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Introduction. – Pourfour du Petit syndrome, rarely reported, is the opposite of Claude Bernard-Horner syndrome.Exegesis. – A 67 years old female is hospitalised for dysphagia, allowing the discovery of oesophagus carcinoma with mediastinal, pleural and costal extension. The discovery of left unilateral mydriasis associated with exophthalmos and eyelid retraction suggest Pourfour du Petit syndrome ; this diagnosis is confirmed by CT-scan, finding pedicular lysis of high dorsal vertebras and intra-canalar tumoral extension.Conclusion. – Pourfour du Petit syndrome has the same localisation value and the same aetiologies as Claude Bernard-Horner syndrome, but its mechanism proceeds byan exciting lesion of cervical sympathetic nervous system. The recognition of this entity can allow the diagnosis of pathologies that need emergency treatment. [Copyright &y& Elsevier]

Invasion of the central nervous system by the larvae of Tenia Solium classically leads to severe illness. In some instances, however, the course is protracted and benign. The authors report on two patients with cysticercosis cerebri, revealed by delayed seizures without cerebral hypertension or any other manifestation. Computerized tomography established the diagnosis by demonstrating calcifications disseminated throughout the cerebral parenchyma. Such calcifications result from encapsulation of dead larvae. The possible diversity of the anatomic lesions caused directly or indirectly by the parasite explains why clinical manifestations are polymorphic. Diagnostic procedures are discussed.

A pathological study has been carried out of 49 examples of medullary infarction in 33 patients. The medial infarcts, very seldom single (2 /12), spared the subolivary levels. The pontomedullary junction was affected in 3 /9 cases studied. The lesions were more frequent in the ventral part of the arterial zonal pattern. They more often extended to its dorsal part at the level of the middle and upper one-third of the olive. The lateral infarcts, seldom single (6/30), extended to the subolivary levels in 6/22 cases studied and to the pontomedullary junction in 9/24 cases. The structures involved in each case and the area of the lesions at each cranio-caudal level have been studied. None of the 7 dorsal infarcts was single; in 6 of these cases there was also a cerebellar infarct involving the area of supply of the posterior inferior cerebellar artery. The subolivary levels (1/6) and ponto-medullary junctions (1/6) were seldom affected. The extent of the lesions in these uncommon infarcts has been described in detail.

A case of trichinosis involving the cental nervous system is presented. The neurological symptoms developed 20 days after ingestion of the larvae and 3 days after the onset of facial oedema. They consisted of behavioural disorders, tetraparesis, incontinence and oculomotor paralysis. All symptoms progressively regressed. Computed tomography showed transient low-density areas in the white matter. The main manifestations and the physiopathological mechanisms (transport of the parasite through the bloodstream, immuno-allergic reaction) of cerebral trichinosis are discussed.

A case is reported of gustatory sudation of the cheek without previous parotid lesions. The results of pharmacological tests confirmed the neurogenic origin, blocked by atropine and stimulated by A.C. The published literature is reviewed and a tentative explanation suggested, based on the physiopathological mechanisms involved in Freis syndrome, that the lesion was of neuritic type but had not been recognized.