Biomedical subjects
Publications and source records attributed to C E Westerberg.
A typical case of pseudoclaudication syndrome (neurogenic intermittent claudication), where the cause of the lumbar spinal canal narrowing was an intraspinal neoplasm, is reported. A neoplasm as the cause of this syndrome seems to be very rare, possibly because of the progressive nature of the space-occupying lesion and hence the rapid development of other predominant symptoms.
The pseudoclaudication syndrome, now a well known neurological entity, can simulate intermittent claudication of arterial origin in its clinical appearance. Walking and sometimes simply standing upright for a while can cause transitory pain, numbness or weakness in the legs. The symptoms are caused by entrapment of the cauda equina fibers. Intermittent bladder paresis with total inability of micturition despite urgency to void may sometimes be a prominent feature of the syndrome, a fact that seems to be less well known as seen from a review of the literature.
A new disorder with possible autoimmune background is described in a 67-year-old man. He had experienced episodes of cerebellar ataxia induced by infections over the last 40 years. In 1963 he had thyrotoxicosis. The patient underwent bilateral subtotal thyroidectomy. Recently it has been possible to detect involvement also of his remaining thyroid gland, with findings compatible with hyperthyroidism concomitant with his cerebellar atixia.
Twenty-two out of 235 patients with undoubted or suspected MS, treated at the Neurological Clinic, Uppsala, during the eight-year period, 1966-1973, had paroxysmal symptoms during the course of their disease. Paroxysmal dysarthria and ataxia (7 cases), and tonic seizures (5 cases) were the most common types of attacks. Some types of attacks (paroxysmal hemiataxia and crossed paraesthesiae, paroxysmal itching, diplopia as the single, paroxysmal symptom) do not seem to have been described previously. A patient with tonic seizures caused by a localized, traumatic lesion of the cervical spinal cord is also described. It is suggested that the paroxysmal phenomena in MS are caused by a transversely spreading ephaptic activation of axons within a partially demyelinated lesion in fibre tracts somewhere in the central nervous system. The different paroxysmal phenomena are discussed in the light of this hypothesis.
The symptomatology in the thoracic outlet syndrome is well known. A patient is reported in whom the finding of a unilateral pulse deficit was the alerting sign that led to the correct diagnosis. Angiography, performed with injections during different respiratory phases, visualized the pathogenetic mechanism underlying some of the clinical findings.