Skew deviation revisited

Background A case of progressive irradiation-induced cerebral vasculopathy with abnormal netlike vessels and transdural anastomoses (moyamoya syndrome) is presented. Radiological findings in an additional 40 cases reported in the literature are analyzed, and their clinical relevance is discussed. Case Description A 19-year-old woman presented with recurrent ischemic brain lesions after radiation therapy for treatment of a craniopharyngioma during childhood. Cerebral angiography 6 and 12 years after completion of radiation therapy revealed progressive cerebral arterial occlusive disease involving the internal carotid artery on either side of the circle of Willis, with abnormal netlike vessels and transdural anastomoses (moyamoya syndrome). Conclusions Extensive similarities between irradiation-induced cerebral vasculopathy and primary moyamoya syndrome (Nishimoto’s disease) support the notion that both disorders share common pathophysiological mechanisms. The occurrence of moyamoya-like vascular changes ma...

Progressive Cerebral Occlusive Disease After Radiation Therapy

Context: Radiation therapy is a potentially curative treatment for corticotroph adenomas refractory to surgery. Protons have an advantage over photons (x-rays) by depositing energy at the target with no exit dose, providing a lower dose to adjacent normal tissues. Until recently, proton stereotactic radiotherapy (PSR) was available at only two U.S. centers; use will increase as proton facilities are under development. Objective: Our objective was to evaluate the efficacy and safety of PSR for persistent Cushing’s disease (CD) and Nelson’s syndrome (NS). Design: This was a retrospective review of 38 patients (33 with CD and five with NS) treated between 1992 and 2005. Participants: All patients had transsphenoidal surgery without biochemical cure. Four had previous irradiation with photons. The patients with NS underwent bilateral adrenalectomy 29–228 months (median 40) before PSR. Intervention: Single-fraction PSR was delivered at a median dose of 20 Cobalt Gray Equivalents (range 15–20) on 1 treatment da...

/pdf/proton-stereotactic-radiotherapy-for-persistent-9luoqccyeg.pdf

Proton Stereotactic Radiotherapy for Persistent Adrenocorticotropin-Producing Adenomas

third and nineteenth day from the beginning of the symptoms, the first one being normal and the second one showing an increase in protein (0-95 g/l) with 11 cells and negative titres to brucella, syphilis, toxoplasma, herpes simplex, varicella-zoster, and a negative anticryptococcal antigen determination. The patient's clinical pattern began to improve two weeks after admission; she was discharged a week later. Follow up a month later revealed only a generalised areflexia and a slight dysmetria on the heel-knee test. Electrophysiological studies (table) were carried out on the sixth and eighteenth day, which revealed absent sensory potentials. Motor NCS showed less abnormality than that of sensory nerves. There was delay in the distal motor latency in all the nerves tested and there was also reduction in motor amplitude in both median nerves, with a 25-3% drop in peak-to-peak amplitude between wrist and elbow, and a 39-2% drop in amplitude between wrist and axilla in the first right median nerve conduction study. Neither temporal dispersion nor motor conduction block in the remaining nerves was noted. EMG studies were normal. A third electrophysiological study performed a month after her discharge showed the recovery of the sensory nerve action potentials in the lower and upper extremities, although the amplitude and sensory conduction velocity of the nerves studied were lower than the normal values. The motor NCS, however, were similar to previous values. The EMG study of the right anterior tibialis and right first dorsal interosseous muscles showed compatible changes with minimum denervation. Until recently the Guillain-Barre syndrome was an entity whose nosological characterisation relied upon a purely descriptive base, with relatively widely accepted diagnostic criteria,' Among these, the presence of muscular weakness is the most noticeable, indicating the main affectation of the motor roots. However, a purely sensory clinical variant of this illness is also believed to be possible and the following features are necessary for it to be accepted:2 rapid onset, distribution widespread and symmetrical, complete or near recovery, high CSF protein content, with few or no cells, and an electrophysiological study compatible with a demyelinative process in the peripheral nervous system. There is still a certain controversy as to whether this clinical variant occurs. In a recent review of 42 patients with acute sensory neuropathy, the authors concluded that this condition is not part of the spectrum of inflammatory demyelinating neuropathies;' nevertheless, it is noticeable that only 2 of the 42 patients had complete remission of symptoms and that the course of their disease was very protracted-from six to nine months. A case of acute polyneuropathy has been published in which the sensory disorders were also prominent and very similar to those of our patient.4 The necropsy carried out after the patient's death from pulmonary embolism revealed inflammatory infiltration with segmental demyelination in the peripheral nerves, posterior roots and spinal ganglia, with a marked preservation of the anterior roots. These findings, except for the preservation of the motor roots, are identical to those which are described in the GuillainBarre syndrome.' Our patient had an acute sensory neuropathy after a presumed viral illness and vaccination with a monophasic course and nearly complete recovery-both clinical and electrophysiological-in a short time; CSF protein content was high with a mild pleocytosis. The evidence suggests that this was probably an acute sensory inflammatory demyelinating polyneuropathy. FRANCEISC MIRALLES JORDI MONTERO RAMON RENE JUAN A MARTINEZ MATOS Department of Neurology, Hospital Princeps d'Espanya Ciutat Sanitaria de Bellvitge, Barcelona, Spain

https://jnnp.bmj.com/content/jnnp/55/5/412.2.full.pdf

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