Noran Neurological Clinic

Managing Diplopia During Recovery From Fisher Syndrome: An Occupational Therapy–Led Oculomotor Rehabilitation Case SeriesManuscript type: Case series: 3 casesKey Clinical MessageDiplopia during recovery from Fisher syndrome can substantially restrict

Since 2004, Presidents of the American Academy of Clinical Neuropsychology (AACN) have provided the readership of The Clinical Neuropsychologist with the President's Annual State of the Academy Rep...

We describe a patient with chronic asymmetric motor neuropathy, which began in the upper extremity. The paretic muscles showed abundant fasciculations and myokymia but only little amyotrophy. Electrophysiologic examination revealed proximal multifocal persistent conduction block (CB) not located at the usual entrapment sites, and arrhythmic isolated or grouped fasciculation potentials originating distally on blocked axons. Over the years, new CBs developed, which led to tetraplegia, and amyotrophy slowly increased with progressive denervation. This patient differs from the cases of chronic acquired demyelinating polyneuropathy described in the literature by the absence of sensory deficit and the proximal location of CB.

Nucl. ventralis intermed. (Vim) of the thalamus, which is lying posteriorly to VL and anteriorly to the sensory relay nuclei, was investigated and proved that in this small nucleus the lowest threshold muscle afferents are sending projection. By using CAT computer, triphasic potential could be recorded from this small area, for ulnar nerve shocks at intensities below the threshold for evoking the muscle contractions.

An 18-year old male, with intractable pain from sarcoma of the left iliac bone, was submitted to bilateral upper thoracic chordotomy in two stages. There was no post-operative relief of pain, and no detectable loss of touch, cutaneous pain or temperature sensibility. The patient finally died from the progress of his primary disease. Histological examination of the spinal cord revealed bilateral ascending degeneration of the spinothalamic tracts, completely on the right and partially on the left. The persistence of left-sided pain may be explained by preservation of ipsilateral spinothalamic fibers. With regard to the absence of cutaneous sensory loss the authors tentatively suggest that the reticular formation of the spinal cord, as a sort of atavism, has been, in this patient, primarily concerned with the transmission of impulses promoting pain and temperature sensations. On the other hand, it may be supposed that the intact ascending fibers, represented by the not interrupted spinothalamic fibers and/or the multisynaptic system, have been directly or indirectly activated, the central differentiation between the various types of stimuli applied depending on the spatial pattern of discharge from the peripheral nerve terminals.