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Biomedical subjects

F E Lepore

Publications and source records attributed to F E Lepore.

At least 37 records · Page 2Linked to original sources
PubMed1987

Bilateral cerebral ptosis.

We studied 13 patients with bilateral ptosis after acute right frontotemporoparietal lobe lesions. All patients had conjugate gaze deviation to the right. The ptosis persisted for about 5 days in five patients, or was still evident at the time of discharge or death. Other cranial nerve findings included lower facial weakness in five patients and both upper and lower facial weakness in eight patients. The transience of cerebral ptosis and conjugate gaze disturbance may imply ability of the intact hemisphere to assume control.

Aged↗
PubMed1987

Progressive supranuclear palsy.

Progressive supranuclear palsy (PSP) was first recognized as a distinct morbid entity by Richardson, Steele and Olszewski a quarter century ago. Subsequent experience has confirmed and extended their original observations. PSP has become familiar as a chronic progressive disorder with extrapyramidal rigidity, bradykinesia, gait impairment, bulbar palsy, dementia and a characteristic supranuclear ophthalmoplegia. It is an important cause of parkinsonism. Its etiology remains obscure. Familial concentrations have not been observed. Some cases exhibit no oculomotor dysfunction. Dementia is usually mild. Recent neuropsychological studies have defined features consistent with frontal lobe cortical dysfunction. Seizures and paroxysmal EEG activity may occur. CT and MRI scans show midbrain atrophy early and later atrophy of the pontine and midbrain tegmentum and the frontal and temporal lobes. PET scans have shown frontal hypometabolism and loss of striatal D-2 dopamine receptors. Postmortem studies have documented involvement of both dopaminergic and cholinergic systems. Treatment remains palliative and unsatisfactory.

Brain↗
PubMed1986

Monocular diplopia of retinal origin.

A 68-year-old man experienced monocular diplopia related to a subretinal choroidal neovascular membrane. His symptom resolved with laser photocoagulation of the choroidal membrane. Retinal disease is an uncommon cause of this uncommon symptom.

Aged↗
PubMed1985

"Apraxia" of eyelid opening: an involuntary levator inhibition.

Apraxia of lid opening was described by Goldstein and Cogan as "a non paralytic motor abnormality characterized by the patient's difficulty in initiating the act of lid elevation." We studied six such patients with this finding accompanied by vigorous frontalis contraction and no evidence of ongoing orbicularis oculi contraction, dysfunction of the oculomotor nerve, or loss of ocular sympathetic innervation. Four patients had Parkinson's disease or atypical parkinsonism, one had progressive supranuclear palsy, and one had Shy-Drager syndrome. At onset of ocular symptoms, mean age was 64 years, and the mean duration of extrapyramidal symptoms was 9.7 years. By definition, the motor system must be intact in any apraxia. Therefore, this disorder of lid opening in patients with extrapyramidal motor dysfunction is not an apraxia, but rather involuntary levator palpebrae inhibition of supranuclear origin.

Aged↗
PubMed1985

Neuro-ophthalmological findings with neuropathological correlation in bilateral thalamic-mesencephalic infarction.

A 91-year-old man presented with the sudden onset of coma, vertical gaze paresis, and transient disturbance of horizontal gaze, with fixed but unequal pupils. Both cranial computed tomography and postmortem study documented infarction of the paramedian thalamus bilaterally and of the ventral mesencephalon, accounted for by presumably embolic occlusion of a single artery. This artery arose as an unpaired perforating artery originating from the proximal segment of one posterior cerebral artery and thus conformed to the variant anatomic configuration associated with such infarcts as described by Percheron.

Aged↗
PubMed1985

A mimic of the "exact diagnostic sign" of Foster Kennedy.

We observed a patient with bilateral nonarteritic ischemic optic neuropathy presenting with gradual loss of vision in the right eye and initially asymptomatic disk swelling in the left. This atypical picture may create diagnostic difficulty, since sudden visual loss, the major distinguishing feature between Foster Kennedy's original syndrome and "pseudo-Foster Kennedy syndrome" of ischemic optic neuropathy, is lacking.

Brain Neoplasms↗
PubMed1984

Alcoholic myelopathy without substantial liver disease. A syndrome of progressive dorsal and lateral column dysfunction.

Five well-nourished, alcoholic patients had a progressive myelopathy. Symptoms began with paresthesias of the feet and progressed to a spastic paraparesis with clinical signs of both lateral and dorsal column involvement. Abstinence from alcohol halted progression but did not cause improvement in the myelopathy. The absence of portacaval shunting or notable liver dysfunction in these patients suggests that a direct toxic effect of alcohol must be considered a possible mechanism of spinal cord damage.

Aged↗
PubMed1983

Ataxic hemiparesis from lesions of the corona radiata.

Ipsilateral cerebellar and pyramidal signs suddenly developed in three patients. Computed tomography revealed small infarcts of the corona radiata in two patients and a small infarct in the posterior limb of the internal capsule in the third. Ataxic hemiparesis can result from lesions of the corona radiata as well as many other points along the corticopontine pathways.

Aged↗
PubMed1983

Neuro-ophthalmology according to Gordon Holmes.

Holmes' priority in establishing an extensive body of knowledge that defines much of neuro-ophthalmology is given. His original descriptions are reviewed and his findings reappraised in light of present-day knowledge.

England↗
PubMed1981

Bilateral internuclear ophthalmoplegia after intrathecal chemotherapy and cranial irradiation.

A 26-year-old man developed transient bilateral internuclear ophthalmoplegia with exotropia after cranial irradiation and intrathecal administration of methotrexate for lymphoma. Resolution of the ophthalmoplegia and the decrease in abnormally high levels of cerebrospinal fluid myelin basic protein after discontinuation of intrathecal medication suggested demyelination from chemotherapy and irradiation.

Adult↗
PubMed1980

Misdirection revisited. A critical appraisal of acquired oculomotor nerve synkinesis.

Two patients exhibiting "primary" oculomotor misdirection caused by intracavernous mass lesions, and a third boy with transient oculomotor synkinesis after migrainous ophthalmoplegia provide background for a reassessment of the currently accepted explanation of anomalous synkineses subsequent to oculomotor nerve palsies. The hypothesis of peripheral misdirection of regenerating motor axons is inconsistent with these clinical observations, and an alternate mechanism is suggested, based on concepts of ephaptic neuronal transmission of impulses or on chromatolysis-induced reorganization of nuclear synapses.

Aged↗