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PubMed1990

Neurological manifestations of osteoid osteoma.

The clinical and radiological features of 38 children with osteoid osteomas were analysed retrospectively. Twenty nine patients had lesions of the femur (n = 17) or tibia (n = 12). The mean duration from the onset of symptoms to diagnosis was 13.8 months. In seven patients the history of pain and abnormalities on examination suggested a possible neurological disorder. Fourteen of 29 patients (48%) with femoral or tibial osteomas had localised muscle atrophy, and 10 patients (34%) had diminished or absent deep tendon reflexes in the affected limb. Two patients had painless lesions. Six patients had normal plain radiographs. Delay in the diagnosis of osteoid osteoma may be prevented by the knowledge that pain may be referred or radicular, that the concomitant occurrence of muscle atrophy and depressed deep tendon reflexes are relatively common findings, and that the characteristic radiological features may only appear late in the course of the disease.

Adolescent↗
PubMed1994

Differential diagnosis of leukokoria: radiologic-pathologic correlation.

Leukokoria is an abnormal pupillary light reflection that usually results from an intraocular abnormality and is seen most often in children. One-half of the cases of childhood leukokoria are caused by retinoblastoma, a malignant tumor of immature retinoblasts that manifests in a normal-sized eye as a calcified mass, is often partially necrotic, and grows into the vitreous and through the choroid. Retinoblastoma enhances with contrast material and, unlike most tumors, may be darker than vitreous on T2-weighted images. When leukokoria is associated with microphthalmia, persistent hyperplastic primary vitreous (PHPV) (28% of cases) or retinopathy of prematurity (ROP) (5% of cases) should be considered. PHPV is a congenital, usually unilateral lesion that appears as a dense tubular mass extending from the lens to the retina along the course of the hyaloid canal. Hemorrhage from PHPV produces a subhyaloid (or subretinal) fluid collection, often with characteristic blood-fluid levels. ROP is bilateral and usually manifests in premature infants who received supplemental oxygen therapy. Coats disease (16% of leukokoria) is a sporadic unilateral idiopathic retinal telangiectasia that produces a lipoproteinaceous subretinal exudate leading to complete retinal detachment. The globe has normal size but increased attenuation and signal intensity from hemorrhage without calcification or enhancement. Toxocaral endophthalmitis (16% of leukokoria) is a granulomatous reaction to the parasite in the vitreous and uveoretinal coat. Retinal astrocytoma (3% of leukokoria), which manifests in a normal-sized globe, is an indolent benign neoplasm commonly associated with phakomatoses (usually tuberous sclerosis).

Child↗
PubMed1991

Impaired venoarteriolar reflex as a possible cause for nifedipine-induced ankle oedema.

Ankle oedema is not an uncommon side effect of treatment with nifedipine. To evaluate the possible effect of nifedipine on the microcirculation of the skin, 18 patients with systemic hypertension who were known to develop ankle oedema after nifedipine and 19 patients with systemic hypertension who did not develop ankle oedema after nifedipine were studied. Following four weeks of nifedipine therapy (10 mg, three times daily), the microcirculation on the dorsum of the foot was measured using laser-Doppler flowmetry. Estimation of the microcapillary flow was made both after supine resting and on standing upright. The venoarteriolar reflex was expressed as the standing flow in percentage of the resting flow. There was no significant difference between the two groups of patients in the resting flow, supine flow, or the venoarteriolar reflex before nifedipine therapy (P greater than 0.4). Before nifedipine, the blood blow in the skin of both groups of patients was reduced from the supine level upon standing, thus indicating a normal response to dependency. After nifedipine administration, no significant difference was observed between the two groups of patients in the resting flow (P greater than 0.5). The flow on standing, however, was 96.2% of that measured during resting supine in patients who developed ankle oedema and 79.8% of the resting flow in the patients who did not develop ankle oedema, suggesting a weaker venoarteriolar reflex in patients who developed ankle oedema following administration of nifedipine (P less than 0.0001). Thus, the microcapillary flow did not decrease upon standing in patients who developed ankle oedema following nifedipine therapy, indicating an abnormal venoarteriolar reflex. This may explain why ankle oedema develops in such patients following nifedipine.

Adult↗
PubMed1992

Primitive reflex profiles in infants: differences based on categories of neurological abnormality.

In order to clarify reflex profiles in the first year of life in connection with categories of neurological abnormality, six primitive reflexes, i.e., the crossed extensor reflex, suprapubic extensor reflex, heel reflex, Galant response, asymmetric tonic neck reflex and plantar grasp response, were examined in 458 normal infants, 78 infants with cerebral palsy (CP) and 81 infants with mental retardation (MR), whose diagnoses were confirmed at a later follow-up examination. The change in the mean score for each of these reflexes with age was characteristic for each category or type of neurological abnormality. This implies that a presumptive diagnosis can be made in neurologically high-risk infants by examination of the primitive reflexes. Such reflexes are therefore of specific significance, among other neurological criteria, in infants within the first year of life.

Ataxia↗
PubMed2003

Hereditary neuropathy with liability to pressure palsies (HNPP) in a toddler presenting with toe-walking, pain and stiffness.

The typical clinical presentation of hereditary neuropathy with liability to pressure palsies is an adult-onset recurrent, painless monoparesis. Electrophysiological abnormalities--decreased nerve conduction velocities and delayed distal latencies--can be detected even in asymptomatic patients. We describe a toddler, who presented with asymmetric toe walking, painful cramps and stiffness in the legs. He had calf hypertrophy, brisk tendon reflexes and bilateral Babinski signs and the electrophysiological examination was normal. The unlikely diagnosis of hereditary neuropathy with liability to pressure palsies was reached 5 years later, when the boy started to complain of episodic numbness and weakness in the upper extremities. His father, paternal aunt and grandmother had similar symptoms, but they had never been investigated. The typical 1.5 Mb deletion on chromosome 17p11.2-12 was found in our patient and his affected relatives.

Child↗