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Biomedical subjects

H Alcalá

Publications and source records attributed to H Alcalá.

16 recordsLinked to original sources
PubMed1993

[The differential diagnosis of poliomyelitis and other acute flaccid paralyses].

Between June 1988 to January 1991 a total of 246 children with acute flaccid paralysis (AFP) were seen at Hospital Infantil de México, Federico Gómez which was the center of study for AFP for the Poliomyelitis Eradication Program of Mexico. Of the 246 children, 42 has poliomyelitis (17%); 156 has Guillain-Barré syndrome (GBS) (63.4%); 16 had traumatic neuritis of the sciatic nerve secondary to IM injections (TNC) (6.5%); five had transverse myelitis (2%); the rest (27) had other diseases misdiagnosed as polio (10.9%). The basic clinical characteristics for the diagnosis of poliomyelitis are: myalgias and fever at the onset AFP, paralysis is asymmetrical, of distal predominance and causes severe muscular atrophy and skeletal deformities; the GBS presents as an ascending, symmetrical, areflexic paralysis of distal predominance. It does not causes atrophy or deformities. TNC presents several days after IM injections with pain and hypothermia in the affected limbs; TM is a flaccid, symmetrical paraparesis with neurogenic bladder and a sensory level. CSF and neurophysiological studies (EMG and NCV) are very useful for diagnosis. Other entities misdiagnosed as poliomyelitis were: osteoarticular trauma, myopathies and dystrophies, viral myositis, acute cerebellitis, retroperitoneal tumors and upper motor neuron syndromes. Viral studies in stool specimens are essential for the diagnosis of poliomyelitis.

Acute Disease↗
PubMed1990

Wakefulness-sleep modulation of EEG-EMG epileptiform activities: a quantitative study on a child with intractable epilepsia partialis continua.

Continuous all night recordings of epileptiform EEG activities from right frontal scalp and thalamic Centromedian regions and EMG activities from left deltoid muscular region were performed on a child with intractable epilepsia partialis continua, with depth stimulating-recording electrodes used for neuroaugmentive seizure control. In addition, "normal" and "mature" sleep indicators in the same child were simultaneously recorded according to the International Procedures. During wakefulness (W), type B seizures consisted of isolated, high amplitude, negative-positive EEG sharp waves recorded from the right Centromedian region (RCM sharp) correlated with isolated bursts of high amplitude EMG potentials recorded from the left deltoid muscle (LEMG jerks). Type C seizures consisted of clusters of repetitive RCM sharp and LEMG jerks, where individual EEG-EMG activities showed poor correlations. Number and amplitude of type B RCM sharp and LEMG jerks significantly decreased when patient directly shifted from W to slow wave sleep I and II (SWSI and II). Number and amplitude of RCM sharp increased while those of LEMG jerks decreased directly from SWS I and II to slow wave sleep III (SWS III); all forms of EEG-EMG epileptiform type B activities significantly decreased directly or indirectly from W and SWS to paradoxical sleep (PS). Scalp EEG spikes from right frontal and central regions showed almost parallel changes to those of RCM sharp, except during SWS II, when amplitude increased in the former and decreased in the later. Occurrence of type C seizures only decreased during PS and duration decreased directly from SWS I to II and indirectly from SWS I to SWS II and PS; and from W to SWS II and III and PS.

Child, Preschool↗
PubMed1990

[Acute hemiplegia in childhood and alternating hemiconvulsions secondary to Moya-Moya disease. Report of a case associated with Down's syndrome].

Moya-Moya disease has been associated to a number of disease entities including Down syndrome. Initial clinical manifestations in our patient were alternating lateralizing seizures with sudden onset hemiparesis. Ct scan demonstrated several infarcts in different stages of evolution, in the territory of left middle cerebral artery. Single digital subtraction angiography showed bilateral occlusion, predominantly on the left side of the supraclinoid portion of the interna carotid arteries with formation of collateral circulation in the diencephalic territory. The association of Moya-Moya disease and Down syndrome is not fortuitous and it is probably due to a congenital vascular dysplasia. It should be suspected in children with trisomy 21 (with or without congenital heart disease) who presents with alternating hemiplegia and convulsions or acute hemiplegia.

Acute Disease↗
PubMed1986

Spinal cord compression due to cystic duplication of the primitive digestive tract.

Three children are described who presented with the syndrome of spinal cord compression. They had intradural-extramedullary masses, which proved to be histologically benign cysts with characteristics similar to those found in the embryonic foregut. Emphasis is placed on the importance of early diagnosis and prompt surgical treatment of these congenital malformations, stressing the fact that complete recovery is possible. The literature is reviewed.

Child↗
PubMed1980

Human cerebellar hypoplasia: a syndrome of diverse causes.

Seven children had congenitally small cerebella. Perinatal asphyxia was not a factor. Clinical signs in infancy were generalized muscular hypotonia, delayed development, truncal titubation, and intention tremor. Most had fixation nystagmus and esotropia. Three had seizures and an abnormal EEG. Pneumoencephalography in each case revealed a small cerebellum with prominent folia, large fourth ventricle, wide vallecula, large cisterna magna, and normal lateral and third ventricles. A computerized tomography scan in one case showed similar findings. One patient had an absent corpus callosum. One patient died at 2 1/2 years. The cerebellar hemispheres and vermis were small. Granular cells were absent throughout. Purkinje's cells were preserved, but had dendritic swellings with radiating fibrils. Cerebellar, pontine, and inferior olivary nuclei showed mild neuronal loss. The clinical and pathologic findings resemble those of animal models of cerebellar hypoplasia produced by fetal exposure to certain viruses, toxins, or repeated low doses of radiation. Cerebellar hypoplasia is a clinical syndrome of several causes, but with many symptoms and signs in common.

Cerebellar Diseases↗
PubMed1980

Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living ameba.

Primary amebic meningoencephalitis and granulomatous amebic encephalitis are well recognized clinicopathological entities caused by free-living amebas. Associated arteritis and "mycotic aneurysms" with infiltration of intracranial arteries by lymphocytes, amebic trophozoites and cysts have not been previously reported. A 26-month-old girl had a 3-week history of encephalitis, characterized, initially, by vomiting and low-grade fever. Subsequently, she developed ataxia, generalized weakness, lethargy, and esotropia. The first CSF showed 490 RBC/microliters, 705 WBC/microliters with 90% mononuclears. Her pupils reacted briskly to light. Moderate nuchal rigidity, nystagmus, fixed downward gaze, anisocoria, bilateral 6th nerve palsy, left arm monoparesis and left Babinski were present. CAT scan revealed slight symmetrical dilatation of anterior horns of lateral ventricles and an area of abnormal enhancement above the 3rd ventricle. She died 14 days after admission, 5 weeks after onset of symptoms. The brain showed focal necrotizing encephalopathy, involving thalami, cerebellum, brain stem, and cervical and upper thoracic spinal cord. Numerous free-living amebic trophozoites and cysts were present within a chronic granulomatous encephalitis. There were trombosis of basilar, posterior cerebral, and vertebral arteries with profuse chronic panarteritis, fibrinoid necrosis, and mycotic aneurysms.

Amebiasis↗
PubMed1978

The effect of size, histologic elements, and water content on the visualization of cerebral infarcts.

We correlated the radiologic and pathologic examination of 13 human brains, analyzing the size, different histologic elements, and water content in 40 ischemic and hemorrhagic infarcts. Acute infarcts appear in the computerized cranial tomographic (CT) image as low density areas due to high content of fluid, however, a histological-chemical correlation is not concomitant. The addition of blood in hemorrhagic infarcts may result in a normal CT image. Subacute infarcts appear as low density areas, with lower attenuation values due to the presence of large amounts of lipids. Subacute lesions with prominent mineral deposits may be negative on CT scan. Chronic infarcts also appear as low density areas due to cavitation and residual fats. Attenuation values are slightly higher than those of subacute infarcts, possibly due to gliosis. Infarcts smaller than 2 cm in diameter are usually not visualized.

Brain↗
PubMedDate not supplied

Epileptiform EEG activity of the centromedian thalamic nuclei in children with intractable generalized seizures of the Lennox-Gastaut syndrome.

Centromedian thalamic nuclei (CM) epileptiform EEG activities were recorded in children with intractable generalized seizures of Lennox-Gastaut syndrome (LGS) through implanted recording-stimulating electrodes used for seizure control. Ictal CM epileptiform activities were consistently correlated to widespread surface cortical EEG activities and symptoms in all patients and all types of generalized seizures; i.e., fast spike discharges at CM correlated at onset of tonic and tonic-clonic generalized seizures; slow (1-2 Hz) spike-wave complex discharges at CM correlated for atypical absence seizures; slow polyspike-wave complex discharges correlated for myoclonic seizures; and spike bursts and suppression patterns correlated for combined tonic-atonic-myoclonic seizures. Ictal EEG activities occurred simultaneously at right and left CM and surface at onset of all seizure types, with the exception of myoclonic seizures where CM complete discharges and individual spike-wave complexes significantly lead those of the surface. Brief tonic-atonic spasms clinically undistinguishable from "real" epileptic seizures showed no EEG counterparts at CM and surface. Interictal CM spike-wave complete discharges and individual spike-wave complexes showed variable amplitude-temporal patterns. Amplitude emphasis on CM and frontopolar regions was observed in most of complete discharges, however, and phase shifts between CM and frontopolar regions were observed in individual spike-wave complexes.

Adult↗