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As has been shown during the course of experimental allergic neuritis, in the Guillain-Barré syndrome there is an invasion of the myelin sheath in certain fibres by a mononuclear cell, with an intact axon. In a series of 45 cases we have been able to show this feature in 31 cases. In certain cases the cytoplasm prolongation of the invading cell was seen in the myelin sheath, forcing apart two neighbouring layers. In five cases we have furthermore observed the presence of mononuclear cells located either between the myelin and the axon which is deformed, or on the inside of the axon. Such an anomaly was frequent in one recent case and was occasionally found in four other cases.

Inflammatory demyelinating polyradiculoneuropathies exhibit well-known ultrastructural lesions of the peripheral nerve, both in acute cases, i.e., Guillain-Barré syndrome, and in relapsing, sub-acute and chronic cases. We present a case of relapsing inflammatory demyelinating polyradiculoneuropathy in a diabetic patient with a biopsy exhibiting these lesions, as well as a widening of the outermost myelin lamellae in some fibers. Such associated lesions are classic in experimental inflammatory demyelinating polyradiculoneuropathies, but have not been reported in human pathology.

Idiopathic polyradiculoneuropathy with primary axonal lesions is rarely encountered. Two cases are reported with a chronic relapsing course and a fatal outcome. Neuropathological examination of biopsied peripheral nerve in the two patients and in a necropsy case showed loss of myelinated fibres, but neither active demyelination nor inflammatory cells were observed. Acute and chronic relapsing axonal polyradiculoneuropathies appear to be two clinical forms of a peculiar entity different from GBS.

A diabetic woman underwent an incision of the right big toe for an abscess and developed a typical Guillain-Barré syndrome 48 h later. A biopsy of a peripheral nerve, performed 10 days later, showed modifications usually seen in diabetic patients, as well as the characteristic ultrastructural modifications of the Guillain-Barré syndrome (GBS). Moreover, 22% of myelinated fibers exhibited vesicular disruption of the myelin sheaths. This lesion is rarely encountered on the biopsies of peripheral nerve in GBS and concerns only a few myelinated fibers. Such a prominence of myelinic vesicular disruption and its occurrence in a diabetic patient are discussed.

A 46-year-old male patient developed the Guillain-Barre syndrome and recovered completely within 3 months. He had been treated 5 years previously for Hodgkin's disease, and during the neurological syndrome, relapse of the malignant lymphoma was discovered. On neuro-muscular biopsy, lymphocytes were observed penetrating Schwann cells. These neuropathological aspects confirm the auto-immune character of the nervous involvement.

65 biopsies of peripheral nerve from patients suffering from Guillain-Barré syndrome were studied by electron microscopy. In 48 cases there was macrophagic invasion of the Schwann cells of certain myelinated fibers, and in 32 of these cases some myelin sheaths were stripped away by an elongated macrophagic process. Vesicular disruption of the myelin sheath was observed in only 8 cases and in less than 1% of the myelinated fibers. Uncompacted myelin lamellae were observed in a few myelinated fibers. These ultrastructural lesions are analysed and commented on with a view to selecting patients who are to undergo plasma exchange.