Cancer of ileostomy: a late complication of colectomy for ulcerative colitis.

Cancer arising at an ileostomy site represents a rare late complication of total colectomy performed for ulcerative colitis. There are no more than 36 published cases in the literature. We describe a case of adenocarcinoma of the mucocutaneous junction at the ileostomy site, occurring 31 years after total colectomy for ulcerative colitis. Wide excision of the moderately differentiated adenocarcinoma was performed with refashioning of the ileostomy. Polypoid adenomas or adenocarcinomas of the ileostomy after colectomy performed for non-neoplastic conditions are extremely uncommon. Biopsies of polypoid lesions at the stoma site are recommended.

Chronic demyelinating neuropathy associated with benign IgM paraproteinaemia.

Twelve cases of chronic sensorimotor neuropathy associated with benign IgM paraproteinaemia are described. The onset was in the sixth or seventh decades and 9 cases were male. Tremor and ataxia were common features. The ESR was raised in 6 cases and the CSF protein content elevated in 10. There was severe reduction of motor nerve conduction velocity. Sera from all cases contained monoclonal IgM antibodies strongly reactive with human peripheral myelin, made up by the paraprotein. Histological studies on nerve biopsies taken from 8 cases all demonstrated a demyelinating neuropathy. Eight biopsies were examined by immunofluorescence. Monoclonal IgM was present on the myelin sheaths of surviving myelinated nerve fibres. The findings suggested that the neuropathy was of autoimmune origin and caused directly by the antimyelin antibody.

Renaut body distribution at sites of human peripheral nerve entrapment.

In an autopsy study of the pathology of chronic subclinical nerve entrapment Renaut bodies showed a strong predilection for sites of nerve entrapment. They were present at these sites in 43 of 74 peripheral nerves but in none of the control sections of the same nerves. Renaut bodies were most frequently encountered in the median nerve at the wrist and in the lateral femoral cutaneous nerve at the inguinal ligament but were rarely seen in sections of the common peroneal nerve at the neck of the fibula. Renaut bodies were closely associated with thickened subperineurial capillaries, and, in successive transverse sections, they terminated in a fibrous mass of these thickened vessels. In several nerves Renaut bodies showed a similar orientation within adjacent fascicles, suggesting that mechanical factors were related to their pathogenesis; despite this finding there was no relationship between their numbers at entrapment sites and the presence of pathological changes in myelinated nerve fibres at the same level. These findings suggest that while mechanical factors are important in the pathogenesis of Renaut bodies there is no evidence to support the theory that these structures protect nerve fibres from mechanical stress.

Acute ischaemic neuropathy in the rabbit.

Ligation of either the common and internal iliac or the internal and external iliac arteries produced ischaemic lesions of the sciatic nerve and its branches, as well as direct muscle damage, in 5 out of 6 rabbits. In one animal, ligation of the aorta and of the internal iliac artery on one side produced a similar mixture of nerve and muscle damage on the side of the double ligation. Ligation of the femoral artery alone in 3 animals failed to produce significant changes. In the 6 affected animals there was paralysis of the hind leg on the side of the iliac ligations, with loss of tendon reflexes. Appreciation of pinprick over the foot and lower leg also appeared to be impaired. Complete ischaemic necrosis with irreversible damage to both neural and connective tissue elements did not occur in the main nerve trunks, but was present in some of the intramuscular nerve bundles as part of generalized coagulative necrosis of the most severely affected muscles. The characteristic pathological changes in the nerve fibres of the main nerve trunks were Wallerin degeneration and paranodal demyelination, the former being more extensive than the latter. In the animals with double iliac ligations, the upper level of ischaemic nerve damage was in the thigh, the tibial portion of the sciatic nerve being more commonly affected than the peroneal. Nerve and muscle damage tended to occur at different levels in the limb, but there was no example of clinical paresis due to neural damage without any ischaemic muscle changes being present. In two of the 3 animals in which the plantar muscles were examined, these muscles appeared to escape direct damage in spite of ischaemic lesions in the more proximal parts of the limb.

Optic nerve fibre lesions in adult cats: pattern of recovery of spatial vision.

Partial deafferentation in the pre-geniculate optic pathways of the adult cat was produced by micro-injection of diphtheria toxin. In this lesion a certain proportion of fibres was damaged while neighbouring fibres remained unaffected. Behavioural methods were used to study the time course, pattern, and extent of recovery of spatial vision after such lesions. Cats were trained to discriminate square-wave gratings from blank fields. A range of grating sizes (0.13--2.61 cycles/degree) at high contrast were presented each day and when performance was consistently 100%, the lesion was placed. At 24 h post-lesion and serially thereafter grating discrimination was tested. Contrast sensitivity was also measured before and after the lesion. All cats recovered to pre-lesion performance levels. The time course of recovery was characterized by an early rapid phase followed by a longer slower phase. The early recovery was temporally coincident with dispersal of oedema at the site of the lesion, while the later slower recovery probably represented a functional reorganization at the synapse. Optic nerve fibre analyses at one year post-lesion showed reduction in fibre content ranging from 33 to 77% in different cats without shift in the fibre size histograms. The length of recovery time was directly related to the magnitude of fibre loss. The return of spatial frequency perception was hierarchical - first medium (1--4 days), then low (1--2 months) and finally high spatial frequencies (5--8 months). Possible mechanisms are discussed and it is suggested that such a pattern of psychophysical results could be accounted for by date than the X-type.

Hereditary sensory neuropathy with spastic paraplegia.

Five cases of spastic paraplegia with a progressive symmetrical sensory neuropathy producing ulceration and osteomyelitis of the hands and feet are reported. The pathology in one patient, who died of secondary amyloidosis, was similar to that found by Denny-Brown in hereditary sensory radicular neuropathy with severe loss of posterior root ganglion cells and loss of myelinated fibres in both peripheral nerves and posterior columns of the spinal cord. A sural nerve biopsy in another case showed a striking loss of both myelinated and unmyelinated fibres, with some evidence of degeneration and regeneration. The inheritance is probably by an autosomal recessive gene. The prognosis in the more severe form of the disorder is poor.

Subclinical entrapment of the lateral femoral cutaneous nerve: an autopsy study.

Five out of 12 lateral femoral cutaneous nerves, removed at routine autopsies, showed pathologic changes in myelinated nerve fibers in the vicinity of the inguinal ligament. These changes included both local demyelination and Wallerian degeneration, particularly affecting the fibers with the largest diameters. The presence of polarized internodal swellings on single nerve fibers from two specimens suggested that mechanical factors were involved in pathogenesis. Endoneurial vascular thickening confined to the region of the inguinal ligament was also seen and may be implicated in the production of some of the symptoms of meralgia paresthetica (MP).

Remyelination in the spinal cord of the cat following intraspinal injections of lysolecithin.

Intraspinal injections of small volumes of lysolecithin were made in the cat. These produced a local area of primary demyelination at the site of injection and all the demyelinated axons were subsequently remyelinated either by oligodendrocytes or Schwann cells. In general the type of remyelination depended on the position of the axon relative to the point of injection; those near the centre of the lesion were remyelinated by Schwann cells while those at the edges were remyelinated by oligodendrocytes. At the very centre of the lesion there was fairly extensive axonal degeneration. Oligodendrocyte-remyelinated axons were enclosed within astrocyte processes which were usually covered by basement membrane on the surface next to Schwann cells. The pattern of remyelination in the cat was compared with similar lesions in the rat and it was concluded that the more vigorous astrocytic response in the cat was responsible for the differences observed in the lesions in the 2 species.

Pathological changes in the optic chiasm of the cat following local injection of diphtheria toxin.

The optic chiasm in 14 cats was injected stereotactically with small amounts of diphtheria toxin and the morphological changes were examined by light and electron microscopy. Phagocytosis was already well-marked at 3 hr after injection and massive at 1 week. Intercellular oedema was extensive in the first week and, though diminished, was still present after 1 month. The oedema was most marked in the subendothelial regions in the early stages but was found among the nerve fibres and glial processes in those animals which survived for longer periods. Demyelination and Wallerian-type degeneration were established at 3 hr after injection and both processes continued up to 2 months and beyond. Scarring and an absolute loss of nerve fibres were present in the longer-surviving animals. Unequivocal evidence of remyelination was not obtained.