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Pituitary tuberculomas, mimicking adenomas are very unusual. We describe a rare case of a patient with an exclusively intrasellar mass, and who presented with severe headaches and loss of libido. The lesion was approached trans-sphenoidally and pathological examination revealed a tuberculoma. Complete removal was achieved and the patient followed on anti-tuberculous therapy.

PURPOSE: We sought to document the appearance of isolated cysticercal infestation of single extraocular muscles on MR and CT studies, and to compare these findings with results of histopathologic examination. METHODS: Six MR and three CT examinations of the orbits of six patients were reviewed. Histopathologic confirmation of the diagnosis was available in three patients, and response to specific medical therapy was available in one. In all, the imaging findings were considered highly suggestive of cysticercal infestation. RESULTS: Typically, the affected extraocular muscle showed fusiform enlargement of its belly and contained a well-defined, spherical cyst with a nodule attached to its wall. The mural nodule was identified in all six cases with varying degrees of visibility. It was best seen on the CT examinations and in all cases in which contrast material had been administered. The nodule and the enlarged muscle showed intense enhancement on the contrast-enhanced studies. Imaging studies of the brain showed no evidence of cerebral cysticerci in any of the patients. CONCLUSION: The MR and CT appearance of isolated infestation of single extraocular muscles by the larva of the pork tapeworm Taenia solium is quite characteristic and often diagnostic of this condition.

A reliable method for identification of the subset of population predisposed to coronary heart disease (CHD) would aid a targetted implementation of intervention strategies. To this end, a mathematical formula was developed based on stepwise linear discriminant analysis. Age, body mass index, the number of associated coronary risk factors and a large number of biochemical markers were analysed by computerised discriminant analysis on a test sample of 203 subjects. Unstandardised canonical discriminant coefficients of statistically significant independent variables were used to derive the total discriminant score or the 'risk score'. The 'low-risk' persons not in need of immediate preventive measures of CHD could be distinguished from the 'high-risk' individuals with an almost 90% correctness. As compared with the existing methods such as clinical evaluation and cardiac stress test, the risk scores derived by the new method, and based chiefly on blood markers besides clinical and anthropometric variables, appeared to correctly predict the future coronary episodes in members of the test sample selected at random. The risk scores were also tested on a new sample of 50 subjects; while low scores were not associated with CHD, high scores in some patients were associated with myocardial ischemia. It appears that the preventive measures of CHD may be directed at people who have no clinical manifestations of CHD, but whose risk scores are greater than 0.1. On the other hand, if the score is less than -1.0, immediate preventive measures may not be necessary. If the score is between -1.0 and 0.1 (borderline), no immediate action may be taken but the score may be determined after six months, and action taken accordingly.

The mechanisms and the changes described herein typically begin with a dense basal meningeal exudate often resulting from a "Rich focus" along the basal surface of the cerebrum or ventricular ependyma. In the interpeduncular fossa, when the exudate is copious, among other structures the proximal parts of the optic nerves and of the internal carotid arteries are seen surrounded and compressed by the exudate. This exudate is made up of small and large mononuclear cells, including epithelioid cells, which also act as macrophages and may fuse to form Langhans' giant cells. Further extension of this exudate along small proliferating blood vessels into the brain substance constitutes a border zone encephalitis with the development of focal and diffuse ischemic brain changes due to vasculitis. Entrapment and occasional arteritic occlusion of larger arteries, such as the middle cerebral in the Sylvian fissures, results in infarction. Blockage of the basal subarachnoid cisterns around the midbrain and pons by the dense basal exudate or narrowing of aqueduct and third ventricle by a small tuberculoma causes consequent hydrocephalus. Development of many or one large focal granuloma (i.e., tuberculoma) occurs in the cerebrum, cerebellum, and/or brain stem. Similar pathogenetic mechanisms produce tuberculous spinal meningitis myeloradiculopathy that may be secondary to or occur before cranial tuberculous meningitis. More extensive damage to the white matter may occur together with the infrequent onset of perivascular demyelination on the basis of a hypersensitivity reaction to tuberculoprotein (i.e., "allergic tuberculous encephalopathy"). Finally, there may be a part played by NO in the production of the vascular and perivascular inflammatory central nervous system changes and a role for the the potential beneficial action of corticosteroids, especially in cases of tuberculous encephalopathy.

Light and electronmicroscopic changes in lung biopsies were studied in six patients with tropical pulmonary eosinophilia, aged 20 to 37 years, of varying duration, and with severe haematologic (blood eosinophil count of 3,600 to 18,200 per mm3), and respiratory changes. On light microscopy the main pathologic reaction consisted of large mononuclear cells and eosinophils in and around the alveoli and blood vessels, and proliferated reticulin. Fine structural changes probably being described for the first time, included the presence of many alveolar macrophages characterised by abundant cytoplasm, irregular or stunted microvilli, increased phagolysosomes with ingested debris, and depletion of other organelles. Eosinophils bearing typical old and young granules, were encountered in and around the alveoli and blood vessels in all case, and collagenosis around alveolar cells in a few. Subacute pneumonitis producing compression and disorganisation of alveoli and blood vessels, and lack of normal apposition of air and blood spaces, appear responsible for the respiratory disability. The detection of mycobacteria, cocci or chlamydia-like bodies in two specimens and of intranuclear virus-like particles in another, could either indicate secondary infection or have an immunogenic significance, in the absence of detection of filarial elements in any of the specimens. Lung biopsies from two additional patients (aged 1332) who had mitral stenosis probably due to rheumatic heart disease, and secondary pulmonary hypertension, were studied as "control" specimens. Both at light and electronmicroscopy these specimens did not show any eosinophils or neutrophils, and fewer macrophages in the lung parenchyma. In contrast to tropical eosinophilia and, as expected, there was considerably more fibrosis of the lung parenchyma, especially in the alveolar subepithelial region and in the vessel walls. This, together with fibroblasts full of endoplasmic cisterns, noted particularly in the younger patient with shorter duration, probably represented an earlier change in this condition.

The anorectic compound fenfluramine hydrochloride was injected into young Holtzman strain rats (from days 6 to 40 of life), at the dose of 75 mg/kg body weight. Intralysosomal lamellar bodies (LBs) were seen in the endothelial cells, pericytes, the perivascular astrocyte processes and occasionally in the lumen. The pathology of myelinated fibres varied from thinning of myelin to complete demyelination and, at times, presence of dense bodies in the axons, the changes perhaps being a result of the oligodendroglia damage. A small group of adult mice was administered three oral doses each of Ponderax equivalent to 5 mg of fenfluramine. The brain stem and cerebellar neurons of these mice showed abnormal dark cytoplasm, without lamellar bodies. Even in this short-term experiment, there was formation of a few LBs in the neuropil, the prominence of dark glial cells, probably oligodendroglia, and some perivascular intracytoplasmic oedema. The earliest detection of dense bodies in the undistended astrocyte processes before they were observed in the cell perikarya, both in the younger rats and the adult mice, suggested the perivascular astrocyte to be the first CNS constituent to come in contact with the toxic agent as it passes the blood-brain barrier. On the basis of our observations, it also appears that the 'myelinosomes' or lamellar phagolysosomes developing due to failure of degradation of drug-phospholipid interaction product, accumulate in different cells of the CNS.

1. The B-vitamin status of fifty-nine patients, mainly from the lower socio-economic classes in Bombay, with a history of chronic malnutrition, and of alcoholism of 1·5–20 years’ duration, was studied before and during treatment, and in relation to their clinical, especially neurological, condition. These patients were divided into two neurological categories: (1) those with peripheral neuropathy (mainly sensory and distal) alone, (2) those with mental changes (mainly confusion and disorientation) also. Both categories frequently showed pellagrous pigmentation and mucocutaneous signs of B-vitamin deficiency.2. Thiamin and erythrocyte transketolase (EC2.2.1.1) activity, riboflavin, nicotinic acid, pantothenic acid, total and pyridoxal fraction of vitamin B6, folate and total vitamin B12were estimated in the blood and the cerebrospinal fluid (CSF) of these patients, and also in the blood of sixty-nine control subjects and in the CSF of some of them. The concentrations of all the vitamins, except vitamin B12, were highly significantly lower in the blood of patients of category 1 compared to the controls, and erythrocyte transketolase activity and pyridoxal concentration in patients of category 2 were significantly lower than those of category 1 patients. Blood pantothenic acid and folate concentrations were reduced less consistently.3. Serum vitamin B12concentration was significantly increased (though within normal range) in the patients compared to the control group, probably because of the moderate hepatic insufficiency (as assessed by liver function tests) in the former.4. The concentrations of thiamin, riboflavin, nicotinic acid and total vitamin B6were also highly significantly lower in the CSF in patients of category 1 compared with controls. Furthermore, thiamin, nicotinic acid and total vitamin B6concentrations were significantly lower in patients of category 2 than those of category 1 patients, indicating that CSF levels reflect better the neurological status of these patients.5. There was a moderate increase in the blood concentration of all the vitamins tested, after a relatively poor hospital diet alone. There was a concurrent increase in the blood levels of thiamin, riboflavin, nicotinic acid and pantothenic acid after parenteral treatment with either thiamin or nicotinic acid. The administration of pyridoxine resulted in a significant increase in the blood levels of riboflavin and the pyridoxal fraction of vitamin B6.

A very brief review of the literature on the clinicopathological aspects of leprosy is given; mainly through references. The salient features of the two main types of leprosy — tuberculoid and lepromatous — are presented in a Table. The surgical and pathological findings are briefly described and the pathogenesis of involvement of the facial nerve (a motor nerve) is discussed. On the basis of (i) the severe histopathologic changes (degeneration) of the most distal part of the zygomatic branch of the facial nerve (innervating the orbicularis oculi), with sparing of the roots of all branches and the trunk of the nerve; (ii) the concurrent loss of cutaneous sensations in the territory of the maxillary division of the trigeminal nerve (the region of the zygoma and the lower eyelid); and (iii) the close approximation or even anastomoses occurring between the ultimate branches of these two nerves, it is postulated that paralysis of orbicularis oculi occurs secondarily to the sensory nerve damage, i.e. due to spread of infection from the sensory branches of the trigeminal to the motor branches of the facial nerve. The surgical and pathological findings of the nerves in the arm, especially the ulnar and the median and their branches are described, in tuberculoid and lepromatous leprosy. The forms of nerve degeneration, the occasional axon regeneration, and the role of the Schwann cell in harbouring the bacilli, are illustrated. The lysosomal enzyme activity in the Schwann cells of nerve fibres, particularly of unmyelinated fibres which preferentially phagocytose the M. leprae, and their role, albeit not very successful, in degrading the bacilli and controlling the infection, are also stressed, through light and electronmicrographs. The constellation of secondary factors of the terrain operating to produce further damage to primarily diseased nerves, is discussed. These factors include indirect compression from unyielding fibroosseous tissues, minor traumata, stretching of the nerves, and their exposure to lower temperatures in subcutaneous tissues.

A case of rabies was treated with intensive medical support. This led to a prolongation of life to 25 days. The neurologic progression of the disease was monitored clinically and with serial EEG. This prolonged course enabled us to witness and manage a wide variety of unusual complications including the adult respiratory distress syndrome, hypothermia, myocarditis, and diabetes insipidus. This report documents the clinical features, diagnostic problems, complications, and management.

The pathology of an unusual intracranial neuroectodermal tumour of the neuron series in described and its possible histogenesis discussed. The tumour, in a child aged 5 years with an enlarged head since infancy, presented as a large solid intra-cerebral mass. Histological examination showed four types of cells; (i) the stroma, forming the bulk of the tumour, was astrocytomatous; (ii) lobules of ill defined cells bearing small circular nuclei, representing immature neuroblasts: (iii) the same of other lobules containing neurons in various stages of development; and (iv) dense clusters of cells with hyperchromatic nuclei attempting rosettes, representing an overtly malignant neuroblastoma. This tumour was designated "ganglioglio-neuroblastoma" and probably originated from a slow growing ganglioglioma.

The clinical features in a 42 year old man with malignant atrophic papulosis with CNS involvement are described. They included mental dysfunction, paraesthesiae, weakness of left limbs, with pyramidal tract signs, bilateral ptosis, progressing to total ophthalmoplegia and obtundation. There were two crops of characteristic papular lesions on trunk and limbs, with terminal evidence of a coagulopathy and bruises, resulting in death in six months. Papular biopsy revealed multiple microinfarcts in the dermal collagen. The brain showed multiple small haemorrhagic infarcts of both hemispheres, the lower mid-brain, pons and a cerebellar peduncle. Microscopy showed fibrin exudation in the leptomeninges, various stages of thrombosis of small arteries without inflammatory reaction, and corresponding acute and subacute microinfarcts. The pathogenetic basis of the disease appeared to be a combined vasculopathy and coagulopathy.

The clinical, histopathologic and fine structural features of multiple unusual tumours detected in a 20-year-old patient with von Recklinghausen's disease, who died within a year of onset of symptoms of a rapidly expanding intracranial tumour, are described. The tumour was found to involve the falx cerebri, the basal leptomeninges and dura mater, both olfactory and optic nerves, both frontal lobes, the right temporal lobe and middle cerebral peduncle, both middle cerebellar peduncles, and with a metastasis in a cervical node. On light and electron microscopy this tumour appeared to be a fibroblastic meningeal sarcoma with giant cells, mitotic figures, a rich reticulin matrix throughout, and tumour cells full of rough ER but without any glial filaments. Also very unusual was the involvement of both vagus nerves in their cervical and intrathoracic portions, by a schwannomatous benign tumour and with a non-chromaffin paraganglioma at its termination in the oesophagus. One of the few cutaneous "neurofibromas" was also schwannian, containing tumour cells with a basement membrane on electron microscopy. Most, if not all, of these tumours appeared mesenchymal in origin, more aggressive in behaviour and carrying a graver prognosis in von Recklinghausen's disease.

Biological effects of cytochalasin H (CH), a newly isolated mould metabolite, have been found to bring about disaggregation of embryonic cells and to inhibit cytokinesis. Disaggregation is known to be a phenomenon related to the cell surface. (The cells are held together by a mucopolysaccharide glycoprotein complex.) In the present work the fact that the mucopolysaccharide glycoprotein surface coat gets affected by CH treatment is confirmed by electron microscopy with the help of Lanthanum, a specific marker, which gets selectively absorbed to the cell surface material and renders it electron dense. The ultrastructural observations indicated the reduction of the cell surface material in treated embryos as compared to the controls. The reappearance of lanthanum-bound cell surface material in the recovered embryos was also observed. However, the exact mechanism of the action of CH on the cell surface remains to be clarified.

Nine patients with characteristic changes of Eales' disease in the eye in whom there was neurological involvement, have been described. The characteristic neurological picture comprised an acute or subacute myelopathy occurring at an interval of a few weeks to a few years after the eye episode; in only 1 patient was there cerebral involvement without any evidence of myelopathy. Besides the involvement of spinal cord at the dorsal level in the 8 patients, there was evidence of additional lesions in the brain stem in 1 patient and in the cervical cord in another.

The term meningocele is used in this communication to include all lesions presenting as swellings associated with spina bifida, when neural tissue is not exposed on the surface. 144 meningoceles were operated on during an 18-year period. The stalk of the meningocele was connected with the neural tissue in 113 of them. Two distinct types of lesions have been noted in these patients and have been designated "meningocele with tethered cord" (52) and "meningocele with tethered roots" (56). In both conditions about half the number of cases presented clinically before the age of 3 months, when paraplegia was evident in only 5 of the 26 infants with tethered cord and 3 of the 25 with tethered roots. In contrast, all or the majority of babies reporting after the age of one year, had paraplegia. Hence, a case is made out for an early operation in all these patients. At surgery the main lesion was a fatty mass in 29 babies with tethered cord, and a cystic mass in 30 with tethered roots. While hydrocephalus was virtually absent in these babies, there were 5 others who manifested obstructive hydrocephalus with meningocele. "Meningomyelocele", the commonest lesion associated with spina bifida, presents with an exposed spinal cord at birth, is associated with communicating hydrocephalus, and can be clearly distinguished from the meningocele.

Pathological features are described, and clinico-pathological correlations are made, in 11 patients presenting the unusual combination of chronic compressive myelopathy of the upper cervical cord due to congenital atlanto-axial dislocation, and sudden haematomyelia and respiratory arrest developing at open surgery for release of pressure on the medullospinal tissues, or as a postoperative catstrophe. Necropsy and histological examination confirmed that the neuropathological substrate of intermittent or progressive quadriplegia and sensory changes (mainly deep sensory loss) was degeneration of the lateral and posterior columns. Loss of anterior horn cells of the lower cervical and upper dorsal cord led to weakness of hand and arm muscles. Acute paracentral haemorrhages occurring at the C1 to C2 or medullospinal level, in the territory of distribution of the sulcal branches of the spinal artery (due to sudden release of pressure at operation) were responsible for postoperative paralysis and sensory loss below C2 segment. In terms of the bony anomaly (dissected at necropsy), the cases fell into 2 sibgroups: a) The majority with the odontoid attached to the body of the axis, but short and ill developed, at times accompanied by other bony anomalies and a poorly formed transverse ligament. This tended to produce a fixed type of dislocation with a higher level (medullospinal) and more severe compression of the CNS. b) Fewer cases with a well formed but detached odontoid, producing a less severe myelopathy at a lower level (C1-C2), and generally more readily reducible on extension.

Eleven cases of Wilms' tumour received at Banglore Medical College, Bangalore are being studied focussing on the histopathological appearance of these tumours. One case exhibiting neuronal and glial differentiation, which is a rare observation, was noticed and is reported. The clinicopathological features and a brief review of literature are being presented.

Fine structural changes are described in 21 muscle biopsy specimens from patients with early and established tuberculoid or treated and untreated lepromatous leprosy. The predominant light microscopic finding on paraffin sections of atrophy of the muscle fiber was confirmed in semithin araldite sections, which also revealed considerable degenerative changes in a few or more fibers. These were more clearly seen in ultrathin sections, especially in the lepromatous muscle specimens. The degeneration was in the form of severe loss or disorganization of the myofibrillar elements and in the most affected muscle fiber, a loss of all sarcoplasmic constituents, with occasional accumulation of lipofuscin in lysosome-like bodies. Only 3 of the lepromatous specimens showed 1 and 2 bacilli each, only 1 being within a muscle fiber. There were also mural changes in the small intramuscular blood vessels with proliferation of their basement membrane and pericytes. The mean serum IgG level in lepromatous patients was significantly elevated. This, together with the vascular change, might perhaps be responsible for the degenerative change in the muscle fiber despite a paucity of M. leprae in the muscle.

In view of the persisting high prevalence (though somewhat reduced compared to 20 years ago) of various forms of neurotuberculosis , especially in economically underpriviledged and undernourished urban paediatric populations of the world, some aspects of the neuropathology relevant to neurosurgeons, are briefly presented and discussed. The most conspicuous of these is the development of brain tuberculomas, which act as both space-occupying and inflammatory masses that result in severe oedema or direct destruction of brain parenchyma. The cellular reaction in the border zone of these tuberculomas is identical to that in tuberculous meningitis and consists of specialized large mononuclear cells-the epitheloid cells-which undertake a phagocytic function and also fuse with one another to form giant cells, as seen by both light and electron microscopy. These cells together with others like lymphocytes and plasma cells, also infiltrate the walls of small blood vessels, constituting vasculitis, and these vessels may undergo necrosis, in both the intracranial (mainly basal) and spinal leptomeningeal exudate. The latter is more frequent in young adults than in children, and may be the primary event in the CNS or secondary to extension downwards of the basal meningitis. The quantity and nature of the spinal exudate vary in duration and severity, the more common being extensively "tubular" and subacute, producing radiculopathy and myelopathy by compression of these structures, and rarely infiltration. The damage to the cord, mainly the white matter, occurs through oedema and ischaemia, rather than frank infarction, the larger arteries being rarely involved.(ABSTRACT TRUNCATED AT 250 WORDS)

Detailed neuropathologic examination was carried out on 1 case of Eales' disease with CNS involvement, in the form of retinal vasculopathy, followed first by signs of brain stem and cerebellar disease and then by a myelopathy, with death 4 years later from retinal infection. There was mild chronic inflammation in the retina, and sub-total demyelination of one optic nerve. The brain stem and cerebellum showed extensive vasculopathy, with various stages of venous change extending from proliferation and dilatation to haemorrhage, or to thickening with hyalinisation. The perivenular brain tissue, particularly of the cerebellum, often showed demyelination, with relative axon preservation, but no inflammation. Similar, but less pronounced venopathy was seen in the dorsal cord. There was ascending degeneration of Goll's columns and descending degeneration of the lateral columns.

Five patients presenting clinically with a form B12-deficiency neuromyelopathy, with cord involvement in all and proximal muscle weakness in two of them, were investigated for their neurologic, hematologic and vitamin status. Megaloblastosis and achlorhydria were present in all, and impaired absorption of 57Co vitamin B12 and of D-xylose was detected in four. Total cyanide extracted vitamin B12 (A) was lowered in all cases and noncyanide extractable (B) in four of the five, being zero in three. All five responded to injections of hydroxocobalamin. In two patients sequential estimations showed that both A and B, especially the latter, rose steeply initially, normalizing at 50% of A after some weeks. Moiety B is suggested to be physiologically the more active and dissociable form of vitamin B12. Markedly elevated initial serum folate levels, and their subsequent fall under treatment with B12, indicated the operation of the "methyltetrahydrofolate trap". Blood levels of thiamin, nicotinic acid and pantothenic acid were within normal limits. However, serum riboflavin (B2) total vitamin B6 and pyridoxal were reduced in all where tested. Vitamin B6 deficiency could have resulted from its own malabsorption and have contributed to be B12 deficiency. Vitamin B2 and B6 levels also corrected themselves on B12 therapy. The B-vitamin deficiencies in our patients probably resulted from intestinal malabsorption, with a possible factor of malnutrition consequent to their strictly vegetarian diet.

1. The B-vitamin status of fifty-nine patients, mainly from the lower socio-economic classes in Bombay, with a history of chronic malnutrition, and of alcoholism of 1-5-20 years' duration, was studied before and during treatment, and in relation to their clinical, especially neurological, condition. These patients were divided into two neurological categories: (I) those with peripheral neuropathy (mainly sensory and distal) alone, (2) those with mental changes (mainly confusion and disorientation) also. Both categories frequently showed pellagrous pigmentation and mucocutaneous signs of B-vitamin deficiency. 2. Thiamin and erythrocyte transketolase (EC 2.2.1.1) activity, riboflavin, nicotinic acid, pantothenic acid, total and pyridoxal fraction of vitamin B6, folate and total vitamin B12 were estimated in the blood and the cerebrospinal fluid (CSF) of these patients, and also in the blood of sixty-nine control subjects and in the CSF of some of them. The concentrations of all the vitamins, except vitamin B12, were highly significantly lower in the blood of patients of category I compared to the controls, and erythrocyte transketolase activity and pyridoxal concentration in patients of category 2 were significantly lower than those of category I patients. Blood pantothenic acid and folate concentrations were reduced less consistently. 3. Serum vitamin B12 concentration was significantly increased (though within normal range) in the patients compared to the control group, probably because of the moderate hepatic insufficiency (as assessed by liver function tests) in the former. 4. The concentrations of thiamin, riboflavin, nicotinic acid and total vitamin B6 were also highly significantly lower in the CSF in patients of category I compared with controls. Furthermore, thiamin, nicotinic acid and total vitamin B6 concentrations were significantly lower in patients of category 2 than those of category I patients, indicating that CSF levels reflect better the neurological status of these patients. 5. There was a moderate increase in the blood concentration of all the vitamins tested, after a relatively poor hospital diet alone. There was a concurrent increase in the blood levels of thiamin, riboflavin, nicotinic acid and pantothenic acid after parenteral treatment with either thiamin or nicotinic acid. The administration of pyridoxine resulted in a significant increase in the blood levels of riboflavin and the pyridoxal fraction of vitamin B6.

A brief account is given of some aspects of Wilson's disease in India, studied during the periods 1959 to 1967 and 1970 to 1978, with emphasis on disordered parameters of copper metabolism. Among the latter, serum copper oxidase (representing caeruloplasmin) was found to be the most constant laboratory evidence of Wilson's disease. It wad drastically lowered in all patients in both periods (25 and 44 patients respectively), when compared to its level in the parents and siblings of the patients, in other neurological patients and in normal subjects serving as controls. The other constantly involved parameter was direct-reacting serum copper which was highly significantly elevated in the patients compared to the other groups. Most of the patients presented with a predominantly neurological form of the disease, smaller groups presenting with predominantly osseomuscular or hepatic forms. The mean age of patients in both periods was approximately 13 years.

The fine structure of cells of the mononuclear phagocyte series (MPS) and a few other cells with phagocytic capacity, has been critically evaluated, mainly from an electronmicroscopic examination of the reactive border zone of 11 human brain tuberculomas, which provide ideal material for the study of macrophages. Most of them appeared to be blood monocyte-derived epithelioid cells of various forms and stages. The cytoplasm of these cells showed either more rough ER representing protein synthesising activity; or more frequently, phagosomes, phagolysosomes, dense bodies or empty vacuoles, representing various stages of ingestion and digestion of necrotic material. Often such material, which was more or less osmiophilic, was seen abundantly between the cells. These actively phagocytic cells occasionally undergoing, mitosis, are referred to as "epithelioid macrophages" and were morphologically similar to the "activated microglia" described in other conditions. They also showed a tendency to be closely adjacent to each other and occasionally fuse to form giant cells. There were also a number of lymphocytes and plasma cells. The latter showed various stages of active and granular or depleted and distended rough ER tubules, phagocytic activity and tendency to fuse. Expected vasculitis and small vessel necrosis formed part of this granulomatous reaction. Constituents of oedematous or necrosed brain tissue were seen immediately around the reactive zone of these tuberculomas, the most frequent being reactive astrocytes, many of which showed membrane-bound vacuoles. It is conceivable that the excessive pleomorphic cellular, vascular and necrotic reaction in these brain tuberculomas could have resulted from a delayed type of hypersensitivity to a very small quentity of antigenic tuberculoprotein, which probably initiates the chain of immunologic responses.

A brief illustrated account is presented of the light microscopic pathology, histochemistry of lysosomal enzymes, and fine structural changes in the nerves of patients with untreated or treated lepromatous leprosy. Predominant bacillation of the Schwann cells of unmyelinated fibres, degeneration of their axons, prominence of phagolysosomes, and disappearance of these cells with endoneurial collagenosis were observed on electronmicroscopic examination of the index branch of the radial cutaneous nerve. Although there were changes in the blood vessels and proliferation of perineurium, bacillation of endothelial or perineurial cells was much less conspicuous. Intact and degenerating forms of M. leprae were found in both treated and untreated patients, fragmenting or crumpled forms being more frequent in the treated. Both groups of patients also showed increased lysosomal enzyme activity, evidenced by single or paired paranodal spots of acid phosphatase and beta-glucuronidase in Schwann cells in histochemical preparations of the nerve. There was lesser activity, and activity in fewer cells, in the case of beta-glucuronidase than of acid phosphatase. Diffuse beta-glucuronidase activity was found in the wall of empty-looking oval chambers in the Schwann cells, and acid-fast bacilli were seen in these chambers. In teased fibre preparations, both axonal degeneration and segmental demyelination were found. In semi-thin araldite sections, the myelinated fibre density was either preserved or reduced; large diameter fibres were more frequently depleted, with tall peaks of smaller fibres seen on plotting diameter spectra.