Dysphagia can be caused by a rare anomaly of the subclavian artery. The diagnosis can be overlooked at endoscopy, but barium contrast study of the esophagus will reveal the abnormality. In patients with coexisting esophageal abnormalities the finding may be incidental and specific conservative treatment may be sufficient. Manometry cannot be used to diagnose this condition or to predict surgical outcome. When the symptoms are intractable, surgical correction should be considered even if coexisting esophageal abnormalities are present.

A 78-year-old woman with long-standing obstipation presented herself to the hospital with diarrhoea and progressive abdominal cramping since 2 days. Acute abdomen developed and an emergency exploratory laparotomy was indicated, which showed no signs of bowel ischaemia. After admission to the internal ward, stool Clostridium difficile PCR was tested positive. Hence the diagnosis of pseudomembranous colitis became apparent. Abdominal imaging demonstrated multiple gas foci in the wall of the bladder and extensive pseudomembranous colitis. The patient was initially treated with oral vancomycin and secondarily with metronidazole for recurrent C. difficile infection. Resolution of diarrhoea and abdominal cramping was noted on 6-week follow-up visit.

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Intra-abdominal arterial bleeding is a life-threatening condition, warranting immediate causal therapy. Polyarteritis nodosa is a rare type of necrotizing vasculitis that affects medium-sized arteries. We present a patient with severe arterial bleeding as the first symptom of polyarteritis nodosa. Because the bleeding took place intra-abdominal instead of gastro-intestinal, there was no macroscopic blood loss. She was successfully treated with endovascular coil embolization during angiography.

The paper by Anzola et al' addressed the important issue of cognitive functioning in patients suffering from MS. We appreciate their study, and share to a large degree their conclusions concerning cognition in MS patients, and we can contribute some additional information.A) The authors did not mention the exact number or the percentage of patients with deficits on neuropsychological assessment; apparently, number as well as degree of impairment allowed characterisation of the deficit as "very mild". B) The authors attributed their deviating results to their selection of ambulatory patients with relapsing-remitting course of MS. C) They considered the pattem of impairment (inferior performances in concept formation, non-verbal reasoning and verbal memory tests) as indicative of so-called subcortical disruption. We wish to confirm A, comment on B and query C.A) For counselling and management it is important to know that MS is not a sufficient or necessary condition for suffering cognitive defects, let alone dementia. Findings that are at variance with current quite high estimations of cognitive defects in MS will ultimately add to revealing the as yet insufficiently known spectrum of severity in MS.2 Our findings concur with those of Anzola et al. In a comprehensive neuropsychological study of 39 outpatients with relapsing-remitting (n = 20) and chronically progressive (n = 19) MS, who presumably were slightly more handicapped than the patients oftheir study (table), and all ofwhom were in quiescent disease stages, we also found evidence of generally adequate cognition. On a case by case basis we found signs of cognitive decline in 18% of the patients.3B) The suggestion of mild physical handicap and relapsing-remitting course of MS explaining the absence ofMS-related dementia cannot be endorsed by our findings. We studied the explanatory value of several illness variables, among which Kurtzke DSS, duration of illness, and course of MS (RR versus CP). However, using parametric and, when appropriate, nonparametric procedures, we failed to identify a significant influence ofany ofthese variables in any ofthe behavioural measures (table). The critical illness variables, apart from extensive periventricular demyelination, as stressed by the authors, remain to be identified. C) In our view, the presence of weak memory performance, poor concept formation and poor nonverbal problem solving is insufficient to result in subcortical dysfunction. The distinction between cortical and subcortical "dementia" rests on inferring the mental disorganisation underlying poor overt performances. Important variables underlying so-called cortical performance deficit should be disordered instruments of cognition. Key variables underlying so-called subcortical performance deficit should be apathy and slowness of information processing. The discrepancy between relatively adequate acquisition and poor retrieval should be taken as the distinguishing feature of so-called subcortical memory failure.' The authors present no data that may help t...