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To the Editor: I found it surprising that in their study, intended to be an exhaustive analysis of sensory findings in lateral medulary infarction (LMI), Kim et al.1 did not mention the abnormality so peculiar to this condition: dissociation of pain and temperature sensations. The first patient I saw with this condition-a physician himself-mentioned that although he had no difference in …

• 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 juvenileonset spinal muscular atrophy should raise the suspicion of the presence of hexosaminidase-A deficiency and GM 2 gangliosidosis that can be proved by appropriate enzyme assays.

SUMMARY: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.

10 healthy volunteers, ranging in age from 20 to 30 years, were subjected to rotatory stimulation at 1°, 2° and 4°/s2 acceleration and deceleration, repeated four times at weekly intervals. Nystagmus was recorded with electronystagmography. Slowphase 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.

To the Editor. —I am sure many of my colleagues find the meticulous description of patient histories and phenomena by C. Miller Fisher as educational and informative as I do. I was hoping to find some reference to possible legal implications of transient global amnesia (TGA) in his recent article on the subject (Archives1982;39:605-608). From time to time, neurologists are requested to provide information to lawyers and to give evidence as expert witnesses at court proceedings. Not infrequently, persons charged with some illegal activity claim amnesia for it. It is conceivable that some of them had episodes of TGA. Much has been written about TGA over the years, and it is surprising that, to my knowledge, no one has addressed even the possibility that rules and laws might be broken during an episode. The pathophysiologic basis for TGA is a temporary functional separation of the areas of the brain

To the Editor.— I found the recent publication by McCarthy and Marshall on suppression-burst pattern with associated eyelid opening (Archives1981;38:754-756) to be most interesting. They seemed certain that the eyelid movements were the motor manifestation of the seizure activity also causing the EEG discharges, and did not believe that the changes observed on the EEG were the result of eye opening and closure. Their assumption is probably correct for several reasons: (1) The onset of EEG discharges corresponds to eye opening, and not to eye closure as usually seen in light-sensitive epilepsy 1 in cases where such discharges are observed as a result of the motor act of eye closure. 2 (2) The intermittent EEG discharges continued without associated eyelid movement in the follow-up tracing of patient 2. (3) There is a significant delay in two of their cases between termination of EEG discharges and eyelid closure. (4) The