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Biomedical subjects

F Gray

Publications and source records attributed to F Gray.

At least 235 records · Page 13Linked to original sources
PubMed1983

[Crossed cerebellar atrophy following hemispheric lesions occurring in adulthood].

Crossed cerebellar atrophy generally results from a large contralateral hemispheric lesion involving the cortico-spinal tract in neonates or infants. Two cases of crossed cerebellar atrophy which were particular from two points of view are reported: 1) the cerebellar alterations resulted from cerebral lesions which had occurred in adult life, after complete maturation of the central nervous system. One was observed in a 78 years old hypertensive woman who had presented 24 years before a right lenticular haemorrage, the other in a 73 years old woman who when aged 18 had presented a left cortical frontal traumatic lesion. The clinical and pathological data are compared to 13 similar cases reported in the literature. The retrograde or anterograde route of this transneuronal degeneration is discussed. The pathological features of those 2 cases lead the authors to favor the anterograde route; 2) the cerebral lesion was small and strictly limited to F2 in 1 case, the secondary lesions involving then, only the medial pontine nuclei and the quadrangular cerebellar lobule. This allows a clear demonstration, in man, of a systematisation of the cortico-pontine and ponto-cerebellar fibers similar to what has been described in the animal (Brodal, 1980).

Age Factors↗
PubMed1983

[Lasting focal signs in 2 cases of progressive multifocal leukoencephalopathy].

Two cases of progressive multifocal leukoencephalopathy, which occurred without a clinical setting of immune deficiency and developed as a unifocal brain lesion during 14 and 4 months, are reported. The diagnosis was established only by post mortem study in the first case and after five months by a brain biopsy in the second one. The difficulties of an early diagnosis in such cases should be now reduced with CT scan which may show a relatively specific picture, even when there is only one visible lesion.

Female↗
PubMed1982

Parinaud's syndrome: electro-oculographic and anatomical analyses of six vascular cases with deductions about vertical gaze organization in the premotor structures.

Six cases of Parinaud's syndrome, with downward (Cases 1, 2), upward (Cases 3, 4) and both downward and upward gaze paralysis (cases 5, 6) are reported. Four cases (Cases 1, 2, 3, 5) were studied anatomically using serial sections of the brain and 3 cases (Cases, 1, 4, 6) analysed electro-oculographically. In all the cases there were rather small vascular lesions in the mesodiencephalic region, sparing the oculomotor nuclei. Since the rostral interstitial nuclei of the medial longitudinal fasciculus (riMLF), located above the oculomotor nuclei, contain the final relays producing all vertical saccades, it is suggested that the different aspects of Parinaud's syndrome may result from damage to their cells or to their excitatory efferent tracts, or even to their afferent pathways. Downgaze paralysis results from bilateral lesions involving the regions located just caudal, medial and dorsal to the upper poles of the red nuclei. The critical area is probably related to the mediocaudal part of the riMLF, the lateral portion of which appears to be spared. These anatomical data, combined with the clinical observation that most downward eye movements (except slow reflex movements) are affected in the case with such paralysis, lead us to propose that it is the riMLF efferent tracts mediating downgaze and projecting on to the oculomotor nuclei that are principally damaged by the lesions. Upgaze paralysis results from unilateral lesions in or near the posterior commissure. The clinical data allow us to propose that it is also the riMLF efferent tracts, mediating upgaze, that are damaged in such cases. consequently these tracts, probably originating from the dorsolateral part of the riMLF, would decussate through the posterior commissure before they reach the oculomotor nuclei. Combined downgaze and upgaze paralysis results from bilateral lesions involving the region related to the whole riMLF on both sides. The principal conclusion is that the riMLF efferent tracts mediating upward and downward gaze have clearly separate courses in the immediate premotor structures.

Adult↗
PubMed1982

[Cerebellar atrophies].

The concept of cerebellar atrophy was first introduced by Pierre Marie in 1893 in his description of hereditary cerebellar ataxia. Subsequent criticism of this notion was refuted by the report of new clinicopathological entities which are compatible with it. The contributions of the Clinic for Diseases of the Nervous System are discussed in this paper. Etiological classification is difficult, in spite of progress made in the genetic, epidemiologic, and biochemical approaches to cerebellar atrophies. Pathologic findings appear to supply the most secure basis for presentation of these affections. Predominantly cortical atrophies may be localized to the vermis. This is the case in the familial cerebello-olivary atrophy of Holmes (1907), in tardive cortical atrophy (Pierre Marie, Foix and Alajouanine, 1922), and in the cerebellar atrophy of alcoholics (Alajouanine, Castaigne, Contamin and Lebourges, 1959; Victor, Adams and Mancall, 1959), in which the lesions are similar. The frequent intrication of the various etiological factors: age, deficiencies, alcohol, heredity, suggests the role of a sometimes primary, sometimes latent genetic predisposition, revealed during various pathological conditions. Cortical cerebellar atrophy may be of the diffuse type, as in paraneoplastic cerebellar atrophy (Brouwer and Biemond, 1938), which is closely related to subacute polioencephalomyelitis in cancer patients (Dubas et al., 1982), and in congenital atrophy of the granular layer (Norman, 1940), which is more a dysgenesis than a true degenerative affection. Lesions affecting mainly the efferent or afferent cerebellar pathways include olivopontocerebellar atrophy (Dejerine and André Thomas, 1900) which should be included in the larger overall concept of multiple system atrophy (Oppenheimer, 1976), and dentorubric atrophy (Ramsay Hunt, 1921) which themselves should be integrated in the group of spinocerebellar atrophies. Finally, olivorubrocerebellar atrophy (Lejonne and Lhermitte, 1909) and crossed cerebellar atrophy, traditionally studied together with cerebellar atrophies, are only the result of a pre-existing lesion.

Atrophy↗
PubMed1982

[Rigid-spine syndrome in a female patient (author's transl)].

A case of rigid spine syndrome in a woman is reported. There were a diffuse myopathic process, with atrophy and mild weakness not involving the face and a major rigidity of the spine. Contractures were present as well as a pure restrictive respiratory failure. Heart-rythm disorders and prolapse of the mitral valve were present. Histological features of a deltoid muscle biopsy were slight necrosis, lack of fibrosis and major disproportion in fiber-types. There were a high rate of fiber I and absence of fiber IIB. This case was similar to others described as Dubowitz's rigid spine syndrome. The histological features belonged to the second neuropathological group of cases, with disproportion in fiber-types. The rigid spine syndrome may be considered as a clinically definite disease and distinguished from other myopathies with orthopedic deformations. It should not be confused with arthrogryposis multiplex. The disease is probably autosomic recessive.

Adult↗
PubMed1982

[Giant aneurysm of both vertebral arteries. Drop-attacks (author's transl)].

A 79 year-old woman suffered from drop-attacks for 2 years. There were in addition disorders of swallowing. She then had a mild right hemiplegia. At age 81, she had a mild spastic quadriparesis with paresis of the right sterno-mastoid and trapezius muscles and of the right side of the tongue. She died from bronchopneumonia. At autopsy a giant aneurysm involving both vertebral arteries was present. This case exemplifies: 1) drop-attacks due to a lesion near the foramen magnum; 2) signs which may suggest an aneurysm of the posterior fossa; 3) an apparently very rare kind of aneurysm of the vertebral arteries.

Aged↗
PubMed1982

[Parinaud's syndrome and tonic vertical gaze deviation. 3 anatomo-clinical observations].

Two anatomo-clinical cases of downward gaze palsy and one case of upward gaze palsy are reported. A tonic and intermittent downward gaze deviation is described. The supranuclear palsies of the downward gaze were related to paramedian lesions of the rostral mesencephalon; the lesions involved the rostral interstitial nucleus of the medial longitudinal fasciculus, the nucleus interstitial of Cajal, and/or their afferent and/or efferent pathways. The supranuclear palsy of the upward gaze was related to lesions of the posterior commissure. Tonic and intermittent downward deviation of gaze and ocular bobbing have opposed features. The former could be related to disinhibited reticular mesencephalic neurones activated by vestibular inputs. Tonic upward deviation of gaze is also related to a vestibulo-ocular reflex. In this case, partial or total damage of the nucleus of Cajal, and/or its input and/or its output fibers appears to have a critical role.

Aged↗
PubMed1981

Cerebellar changes in 50 cases of Creutzfeldt-Jakob disease with emphasis on granule cell atrophy variant.

Cerebellar changes have been found in 41/50 cases of Creutzfeldt-Jakob disease. They were severe in 9 cases. We did not find significant correlation between the cerebellar symptoms and signs pointed out in clinical records and prominent cerebellar changes. The only exception consisted in dentate nucleus involvement which was more frequently related to those symptoms and signs. 5 of the cases with severe changes were characterized by predominant granule cell atrophy without kuru plaques. The mean age of death (56.0) was significantly lower in this variant than that of patients with other cerebellar changes (64.4) (p less than 0.01). The granule cell atrophy seems a distinct variant on the basis of age of death and pathological changes. However, it is not characterized by the presence of kuru plaques.

Atrophy↗