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Biomedical subjects

C Leno

Publications and source records attributed to C Leno.

At least 19 recordsLinked to original sources
PubMed1991

Presynaptic parkinsonism in olivopontocerebellar atrophy: clinical, pathological, and neurochemical evidence.

The substrate for olivopontocerebellar atrophy parkinsonism is obscure due to the lack of clinical and pathological reports and the absence of studies on dopamine receptors in this entity. We describe a patient with olivopontocerebellar atrophy whose clinical presentation was levodopa-responsive parkinsonism in whom pathological examination disclosed pronounced nigral cell loss with no striatal damage. Autoradiographic labeling with 3H-spiperone showed normal densities of D2 dopamine striatal receptors. These data show that indistinguishable nigral, presynaptic parkinsonism occurs in patients with idiopathic Parkinson's disease and in patients with olivopontocerebellar atrophy, and also how a favorable response to levodopa is neither synonymous with idiopathic Parkinson's disease, nor does it exclude multiple-system, atrophy-related parkinsonism.

Aged↗
PubMed1990

Prevalence of primary Sjögren's syndrome in patients with multiple sclerosis.

Sixty-four consecutive patients with clinically or laboratory-supported definite multiple sclerosis (MS) were evaluated prospectively for evidence of primary Sjögren's syndrome (SS). This diagnosis was established when a patient had objective keratoconjunctivitis sicca, xerostomia, or both together with positive labial salivary gland biopsy. We found 2 patients (3.1%) with clinical evidence of primary SS. Whether this association is fortuitous or whether there is pathogenetic linkage between MS and primary SS remains to be established.

Adult↗
PubMed1989

The application of nerve conduction and clinical studies to genetic counseling in hereditary motor and sensory neuropathy type I.

One hundred and thirty two individuals at risk for hereditary motor and sensory neuropathy (HMSN) type I from 11 unrelated families were evaluated by physical examination. Motor conduction velocity (MCV) studies of median and/or peroneal nerves were performed on 99 of them. Seventy-three subjects were found to be affected. In all age categories including the first decade of life, the ratio of affected individuals at risk did not significantly differ from the expected 1:1 ratio; that is, penetrance of the gene was complete. The majority of affected members in the first decade had no clinical features considered diagnostic of peroneal muscular atrophy syndrome, and full clinical expression developed in the second decade. Marked slowing of MCV was already present in the early years of life, even as young as 6 months. Moreover serial MCV studies carried out throughout the first year of life in an affected girl showed no physiological increase in conduction velocity. For purposes of genetic counseling, our experience suggests that, starting from 6 months of age, a clinically and electrophysiologically normal subject has a zero risk of having inherited the HMSN type I gene. However given the limited numbers in this series, infants at risk with normal clinical evaluation and MCVs should be followed up yearly up to 5 years of age.

Adolescent↗
PubMed1983

Voluminous benign osteoblastoma of the skull.

A case of benign osteoblastoma of the skull is reported. The clinical picture began when the patient was 15 years old, with exophthalmos and blindness in the right eye. After the enucleation of this eye, the only symptoms were repetitive convulsive seizures. Radiologic studies done when the patient was 76 years old, and a postmortem examination following her death at this age, revealed a voluminous osteoblastoma localized in the anterior cranial fossa and invading the structures below. The clinical characteristics of osteoblastomas of the skull are briefly reviewed.

Aged↗
PubMedDate not supplied

CT findings in spinocerebellar degeneration.

Thirty-five CT scans were studied from patients with several forms of spinocerebellar degeneration. Atrophy was determined by objective measurements of the number and width of cerebellar sulci, transverse diameter and surface area of the fourth ventricle, brainstem ratio, cerebellopontine angle cistern, and Evans' index. Two-thirds of the patients with Friedreich's ataxia showed moderate cerebellar atrophy and an increase in the surface area of the fourth ventricle. Severe cerebellar atrophy and enlargement of the cerebellopontine angle cistern was seen in patients with olivopontocerebellar (OPC) atrophy and idiopathic cortical cerebellar atrophy. In the OPC atrophy group there was also prominent atrophy of the brainstem and an increase in the fourth ventricle parameters. Alcoholic cerebellar degeneration showed a specific pattern of cerebellar atrophy most prominent in the superior vermis, together with a slight increase in the fourth ventricle surface, a reduction in the size of the brainstem, and an enlargement of the cerebellopontine angle cistern. Supratentorial atrophy was present only in the OPC and alcoholic atrophy groups. In one patient with spastic ataxia, CT was normal but MR imaging revealed prominent atrophy of the spinal cord. These CT patterns appear to be distinctive enough to permit the diagnosis and classification of the various forms of spinocerebellar degeneration.

Adolescent↗