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Biomedical subjects

J C Masdeu

Publications and source records attributed to J C Masdeu.

At least 73 records · Page 4Linked to original sources
PubMed1988

Multifocal cytomegalovirus encephalitis in AIDS.

A 43-year-old man with the acquired immunodeficiency syndrome had clinical evidence of multifocal disease of the brain, but computed tomography was negative. Magnetic resonance imaging revealed multifocal lesions, histologically proven to be caused by cytomegalovirus. Therapy with 9[2-hydroxy-1-(hydroxymethyl) ethoxymethyl] guanine (BW B759U) resulted in stabilization of the patient's clinical disease and radiographic improvement of the lesions.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Thalamic astasia: inability to stand after unilateral thalamic lesions.

Inability to stand in the absence of motor weakness or marked sensory loss is usually considered to reflect midline cerebellar disease. However, the 15 patients reported here had astasia related to unilateral thalamic lesions, documented by autopsy and computed tomography in 2 patients and by computed tomography in 13. The lesions, including infarction (6), hemorrhage (7), and tumor (2), involved primarily the superoposterolateral portion of the thalamus, but spared the rubral region. Alert, with normal or near-normal strength on isometric muscle testing and a variable degree of sensory loss, the patients could not stand and 7 of them could not sit up unassisted. They fell backwards or toward the side contralateral to the lesion. They appeared to have a deficit of overlearned motor activity of an axial and postural nature. In the vascular cases, the deficit improved in a few days or weeks. However, these patients had a tendency to sustain falls during the rehabilitation period.

Aged↗
PubMed1988

Medullary satiety.

A 62-year-old man with a tegmental medullary glioma lost 30 pounds of weight in several months because of lack of appetite and early satiety. The medullary tegmentum may play an important role in regulating feeding behavior in humans.

Brain Neoplasms↗
PubMed1987

Midbrain-diencephalic horizontal gaze paresis.

Four patients with predominantly right-sided infarcts at the midbrain-diencephalic junction had an ipsilateral oculomotor palsy and contralateral gaze palsy. The gaze palsy to the left was supranuclear in nature, because the restriction of abduction was overcome by the oculocephalic reflex. However, it was masked on the right eye by the third nerve palsy. In all cases upgaze was impaired bilaterally, and infraduction was absent on the right. The restriction of abducting saccades remained for months, considerably longer than with supranuclear cortical lesions, suggesting that the damage extended beyond involvement of the frontopontine pathways. These cases represent clinical instances of a recently described experimental syndrome of impaired horizontal saccadic eye movements with lesions at the paramedian midbrain-diencephalic junction.

Cerebral Infarction↗
PubMed1986

Hemispheric white matter lesions in the elderly prone to falling.

Brain computed tomography studies of two groups of elderly (mean age 83.3 years, SE 1.7) with no neurologic diagnoses were compared. Sixteen of the subjects were non-fallers and the remaining 17 had frequent unexplained falls. The group of fallers had a significantly greater degree of white-matter hypodensity of the elderly (Student's t-test = 2.7, p less than 0.01).

Accidental Falls↗
PubMed1985

Incidence of seizures with phenytoin toxicity.

Among 50 patients with phenytoin intoxication, 14 had seizures during the episode. Seizures in 9 of these 14 patients probably resulted from poor seizure control despite high phenytoin levels, but in 5 cases, attacks were attributed to phenytoin toxicity. The only factor that seemed to correlate with seizures was a serum phenytoin level over 30 micrograms/ml. No demographic, metabolic, neuropsychiatric, or therapeutic variables were predictive; nor were any other symptoms of toxicity particularly likely to be found in association with seizures. Seizures are an occasional manifestation of phenytoin toxicity, particularly when levels are high.

Adult↗
PubMed1984

Hyperekplexia: a syndrome of pathological startle responses.

We describe a family and three sporadic cases of startle disease, or hyperekplexia. Sudden unexpected noises caused the patients to fall rigidly, often injuring themselves but retaining consciousness. This unusual entity differs from startle epilepsy and cataplexy. Clonazepam proved ineffective in three patients. Valproic acid, 5-hydroxytryptophan, or piracetam markedly reduced the abnormal startle in three patients.

5-Hydroxytryptophan↗
PubMed1984

Startle epilepsy: a clinical study.

Twelve patients with perinatal anoxic encephalopathy, 1 with encephalitis, and 1 with Down's syndrome had startle epilepsy. Hemiparesis, startle-induced seizures involving the hemiparetic side, focal electroencephalographic abnormalities, and unilateral lesions evident on computed tomographic scan were found in 6 patients, all of whom responded favorably to carbamazepine. The remaining 8 patients had severe intellectual impairment, bilateral motor deficits, generalized startle-induced seizures, diffuse and lasting electroencephalographic abnormalities, and widespread cerebral lesions evident on computed tomographic scan. Of these, 2 patients with Lennox-Gastaut syndrome responded to clonazepam, 4 others responded to valproic acid, and 2 others, with predominantly focal hemispheric lesions, improved on a regimen of carbamazepine.

Adolescent↗
PubMed1984

Familial photosensitive epilepsy: effectiveness of clonazepam.

We describe the clinical features of a family with photosensitive epilepsy, followed for 13 years. Generalized paroxysmal discharges induced by photic stimulation appeared in all 9 siblings. Generalized seizures, myoclonic jerks, and absences appeared in variable combination in 7 of them who on clonazepam remained free from seizures for a seven-year follow-up period. On EEG the paroxysmal abnormalities induced by photic stimulation abated during clonazepam medication.

Adolescent↗
PubMed1984

Management of lobar intracerebral hemorrhage: medical or surgical.

Two case histories of left parietal hemorrhage, with CTs, were evaluated by 88 board-certified neurologists and 114 board-certified neurosurgeons. Among the neurologists, 24% would have referred both patients for removal of the hemorrhage, 24% would have referred one of them, and 52% would have referred neither. Among the neurosurgeons, 47% would have operated on both patients, 25% on one of them, and 28% on neither. The lack of consensus probably results from an imperfect understanding of the natural history of these lesions. Controlled studies, or at least large retrospective studies, are needed to clarify this important therapeutic issue.

Cerebral Hemorrhage↗
PubMed1983

Dandy-Walker syndrome studied by computed tomography and pneumoencephalography.

Based on air studies, some authors have disputed the ability of computed tomography (CT) to diagnose posterior fossa cysts. The authors correlated the pneumoencephalographic, CT, and pathological findings in 4 patients with classic Dandy-Walker syndrome. Three cases had been misdiagnosed as retrocerebellar arachnoid cysts because the fourth ventricle was incorrectly considered normal on brow-up or erect air studies, reflecting the inability of such studies to evaluate an agenetic vermis and deficient posterior medullary velum which are characteristic of Dandy-Walker malformation. Careful correlation with autopsy findings showed that even with complete agenesis of the inferior vermis, if the slit between the cerebellar hemispheres is narrow, the fourth ventricle could be misinterpreted as normal on pneumoencephalography and sagittal CT. Radionuclide studies, a small amount of air, or metrizamide may be needed to determine whether the cyst communicates with the subarachnoid space.

Adult↗
PubMed1983

Motor aphasia unaccompanied by faciobrachial weakness.

Most patients with motor aphasia resulting from lesions of the left frontal opercular region have weakness of the right face and arm. We report a 43-year-old man who suffered mutism and agraphia unaccompanied by right-sided weakness after embolic infarction of Broca's area.

Adult↗
PubMed1983

Enhancing mass on CT: neoplasm or recent infarction?

On CT, mass effect and contrast enhancement have limited value in separating brain neoplasm from infarct, because both findings are frequent with recent infarction. Review of CT in 100 patients with histologically proven supratentorial lesions (35 infarcts and 65 tumors) indicated the specificity of three helpful signs: (1) White matter edema outlined the uninvolved cortex in 73% of metastases and in 74% of gliomas but only in 14% of infarcts. (2) The cortical ribbon was enhanced in 43% of infarcts, in 7% of gliomas, and in 4% of metastases. (3) Selective sparing of the thalamus occurred in 31% of infarcts but only in 7% of tumors.

Brain Edema↗
PubMed1982

Inclusion body myositis. A corticosteroid-resistant idiopathic inflammatory myopathy.

In seven patients with slowly progressive muscle weakness, inclusion body myositis (IBM) was diagnosed on biopsy. None had stigmata of collagen-vascular disease or malignancy. Serum creatine kinase levels were mildly or moderately increased. The six patients treated with prednisone did not improve. Needle electromyography showed a "myopathic" pattern in all patients, but four also had diffuse neurogenic changes with normal nerve conductions. Histologic study of muscle showed a mixture of small rounded fibers varying in size, atrophic angulated fibers forming small groups, and hypertrophic fibers. Variable amounts of inflammation, necrosis, and regeneration were seen in all specimens. All showed numerous intracytoplasmic vacuoles lined with purple-blue granules. Electron microscopy showed membranous whorls and masses of abnormal filaments measuring 14 to 18 nm in diameter. Although IBM seems to be a distinct type of inflammatory myopathy, its etiology and pathogenesis are not clear.

Adult↗