 0.01). A history of progressive intellectual impairment (23%) and the finding of a mild or moderate impairment, or severe dementia (84%) were more frequent in study patients (p less than 0.05) than in 31 sex- and age-matched controls with an acute infarct of same size and topography but without leukoencephalopathy. A history of hypertension (81%) and high blood pressure on admission (166 +/- 19/96 +/- 12 mm Hg) were the most common risk factors and were more frequent in study patients (p less than 0.05) than in controls. On the other hand, study patients had a greater than or equal to 50% stenosis or occlusion of the carotid artery (13%) less often than controls (35%) (p less than 0.05). Diabetes (23%), elevated blood cholesterol (13%), hematocrit greater than 45% (23%), smoking (32%), and myocardial ischemia by history or ECG (45%) did not differ. These findings suggest that hypertension may be more strongly associated with leukoencephalopathy than with deep infarcts. In acute stroke patients, leukoencephalopathy on CT should not be considered a fortuitous finding.

Aged↗
PubMedDate not supplied

Effects of proximal and distal muscles' groups contraction and mental stress on the amplitude and frequency of physiological finger tremor. An accelerometric study.

Physiological finger tremor was assessed by two-dimensional solid accelerometry in 40 healthy normal subjects at rest (R) with the hand hanging over the armrest of a chair, in posture (P) with the arm rested on the armrest but the hand extended from the wrist, and finally adding proximal muscles contraction in extension (E) with the arm extended in front of the patient, each time with and without mental stress. The mean amplitude for physiological tremor, about 30 microns, was almost doubled by hand extension and increased by 4 to 5-fold by arm extension with further increase by mental stress in each position, which gives a good estimation of the contribution of proximal and distal muscles into the amplitude of physiological tremor. There was no significant effect of age between 20 and 60 years on tremor amplitude, but mean tremor frequency decreased significantly between 40 to 60 years. Mental stress increased amplitude but decreased tremor frequency of both across all position, possibly by increasing the synchronization of motor unit firing and by modifying the gain of the motoneurones and the stretch reflex as shown by electrophysiological studies.

Adult↗
PubMedDate not supplied

[Characteristics of chronic headaches after whiplash injury].

OBJECTIVES: The aim of this study was to identify the characteristics of post-traumatic headache after whiplash injury in order to obtain some indications as to the pathogenesis of this particularly frequent clinical entity. METHODS: A retrospective study of 63 patients who had suffered whiplash injury and who had persistent chronic pain was conducted. RESULTS: Forty-seven patients complained of headache and pain in the cervical spine and 16 of pain in the cervical spine alone. Among the patients with headache 74% complained of tension-like pain, while only about 10% had identifiable post-trauma migraine headache with or without aura. Current neurophysiological hypotheses of central dysfunction due to neurochemical disorders induced by the initial nociceptive stimuli, frequently found in the general population, would not explain the disabling characteristics observed in these patients with chronic pain. CONCLUSION: A multifactorial pathogenesis of post-traumatic chronic headache should be entertained, suggesting that not only trauma but also extra-trauma factors unrelated to whiplash would be involved.

Accidents, Traffic↗
PubMedDate not supplied

A case of dissection of intracranial cerebral arteries with segmental mediolytic "arteritis".

The intravital diagnosis of intracranial arterial dissection is not always possible due to atypic and non-specific clinical and radiological presentations. The postmortem pathological examination of cerebral blood vessels is therefore necessary to establish or confirm the presence of a dissecting aneurysm of intracranial arteries. Most of the described cases showed no significant underlying vascular pathology. Here we present the case of a 24-year-old women who died 5 days after admission to the hospital for a rapidly developing right-sided hemisyndrome. Neuroradiological examination had revealed ill-defined bifrontal hypodense lesions and angiographic findings were compatible with a dissection of the left extracranial internal carotid artery with embolic subocclusion of both anterior cerebral arteries. The pathological evaluation ruled out a thromboembolic occlusion of cerebral arteries and an extracranial internal carotid artery dissection but showed an extended dissecting process of variable age in the anterior circulation of the circle of Willis. The dissected vessels showed pathological changes characteristic of segmental mediolytic "arteritis" [Slavin and Gonzalez-Vitale 1976]. To our knowledge this is the first report on intracranial arteries being affected by this pathologic entity. Our case illustrates the importance of a postmortem examination of dissecting aneurysms of intracranial arteries. Careful serial section studies of dissected intracranial arteries in young subjects should be performed and may allow for a better understanding of the vascular pathology underlying the dissection processus.

Adult↗
PubMedDate not supplied

[Familial hyperekplexia: startle disease. Clinical, electrophysiological and genetic study of a family].

The major form of familial hyperekplexia, a rare autosomal dominant disorder, is characterized by an abnormal startle reaction elicited by auditory and somatosensory stimuli, with transitory stiffness during the neontam period, followed later by falling attacks accompanied by momentary generalized muscular stiffness. Affected neonates occasionally have fatal hypertonia. The minor form is characterized only by an inconstant excessive startle response. We encountered a family in which three females presented with a partial or complete major form of the disease. All our patients were hyperreflexic, insecure gait was present in two subjects, without concomitant spontaneous nocturnal myoclonus. The pathophysiological basis of the hyperekplexia remains unclear. The abnormal startle reflex, probably related to the lack of inhibition by higher centers, is relayed in the caudal brainstem (ponto-medullary reticular formation), where bulbospinal motor efferents originate. Moreover, nonspecific changes such as large somatosensory evoked potentials and long-loop reflexes ("C-responses") may indicate increased cortical neuronal excitability. Polygraphic studies in these patients were normal. The locus of the major form of the disorder is located on chromosome 5q33-q35. Sequence analysis of the alpha 1 subunit of the inhibitory glycine receptor (GLRA1) revealed a mutation at the same codon 271 in several families (G1192A and G1192T). We analyzed this gene and found a G1192A mutation changing an ARG to a LEU codon in all three presented patients. Sporadic cases may represent new mutations or lack of penetrance in some family members. Only one of our three patients needed clonazepam. The diagnosis of this disorder rules out epilepsy, or psychogenic pathological startle reaction. Electrophysiological criteria are useful, however perinatal hypertonia or a tonic generalized spasm accompanied with falls following an abnormal startle reaction and genetic studies remain the diagnostic milestones of familial hyperekplexia.

Adolescent↗