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Biomedical subjects

L Suranyi

Publications and source records attributed to L Suranyi.

15 recordsLinked to original sources
PubMed1985

Hexosaminidase-A deficiency presenting as atypical juvenile-onset spinal muscular atrophy.

Three patients from two families had an unusual phenotypical variant of late-onset hexosaminidase-A deficiency. The clinical picture was dominated by spinal motor neuron involvement mimicking juvenile-onset spinal muscular atrophy. Atypical features included prominent muscle cramps, postural and action tremor, recurrent psychosis, incoordination, corticospinal and corticobulbar involvement, and dysarthria. The presence of these atypical features in patients whose lower motor neuron involvement would otherwise be consistent with juvenile-onset spinal muscular atrophy should raise the suspicion of the presence of hexosaminidase-A deficiency and GM2 gangliosidosis that can be proved by appropriate enzyme assays.

Adult↗
PubMed1983

Median nerve compression by Struthers ligament.

A 61-year-old patient presented with progressive weakness, pain and numbness in the left arm and hand. On examination the abnormalities were confined to the distribution of the median nerve, and electrophysiological testing localised the lesion to the segment just proximal to the elbow. At surgery Struthers ligament was found compressing the median nerve. No bony spur was found by palpation or on radiological examination.

Electromyography↗
PubMed1982

Study of nystagmus suppression in the Rotatory Tests.

Thirty one healthy subjects ranging in age between 21 and 50, participated voluntarily in the following experiment: they underwent programmed sequential alternating rotations, while their nystagmus was recorded by way of electronystagmography. The direction of rotation was changed every minute, and the total rotation time was 36 minutes. The subjects were rotated under external conditions which were altered every six minutes; these conditions included the following: 1. Rotation in the light with visual fixation and convergence. 2. Rotation in the light with visual fixation without convergence (one eye closed, the other looking at the target). 3. Rotation in the light without visual fixation (both eyes covered by a shade or by Frenzel's glasses). 4. Rotation in the dark without convergence (looking straight ahead). 5. Rotation in the dark with convergence (looking at the thumb, closely placed in front of the nose). The purpose of the experiment was to study the phenomenon of nystagmus suppression observed with visual fixation and often attributed to cortical activity. The conclusion of the study is that nystagmus may be suppressed by light alone as well as by visual stimuli, convergence and proprioceptive stimuli. The inference is that the mechanism involves brain stem reflexes and not necessarily visual cortex activity.

Adult↗
PubMed1982

Is there nystagmus habituation to angular acceleration in man?

10 healthy volunteers, ranging in age from 20 to 30 years, were subjected to rotatory stimulation at 1 degree, 2 degrees and 4 degrees/s2 acceleration and deceleration, repeated four times at weekly intervals. Nystagmus was recorded with electronystagmography. Slow-phase velocity and the total numbers of nystagmic spikes were analyzed. There was no evidence for habituation in this experiment, which is in agreement with the majority of previous publications.

Acceleration↗
PubMed1975

Respiratory inhibitory apraxia.

Ten patients have been described showing inability to stop breathing on command, spontaneous respiration and voluntary respiratory stimulation being unaffected. This abnormality not previously described in the literature, we feel should be named respiratory inhibitory apraxia (R.I.A.). The anatomical organization of respiration is briefly reviewed. R.I.A. is often associated with other forms of apraxia or motor impersistence. It is thought that the urinary and bowel incontinence present in some of these cases might also represent a form of inhibitory apraxia. Information is presented which supports the view that respiratory inhibitory apraxia is due to a minor hemisphere lesion, usually deepseated. Our one autopsied case showed a lesion in the descending motor pathways in the internal capsule, in middle cerebral artery branch territory, disconnecting the voluntary respiratory inhibitory center in the cortex in anterior and middle cerebral cortical branch territories.

Aged↗