bluuebunny/crossref_metadata_2025 huggingface dataset:
ANTISERA AGAINST GANGLIOSIDE GM2: IMMUNOCHEMICAL AND IMMUNOHISTOLOGICAL STUDIES
Authors: SCHWERER BEATRIX , LASSMANN H. , BERNHEIMER H.
Published: May 2008

Schwerer B., Lassman H. & Bernheimer H. (1982) Neuropathology and Applied Neurobiology 8, 217–226

Antisera against ganglioside GM2: immunochemical and immunohistological studies

Antisera against ganglioside GM2 were raised in rabbits and tested by immunodiffusion, complement fixation and immunohistology. The presence of precipitating antibodies was demonstrated by immunodiffusion techniques (Ouchterlony and reversed Mancini). GM2‐antibody titres were determined by a quantitative microcomplement fixation assay. The GM2‐antibodies were shown to be specifically directed against GM2 and did not cross‐react with the major brain gangliosides. Application of GM2‐antiserum to brain sections from a case of GM2‐gangliosidosis (Sandhoff s disease) in an immunofluorescence study produced a specific fluorescence of the granular GM2‐storage material within the cytoplasm of cortical neurons. With immunoperoxidase staining by electron microscopy, labelling of the surface of the membraneous cytoplasmic bodies was obtained.
THE EFFECT OF X‐RADIATION GIVEN AFTER NEONATAL ADMINISTRATION OF ETHYL NITROSOUREA ON INCIDENCE OF INDUCED NERVOUS SYSTEM TUMOURS
Authors: KNOWLES J. F.
Published: May 2008

Knowles J.F. 1982 Neuropathology and Applied Neurobiology 7, 265–276

The effect of X‐radiation given after neonatal administration of ethyl nitrosourea on incidence of induced nervous system tumours

Neonatal rats were injected with neurocarcinogenic amounts of ethyl nitrosourea (ENU) and whole‐body X‐irradiated 24 h later. An absorbed radiation dose of 1–25 Gy caused a statistically significant decrease in the incidence of nervous system tumours induced by ENU (10 mg/kg). Absorbed doses of 0–2 Gy or 1–25 Gy given after ENU (4 mg/kg) also reduced their incidence, but not significantly so. The X‐irradiation did not affect the range of histological appearances amongst the tumours but malignant schwannomas, particularly those of the trigeminal nerve, were significantly reduced by 1–25 Gy given after ENU (10 mg/kg). The mean latency for clinical signs of tumour appearance was not affected by radiation. A small number of nervous system tumours occurred in rats given neonatal X‐radiation only and it seems highly likely that these were radiation‐induced.
GLIAL CELL RESPONSES IN THE ADULT RABBIT DORSAL MOTOR VAGAL NUCLEUS DURING AXON REACTION
Authors: ALDSKOGIUS HÅKAN
Published: May 2008

Aldskogius H.1982 Neuropathology and Applied Neurobiology 8, 341–349

Glial cell responses in the adult rabbit dorsal motor vagal nucleus during axon reaction

Following transection of the vagal nerve on the neck, a dramatic loss of neurons occurs in the dorsal motor vagal nucleus (DMV) of the adult rabbit. The present study describes the light and electron microscopical characteristics of the accompanying glial cell response. The number of microglial cells was considerably increased a few days after nerve injury and remained at a higher than normal level throughout almost the whole period examined. Astrocytes increased to some extent at a later postoperative stage. Ultrastructurally, microglial cells hypertrophied, surrounded degenerating neurons, and contained a variety of inclusion bodies, some of which appeared to be derived from degenerating neuroplasm. Astrocytes also hypertrophied, displayed numerous filaments and glycogen granules in their cytoplasm as well as a substantial number of heterogenous dense bodies. The findings indicate that the principal features of the glial cell response in the rabbit DMV is similar to previously described glial cell changes in other systems. However, the intensity in the response of astroglial cells in the DMV appears to be greater than usually observed, possibly reflecting the degenerative nature of the nerve cell body response.
THE EFFECT OF MATERNAL AND FETAL THYROIDECTOMY ON FETAL BRAIN DEVELOPMENT IN THE SHEEP
Authors: McINTOSH G. H. , POTTER B. J. , MANO M. T. , HUA C. H. , CRAGG B. G. , HETZEL B. S.
Published: May 2008

The combination of maternal and fetal thyroidectomy was found to have a significant influence on brain development in the fetal sheep at 140 days. There was reduced body weight (36%), brain weight (23%), DNA (26%) and protein (34%) content in five fetuses of ewes, subjected to thyroidectomy six weeks before mating and fetal thyroidectomy at 98 days gestation, compared with six sham operated controls. Cholesterol content was also reduced (36%) and water content increased (2–4%). The cerebellum was most severely affected and showed histologically an increased cell density associated with a significant reduction in the ratio of the molecular to granular cell layer area. The cell density was also significantly increased in the CA1 region of the hippocampus, but not in the CA4 region. It was also increased in the parietal layer of the cerebral cortex but not in the motor region. There was a significant reduction in the weight of heart (28–6%) and lungs (33–4%), while the kidneys and pituitary were enlarged (20–5% and 48–5% respectively) as a result of double thyroidectomy. The combined thyroidectomy was similar to iodine deficiency in its effect on fetal brain development, indicating that it is probable that iodine deficiency has its effects in the sheep by a combination of maternal and fetal hypothyroidism.
EARLY CHANGES IN THE RAT HIPPOCAMPUS FOLLOWING SEIZURES INDUCED BY BICUCULLINE OR L‐ALLYLGLYCINE: A LIGHT AND ELECTRON MICROSCOPE STUDY
Authors: EVANS MARY , GRIFFITHS T. , MELDRUM B.
Published: May 2008

Evans M, Griffiths T & Meldrum B (1983) Neuropathology and Applied Neurobiology 9, 39–52

Early changes in the rat hippocampus following seizures induced by bicuculline or L‐allylglycine: a light and electron microscope study

Status epilepticus was induced in thirteen paralysed and ventilated rats by the injection of either bicuculline or L‐allylglycine. After 1–2 h of seizure activity the animals were intracardially perfused with a 2% glutaralde‐hyde/3% paraformaldehyde solution. Hippocampal blocks from each rat were processed for light and electron microscopy. The effects of L‐allylglycine were more severe than those of bicuculline. Changes include perivascular and perineuronal swelling of astrocytic processes, and neuronal alterations which were graded as follows: Grade I (least severe), neuronal cytoplasm appears slightly darker than usual; Grade II, condensed or dark neurons, usually with microvacuoles; and Grade III classical ‘ischaemic cell change’—the cytoplasm and karyoplasm is dark and shrunken, with or without microvacuoles. Many of the microvacuoles originate from mitochondria. In a few cases swollen and disrupted mitochondria are also seen is distended basal dendrites of the CA3 and CA1 pyramidal neurons. Dentate granule cells appear unaffected. The hippocampal neuronal alterations induced by seizure activity include those of ‘ischaemic cell change’. The pathogenetic factors common to hypoxia/ischaemia and status epilepticus remain to be identified.
A MODEL OF CHRONIC SPINAL CORD COMPRESSION IN THE CAT
Authors: FISH C. J. , BLAKEMORE W. F.
Published: May 2008

Fish C.J. & Blakemore W.F. (1983) Neuropathology and Applied Neurobiology9, 109–120

A model of chronic spinal cord compression in the cat

An experimental method of producing chronic compression of the cat spinal cord is described. A ligature placed around the lumbar spinal cord of 3‐month‐old kittens restricts the growth of the spinal cord to produce compression with a slow onset and an insidious progression. The methods of following the clinical progress of affected animals and of sampling the spinal cord after perfusion fixation are presented. The sampling method used allowed analysis of the three dimensional distribution of the pathological changes caused by the compression. These changes were not symmetrically distributed: the spinal cord caudal to the ligature became swollen and extensive partial demyelination occurred under the ligature and caudal to it, in the swollen region of the cord, whereas cranial to the ligature there was only minimal damage. It is concluded that the method produces a useful model of chronic compression of the spinal cord, which will be of value in studying partial demyelination.
DENERVATION CAUSED BY TULLIDORA(Karwinskia humboldtiana)
Authors: MUNOZ‐MARTINEZ E. J. , CUEVA J. , JOSEPH‐NATHAN P.
Published: May 2008

Munoz‐Martinez, E. J., Cueva J. & Joseph‐Nathan P. (1983) Neuropathology and Applied Neurobiology 9, 121–134

Denervation caused by tullidora (Karwinskia humboldtiana)

Crude homogenate of the seed of the tullidora (Coyotillo, buckthorn; Karwinskia humboldtiana) fruit or a purified neurotoxin extracted from it was administered orally to male Wistar rats. Three to 5 weeks later, gait disturbances and progressive flaccid paralysis of the hindlimbs appeared in these animals which were then submitted to acute experiments. Single twitch and tetanic contractions of the soleus muscle were studied in the tullidora treated rats. The twitch tension elicited by direct stimulation of the muscle was greater than that produced by nerve stimulation. In addition, the tension of nerve‐elicited twitches diminished as the stimulating electrode was moved towards the spinal cord, suggesting failure of nerve conduction. When the muscle was directly stimulated, contraction and relaxation were slower than normal and the tetanus/twitch tension ratio was subnormal. These data suggest partial denervation of the soleus muscle under the action of the toxin. Electron microscopy revealed abnormal motor‐nerve endings with few synaptic vesicles and denervated end‐plates. Degenerative changes of axons and myelin disturbances were frequently seen in the intramuscular branches of the soleus nerve. However, alterations of this type were less severe in the nerve sections closer to the spinal cord and no significant changes were detected at the upper portion of the sciatic nerve. It is concluded that the paralysis produced by the tullidora toxin is the result of both conduction block of the nerve impulses and muscle denervation.
SPINAL CORD TRANSECTION, CEREBRAL ISCHAEMIC AND BRAIN‐STEM INJURY IN A BABY FOLLOWING A KIELLAND'S FORCEPS ROTATION
Authors: GOULD S. J. , SMITH J. F.
Published: May 2008

A full‐term infant suffered a high cervical cord transection after a Kielland's forceps rotation and extraction. Quadriplegia developed immediately and initial cerebral swelling was followed by atrophy with ventricular dilatation on CT examination. Death occurred at 60 days. At post‐mortem complete necrosis of the cervical cord at C2–C3 with old haemorrhage in the meninges was found, with damage to the inferior corpora quadrigemina, the thalamus, striatum, cerebellar and cerebral cortex. The mechanism is discussed briefly.
SEQUENCE OF MURINE CORONAVIRUS JHM INDUCED NEUROPATHOLOGICAL CHANGES IN RATS
Authors: KOGA M. , WEGE H. , MEULEN V. TER
Published: May 2008

Infection of 21–25‐day‐old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6–12 days pi. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14–30 days pi. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time‐course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10–12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. These observations indicated that SDE was preceded by clinically silent AE lesions.
ASYMMETRIC BUDDING OF VIRUSES IN EPENDYMAL AND CHOROID PLEXUS EPITHELIAL CELLS
Authors: KRISTENSSON K. , LUNDH B. , NORRBY E. , PAYNE L. , ÖRVELL C.
Published: May 2008

Sendai virus injected intracerebrally into %week‐old mice caused infection of ependymal and choroid plexus epithelial cells. Budding of mature viruses occurred only from the apical surfaces of these cells. The viral peplomere proteins, haemagglutinin‐neuraminidase and fusion, were concentrated on the apical portion of the ependymal cells, while the nucleocapsid‐associated polymerase protein was dispersed throughout the cytoplasm. This indicates that intracellular routing of the virus envelope glycoproteins to the cell surface may be one of the factors that determines the site of virus budding. Vesicular stomatitis and vaccinia viruses, on the other hand, budded or egressed predominantly from the baso‐lateral cell surfaces.
KAINIC ACID SEIZURES AND THE REVERSIBILITY OF CALCIUM LOADING IN VULNERABLE NEURONS IN THE HIPPOCAMPUS
Authors: EVANS M. C. , GRIFFITHS T. , MELDRUM B. S.
Published: May 2008

The threshold pathological changes in the rat hippocampus following systemic administration of kainic acid (12–15 mg/kg) have been studied in relation to i the duration of EEG seizure activity and ii calcium accumulation in post‐synaptic neurons, using the oxalate‐pyroantimonate method. The reversibility of the pathological changes and calcium loading has been studied from 40 min to 48 h after the termination of seizure activity. Little or no changes were visible 2–3 h after 12 mg kainic acid per kg, but changes were obvious in most hippocampi directly after 2–3.5 h of seizure activity induced by 15 mg kainic acid per kg. These consisted of generalized swelling of perineuronal and perivascular astrocytic processes, neuronal hyperchromasia and microvacuolation, and swelling of CA1 basal dendrites. ‘Ischaemic cell change’ occurred in a small number of pyramidal neurons. Calcium accumulated in mitochondria of basal dendrites and in the soma of pyramidal neurons in CA1 and CA3. Astrocytic and dendritic swelling and mitochondrial calcium accumulation were rapidly reversed during 40 min of seizure suppression with diazepam. Calcium accumulation in astrocytic processes recovered more slowly (≥4h). After a recovery period of 24–48 h, ischaemic cell changes were seen only in very occasional pyramidal neurons. The pattern of pathological changes is very similar to that seen after L‐allylglycine or bicuculline‐induced seizures. If the dendritic and other changes are a direct consequence of agonist actions at excitatory amino acid receptors (pre‐ or post‐synaptic) then similar actions must be occurring in seizures induced by agents acting primarily on GABAergic inhibition.
A RODENT MODEL OF ORGANOPHOSPHORUS‐INDUCED DELAYED NEUROPATHY: DISTRIBUTION OF CENTRAL (SPINAL CORD) AND PERIPHERAL NERVE DAMAGE
Authors: VERONESI BELLINA
Published: May 2008

Central and peripheral nerve fibre damage has been produced in Long‐Evans hooded male rats with tri‐ortho‐cresyl phosphate. Animals were dosed by gavage with intermittent or daily amounts of the organophos‐phate and examined after 2, 6, 12, 18 and 24 weeks. The distribution of central nervous system (spinal cord) damage and the differential vulnerability among various peripheral nerves supported a ‘dying‐back’ classification for the neuropathy. Giant axonal swellings, containing massive accumulations of smooth endoplasmic reticulum, hallmarked the neuropathy. In spite of severe neurological damage the animals displayed only moderate functional disturbances. These findings have shown that the rat is highly sensitive to the structural damage caused by organo‐phosphates, although resistant to the ataxia.
CARCINOID TUMOUR ARISING IN A RECURRENT INTRADURAL SPINAL TERATOMA
Authors: IRONSIDE J. W. , JEFFERSON A. A. , ROYDS J. A. , TAYLOR C. B. , TIMPERLEY W. R.
Published: May 2008

Carcinoid tumour arising in a recurrent intradural spinal teratoma

We report the case of a recurrent intradural spinal teratoma in a 44‐year‐old woman. Histological examination showed the lesion to be composed entirely of mature elements including an argyrophil carcinoid tumour. Electron microscopy showed the neoplastic cells to possess the ultrastructural features of a foregut type APUDoma. Gamma enolase, a marker of APUD cells, was demonstrated in the neoplasm by the peroxidase‐antiperoxidase technique. This method was also used to demonstrate the presence of cytokeratins in the neoplastic cells and the squamous and columnar epithelia within the teratoma. These results are consistent with the suggestion that APUD cells of foregut type may be of endodermal rather than neuroectodermal origin.
IMMUNOCYTOCHEMICAL LOCALIZATION OF ENKEPHALIN‐LIKE IMMUNOREACTIVITY IN NEURONS OF HUMAN HIPPOCAMPAL FORMATION: EFFECTS OF AGEING AND ALZHEIMER'S DISEASE
Authors: KULMALA H. K.
Published: May 2008

Immunocytochemical localization of enkephalin‐like immunoreactivity in neurons of human hippocampal formation: effects of ageing and Alzheimer's disease

The localization of neurons containing enkephalin‐like immunoreactivity was studied within the human hippocampal formation. It was present in numerous dentate granule cells and a few larger neurons within the dentate molecular layer. In hippocampus proper, numerous pyramidal cells also demonstrated it, especially in field H1 of Rose (1926) and subiculum. No difference attributable to ageing or to dementia of the Alzheimer type was seen in this distribution. Post‐mortem delay was the major factor affecting the intensity of its immunocytochemical localization to hippocampal cells and nonspecific background staining, due to binding of the secondary antiserum, increased directly with this. Some dendrites of dentate granule cells with immunoreactivity were found entering senile (neuritic) plaques in tissue from cases of Alzheimer's disease. These dendrites appeared morphologically normal.
TRANSIENT UNCROSSED CORTICOSPINAL FIBRES IN THE NEWBORN RAT
Authors: KATO T. , HIRANO A. , KATAGIRI T. , SASAKI H.
Published: May 2008

Kato T., Hirano A., Katagiri T. & Sasaki H. (1985) Neuropathology and Applied Neurobiology 11, 171–178

Transient uncrossed corticospinal fibres in the newborn rat

A small number of uncrossed corticospinal fibres were demonstrated in a 1‐day‐old rat by injection of horseradish peroxidase into one hemisphere of the cerebral cortex. These fibres were not demonstrable after the age of 7 days.
CAN THE BB‐RAT HELP TO UNRAVEL DIABETIC NEUROPATHY?
Authors: SIMA A. A. F.
Published: May 2008

A. A. F. Sima (1985) Neuropathology and Applied Neurobiology 11, 253–264

Can the BB‐rat help to unravel diabetic neuropathy?

Diabetic neuropathy is probably the most common and one of the most disabling complications of diabetes mellitus. Although several possible pathogenetic mechanisms for this complication have been suggested, they cannot easily be tested in man. Therefore animal models with induced or spontaneous onset of diabetes mellitus have been used. The spontaneously diabetic BB‐rat may provide a valuable model, since it displays both metabolic, functional and structural abnormalities of peripheral nerve similar to those present in humans. Based on systematic studies of these abnormalities in peripheral nerve in this model, inter‐relationships between diabetic dysmetabolism, dysfunction and structural changes are starting to emerge. These findings are reviewed and a scheme of proven and proposed correlations which now can be tested in this animal model is presented.
ADENOID CYSTIC CARCINOMA PRESENTING AS INTRACRANIAL TUMOUR
Authors: McLELLAN D. R. , ADAMS J. H.
Published: May 2008

McLellan D. R. & Adams J. H. (1985) Neuropathology and Applied Neurobiology 11, 309–315.

Adenoid cystic carcinoma presenting as intracranial tumour

Two women are described in whom adenoid cystic carcinoma of upper respiratory tract origin presented as a large intracranial tumour with involvement of cranial nerves. Smears of the neurosurgical biopsies were distinguished by abundant metachromatic mucin.
SIMULTANEOUS EXPRESSION OF GLIAL FIBRILLARY ACIDIC (GFA) PROTEIN AND NEURON‐SPECIFIC ENOLASE (NSE) BY THE SAME REACTIVE OR NEOPLASTIC ASTROCYTES
Authors: VINORES S. A. , RUBINSTEIN L. J.
Published: May 2008

Vinores S. A. & Rubinstein L. J. (1985) Neuropathology and Applied Neurobiology 11, 349–359

Simultaneous expression of glial fibrillary acidic (GFA) protein and neuron‐specific enolase (NSE) by the same reactive or neoplastic astrocytes

In normal cells of the central nervous system (CNS), glial fibrillary acidic (GFA) protein is demonstrable by immunohistochemistry in fibrillated astrocytes, and neuron‐specific enolase (NSE) in neurons and their processes. However, it has been shown that NSE may also be expressed in reactive astrocytes and in various neoplastic cells of non‐neuronal origin, including those of astrocytomas and glioblastomas. In the present study, a double‐labelling technique using immunoperoxidase (PAP) and immunofluorescence (FITC) was employed to determine whether GFA protein and NSE could be expressed simultaneously by the same cell. This was found to be the case in some, but not in all reactive astrocytes in the human brain. In glial tumours, many of the neoplastic cells in the glioblastomas and astrocytomas examined demonstrated either GFA protein or NSE, but usually not both. However, occasional neoplastic cells in those gliomas were found to show both proteins. Because of the relatively low sensitivity of the FITC technique, the percentage of cells expressing both proteins could not be determined, but it is clearly possible for a single reactive or neoplastic astrocyte to demonstrate both GFA protein and NSE.
CONGENITAL AMAUROTIC IDIOCY ‐A PATHOLOGICAL, HISTOCHEMICAL, BIOCHEMICAL AND ULTRASTRUCTURAL STUDY
Authors: HUMPHREYS S. , LAKE B. D. , SCHOLTZ C. L.
Published: May 2008

Humphreys S., Lake B. D. & Scholtz C. L. (1985) Neuropathology and Applied Neurobiology 11, 475–484

Congenital amaurotic idiocy‐a pathological, histochemical biochemical and ultrastructural study

A case of congenital amaurotic idiocy, a subgroup of the neurovisceral lipidoses, is described. This is a rare condition of which only five cases have been reported previously. The brain was small and firm with marked neuronal loss and gliosis. Granular material with histochemical properties of the ceroid‐lipofuscin group of lipopigments was found deposited within astrocytes, macrophages and residual brain stem neurons. Cells of the mononuclear phagocyte system within the liver, spleen, thymus and lungs contained similar material. Ultrastructurally this substance appeared as intracytoplasmic membranous and granular deposits within limiting membranes, and biochemical analysis of formalin‐fixed tissue did not identify a specific material. Comparison is made with the Batten group of disorders.
A MONOCLONAL ANTIBODY TO AMYLOID IN THE BRAINS OF PATIENTS WITH ALZHEIMER'S DISEASE
Authors: ISHII T. , SATO M. , HAGA S. , SHINODA T. , KATO K. , SAITO T.
Published: May 2008

A monoclonal antibody that reacts with the amyloid in senile plaques in the brains of patients with Alzheimer's disease, was produced. The antigen was the crude amyloid protein (DAM, Pras et al. 1968) from the spleen of a patient with primary amyloidosis. The antibody crossreacts with DAM, but does not stain the amyloid of primary amyloidosis in tissue sections. The presence of a common antigenic site or sites in both the amyloid of senile plaques and amyloid of primary amyloidosis which react with this antibody is postulated.
ABNORMAL TUBULAR STRUCTURES ASSOCIATED WITH THE GRANULAR ENDOPLASMIC RETICULUM OF NEOCORTICAL NEURONS IN A BIOPSY FROM A PATIENT WITH ALZHEIMER'S DISEASE
Authors: SLOPER J. J. , BARNARD R. O. , EGLIN R. P. , POWELL T. P. S.
Published: May 2008

The electron microscope has been used to examine a diagnostic biopsy of frontal neocortex which showed the light microscopic features of Alzheimer's disease. In addition to plaques and tangles, the biopsy showed some neurons which contained abnormal tubular profiles specifically associated with their granular endoplasmic reticulum. In transverse section the profiles consisted of two concentric layers of trilaminar unit membrane with an overall diameter of approximately 75 nm and they appeared to lie within the cisternae of granular endoplasmic reticulum. When cut longitudinally, the structures appeared as elongated tubes lying within the endoplasmic reticulum, but a number of ends were found where the inner membrane formed a closed tube and the outer membrane folded back and was continuous with the membrane forming the outer layer of the sac of endoplasmic reticulum. These profiles do not appear to have been described previously although similarities between their ultrastructure and that of the coat of certain unusual forms of Rhabdovirus are noted.
LEPTOMENINGEAL AND ADVENTITIAL GLIOSIS AS A CONSEQUENCE OF CHRONIC INFLAMMATION
Authors: MOORE G. R. WAYNE , RAINE CEDRIC S.
Published: May 2008

Leptomeningeal and adventitial gliosis as a consequence of chronic inflammation

Astroglial cell bodies and processes identified ultrastructurally and immunocytochemically are described within the subarachnoid and Virchow‐Robin spaces of white matter throughout the CNS of Strain 13 guinea‐pigs with chronic relapsing experimental allergic encephalomyelitis. These heterotopic astroglial elements, invariably in close proximity to subpial chronically‐demyelinated lesions, were derived from subpial astrocytes and extended for great distances perpendicular and circumferential to the underlying white matter. Subpial astrocytes overlying adjacent grey matter regions appeared unaffected. This phenomenon is probably a subpial astrocyte response to inflammation and demyelination and may be related to the protection of damaged white matter against subsequent inflammatory events.
CHRONIC HUMAN NERVE COMPRESSION – A HISTOLOGICAL ASSESSMENT
Authors: MACKINNON S. E. , DELLON A. L. , HUDSON A. R. , HUNTER D. A.
Published: May 2008

While compression neuropathy is a common clinical problem, the opportunity to study human nerve material is rare. A histological assessment of the superficial radial nerve of four human cases with entrapment syndrome is reported. Changes in the perineurium and the endoneurial microvessels as well as the presence of Renaut bodies were the earliest histological abnormalities noted. Connective tissue changes included epineurial and perineurial fibrosis. Nerve fibre pathology varied from fascicle to fascicle. The myelinated and unmyelinated fibre populations responded differently to this compression. In the myelinated fibre population, marked thinning of the myelin was noted. In the unmyelinated fibre population, a shift in the fibre histogram due to a new population of very small fibres was observed suggesting degeneration with subsequent regeneration of this fibre population.
A COMPARATIVE STUDY OF MODIFIED BIELSCHOWSKY, BODIAN AND THIOFLAVIN S STAINS ON ALZHEIMER'S NEUROFIBRILLARY TANGLES
Authors: YAMAMOTO T. , HIRANO A.
Published: May 2008

Serial sections of the brains of two cases with Alzheimer's disease were stained with the standard Bodian, modified Bielschowsky (reformed Gros‐Schultze's modification) and thioflavin S methods. The numbers of demonstrated Alzheimer's neurofibrillary tangles (NFTs) were different between the two silver stains: from 15 to 75% more NFTs were shown and more distinctly with the modified Bielschowsky stain than with the Bodian stain. Many of the NFTs in both cases were of eosinophilic and less argentophilic type. Although the NFTs were not counted, the thioflavin S stain seemed to have no apparent advantage over the modified Bielschowsky stain in the demonstration of NFTs.
THE MORPHOLOGY AND MORPHOMETRY OF THE NORMAL HUMAN TIBIALIS ANTERIOR MUSCLE
Authors: HELLIWELL T. R. , COAKLEY J. , SMITH P. E. M. , EDWARDS R. H. T.
Published: May 2008

The light microscopic appearance of the human tibialis anterior muscle is described based on conchotome biopsy specimens from seven healthy volunteers and 20 patients who presented with myalgia but who had no evidence of neuromuscular disease. The morphometric characteristics of these normal muscles are documented and the similarities and differences between the appearances of the tibialis anterior and other muscles discussed.
IMMUNOHISTOCHEMICAL CHARACTERISTICS OF HAEMANGIOPERICYTIC MENINGIOMAS: COMPARISON WITH TYPICAL MENINGIOMAS, HAEMANGIOBLASTOMAS AND HAEMANGIOPERICYTOMAS FROM EXTRACRANIAL SITES
Authors: MOSS T. H.
Published: May 2008

The relationship between malignant vascular meningeal tumours and typical meningiomas remains controversial, despite the need for accurate diagnostic distinction between the two, and some forms of vascular meningioma may be more closely allied to haemangioblastomas or extracranial haemangiopericytomas than to true meningiomas. In order to try to clarify the diagnostic characteristics and origins of the entity known as haemangiopericytic meningioma, 10 histologically typical cases were stained by the immunoperoxidase technique with a panel of seven antibodies. The results were compared with those obtained from typical and angiomatous meningiomas, haemangioblastomas and haemangiopericytomas from extracranial sites. Both the haemangiopericytic meningiomas and the extracranial haemangiopericytomas showed a similar staining pattern, which differed from that of the typical and angiomatous meningiomas in the strikingly focal nature of the vimentin staining and the lack of reactivity with antibodies to epithelial elements. The haemangioblastomas were less consistent in their individual staining characteristics, but had a quite different overall pattern from all the other tumour types. It is, therefore, suggested that so‐called haemangiopericytic meningiomas are in fact primary haemangiopericytomas of the meninges, antigenically distinct from true meningiomas and displaying a malignant potential appropriate to haemangiopericytomas arising in any other sites.
CONGO RED BIREFRINGENT STRUCTURES IN THE HYPOTHALAMUS IN SENILE DEMENTIA OF THE ALZHEIMER TYPE
Authors: SIMPSON J. , YATES C. M. , WATTS A. G. , FINK G.
Published: May 2008

Congo red birefringent structures in the hypothalamus in senile dementia of the Alzheimer type

Serial cryostat sections of hypothalamus from four cases of Alzheimer‐type dementia and four controls were stained with Congo red and examined for birefringence. Green birefringence and dichroism was associated with (a) neurofibrillary tangles, which were most numerous at the level of the tuberomammillary nucleus where they were found in large acetylcho‐linesterase‐positive neurons; (b) neuropil processes within tangle fields; (c) a few plaque cores in the mammillary body; (d) spicules at the ependyma of the third ventricle, and (e) blood vessels. Birefringence (e) had different properties from (a) to (d) and was considered to be due to collagen. The ependymal spicules did not react with an antibody which recognized the tangles and neuropil processes. Each Alzheimer case had many more tangles than the control cases. Birefringence in (b)‐(d) tended to be greater in the Alzheimer than in the control cases. This study confirms previous reports of large numbers of tangles in circumscribed areas of caudal hypothalamus in Alzheimer‐type dementia and demonstrates that Congo red staining reveals abnormalities in hypothalamic structures (neuropil processes and ependyma) not demonstrated by other staining techniques.
SEQUENTIAL STUDIES OF A CHILDHOOD MYOPATHY: A CLINICAL, HISTOCHEMICAL AND MORPHOMETRIC INVESTIGATION
Authors: MAHON M. , KRISTMUNDSDOTTIR F. , CUMMING W. J. K. , NORONHA M. J.
Published: May 2008

Sequential studies of a childhood myopathy: a clinical, histochemical and morphometric investigation

An unusual inherited progressive distal myopathy of early childhood onset is described in two sisters from a consanguineous Asian family. Motor milestones were normal but gait deteriorated slowly thereafter with development of generalized hypotonia and muscle weakness particularly in the wrist extensors and hand muscles.

Muscle biopsies obtained at the ages of 6 and 10 years respectively (Case 1) showed significant differences. At 6 years muscle morphology and histochemical appearance were normal although type I fibres predominated (79%) and a substantial pool of ‘undifferentiated’ fibres (12%) was present. By 10 years there was a significant reduction in type I fibres (‐13%) and in ‘undifferentiated’ fibres (‐10%) with a concomitant increase in type II fibres (+ 23%). Fibre size and shape were normal at the age of 6 years but no further fibre growth was evident 4 years later. The older sister (Case 2, age 13 years) was similarly affected.

The possibility of this progressive myopathy being caused by loss of neural control at two separate stages of development is discussed. The importance of performing sequential morphometric studies of muscle biopsies from patients with unusual childhood myopathies is emphasized.
PROGRESSIVE AXONOPATHY: AN INHERITED NEUROPATHY OF BOXER DOGS. AN IMMUNOCYTOCHEMICAL STUDY OF THE AXONAL CYTOSKELETON
Authors: GRIFFITHS I. R. , KYRIAKIDES E. , BARRIE J.
Published: May 2008

Progressive axonopathy: an inherited neuropathy of Boxer dogs. An immunocytochemical study of the axonal cytoskeleton

The distribution of the major axonal cytoskeletal proteins has been determined in lumbar ventral roots and spinal cord of dogs with progressive axonopathy, an inherited neuropathy of boxer dogs. The three neurofilament proteins, and β‐tubulin, actin and fodrin were localized using immunocytochemistry. The majority of swollen axons in the nerve roots contained excessive, disorientated neurofilaments. In about 5% of such fibres the peripheral filaments in the axoplasm were orientated circumferentially and such zones were deficient in tubulin. Many, but not all, spheroids contained increased amounts of actin, often with internal areas of more intense staining. Similar findings were present in axonal swellings in the CNS, although their contents were more variable. The distribution of axonal fodrin in CNS and PNS appeared unaltered. The perikarya of many motor neurons in the spinal cord and brain stem contained phosphorylated neurofilaments. The results support previous suggestions that defects in slow axonal transport are involved in the pathogenesis of this disease.
MAPPING OF RECEPTORS FOR CARBOHYDRATE CONSTITUENTS OF GLYCOCONJUGATES IN WELL–DIFFERENTIATED AND MALIGNANT EPENDYMOMAS: A GLYCOHISTOCHEMICAL STUDY
Authors: DIMITRI T. , BARDOSI A. , GABIUS H. J.
Published: May 2008

Recognitive interactions between the carbohydrate part of cellular glycoconjugates and endogenous receptors supposedly govern important biological processes. Consequently, their elucidation can be of considerable value in tumour diagnosis. The histochemical patterns of expression of endogenous sugar receptors (e.g. endogenous lectin–like proteins) of 10 cases of well–differentiated ependymoma and 10 cases of malignant ependymoma were analysed, using a panel of 18 biotinylated (neo)glycoproteins and a standardized staining protocol. Within this panel, differences in the extent of staining for intracellular sugar receptors in well–differentiated and malignant ependymomas were histochemically detectable. In comparison to the well–differentiated ependymomas, the anaplastic form of the tumour exhibited a generally higher capacity to specifically bind labelled (neo)glycoproteins, containing α or β–glucosides and a disaccharide, characteristic for one type of β–galactoside–terminated chain structure of glycoproteins. A significantly reduced binding was seen for tumours of the anaplastic type with labelled markers, carrying histochemically indispensable glucuronic acid residues. These findings suggest that labelled neoglycoproteins are a valuable tool for assessing the endogenous sugar–binding capacity in diagnostic histopathology. Our descriptive analysis of endogenous sugar receptors may also be a rational basis for studies on the functional significance of changes in the expression of their endogenous ligands and the cellular glycoconjugates. Further investigations are also possible on the correlation between the degree of differentiation and expression of both parts of a recognitive system, based on protein (receptor)–carbohydrate (ligand) interactions, in tumours of the central nervous system, especially ependymomas.
CEREBELLAR CORTICAL DEGENERATION IN ASSOCIATION WITH SMALL–CELL CARCINOMA OF THE OESOPHAGUS
Authors: COX P. M. , VAZIR M. H. , PETTY R. K. H. , LAW S. , DHILLON A. P.
Published: May 2008

We report the association of paraneoplastic cerebellar cortical degeneration with small–cell oesophageal carcinoma in a 60–year–old woman and describe the histopathological findings. We believe this to be the first report of such an occurrence. The cytoplasmic antigen PGP 9.5, which is strongly expressed in cerebellar Purkinje cells, was identified immunohistologically in the primary tumour and immunoglobulin demonstrated on Purkinje cells. These findings support an immunological pathogenesis for this condition and suggest that it is mediated by antibodies directed against tumour antigen which cross–react with Purkinje cells.
THE NUCLEUS BASALIS OF MEYNERT IN PARKINSONISM–DEMENTIA OF GUAM: A MORPHOMETRIC STUDY
Authors: MASULLO C. , POCCHIARI M. , MARIOTTI P. , MACCHI G. , GARRUTO R. M. , GIBBS C. J. , YANAGIHARA R. , GAJDUSEK D. CARLETON
Published: May 2008

The nucleus basalis of Meynert (nbM) was studied morphometrically in three Guamanians with parkinsonism–dementia (PD) and in two Guamanian and two non–Guamanian controls. Paraffin–embedded blocks of the nbM were serially sectioned (20 μm thick) at increments of 200 μm so that a total of 24 sections (eight each from the anterior, intermediate and posterior sectors of the nbM) were studied. The mean cell density was determined for each sector and the diameter of 50 neurons, randomly chosen in the region of apparent maximal density, was calculated. A decrease of the mean cell density, due to the loss of neurons with diameters larger than 20 μm, was found in the PD cases compared to the controls. Two PD patients exhibited striking neuronal loss (65–95%) with predominant involvement of the intermediate and posterior sectors, while the third case showed only minimal neuronal loss in these sectors (15–40%). In both Guamanian and non–Guamanian controls large neurons (diameters ≥ 20 μm) exceeded small neurons while the reverse was true in all sectors of the nbM for the PD cases. These data, while confirming a previous study reporting neuronal loss in the nbM of PD patients, underline the importance of detailed morphometric analysis of the different sectors of the nbM to recognize those patients in whom lesions are not uniformly distributed.
EVALUATION OF INTRACEREBRAL LESIONS IN PATIENTS WITH ACQUIRED IMMUNODEFICIENCY SYNDROME. NEUROPATHOLOGICAL FINDINGS AND EXPERIMENTAL DATA
Authors: STAVROU D. , MEHRAEIN P. , MELLERT W. , BISE K. , SCHMIDTKE K. , ROTHEMUNDS E. , FUNKE I. , STOCKER U. , BABARYKA I. , ZIETZU C. , FRYDL V. , PRANTL F. , ERFLE V.
Published: May 2008

In this paper we present the results of post–mortem examinations of the central nervous system in 61 male patients who died with Acquired Immunodeficiency Syndrome (AIDS); it includes 23 patients with reported neurological abnormalities at the time of presentation. The analysis revealed central nervous system (CNS) neoplasms (lymphoma, Kaposi's sarcoma) and a variety of inflammatory lesions (bacterial, fungal, protozoal and viral) in 32 cases. A total of 11 patients without opportunistic infections showed significant brain abnormalities characterized by microglial nodules and/or multinucleated giant cells, changes which are probably related to infection by human immunodeficiency virus (HIV). In addition, we describe results from a series of experiments designed to define the target cell population of HIV in the brain. The expression of CD4 complex–putative receptor for HIV–was investigated using short–term cultured brain cells taken from embryonic brain anlage and from different regions of fetal brain; glioma cells were also used. Cells derived from normal embryonic and fetal brain, as well as glioma cells, were examined with respect to their susceptibility to HIV. CD4 antigen expression could be demonstrated only on glioma cells of the permanent glioma line 85HG–59 comprised of cells with properties characteristic of astrocytes. Nevertheless, normal embryonic and fetal brain cells as well as glioma cells could be infected by HIV as documented by immunocytoehemical methods and southern blot analysis. HIV infected brain cells showed reduced growth rate and altered growth pattern. This study emphasizes the diversity of HIV conditioned CNS impairments, suggesting that genomic variability of HIV may result in varying cell type preference of the virus. The experimental data indicate that CD4 expression in brain cells is probably not ‘conditio sine qua non’ for HIV susceptibility. The alterations of HIV–infected brain cells demonstrated provide further evidence for a direct involvement of HIV in the pathogenesis of AIDS–related neurological syndromes.
IMMUNOCYTOCHEMICAL LOCALIZATION OF THE TERMINAL COMPLEMENT COMPLEX IN MULTIPLE SCLEROSIS
Authors: COMPSTON D. A. S. , MORGAN B. P. , CAMPBELL A. K. , WILKINS P. , COLE G. , THOMAS N. D. , JASANI B.
Published: May 2008

Granular deposits of C9 and the terminal complement complex, measuring 0–3–1 2 μm, have been demonstrated immunocytochemically in association with capillary endothelial cells, predominantly within plaques and adjacent white matter, in tissue obtained at autopsy from 5/7 patients with multiple sclerosis (MS) and one individual with subacute sclerosing panencephalitis but not from 7/7 controls. This finding suggests that the evolution of focal tissue damage in MS may involve complement activation associated with passage of humoral and cellular mediators of the immune system through the blood–brain barrier.
DIABETIC NEUROPATHY: ABNORMALITIES OF SCHWANN CELL AND PERINEURIAL BASAL LAMINAE. IMPLICATIONS FOR DIABETIC VASCULOPATHY
Authors: KING R. H. M. , LLEWELYN J. G. , THOMAS P. K. , GILBEY S. G. , WATKINS P. J.
Published: May 2008

During Wallerian degeneration, the Schwann cell basal laminal ensheathment around myelinated nerve fibres remains after the removal of myelin and axonal debris, forming a corrugated tube within which Schwann cell proliferation takes place. In nerve biopsies from patients with diabetic neuropathy, such residual basal laminal tubes tend to be circular rather than corrugated and appear to be more persistent during regeneration; this suggests increased rigidity and durability. These changes could be the result of increased cross–linkage of type IV collagen or alterations to other components of the basal lamina. A similar mechanism may be responsible for the thickening of perineurial basal laminae and the reduplication of basal laminae around endoneurial capillaries in diabetic patients; such reduplication may lead to reduced compliance of the vessel walls and impaired vascular perfusion.
PERLS‘ FERROCYANIDE TEST FOR IRON IN THE DIAGNOSIS OF VASCULITIC NEUROPATHY
Authors: ADAMS C. W. M. , BUK S. J. A. , HUGHES R. A. C. , LEIBOWITZ S. , SINCLAIR E.
Published: May 2008

Preliminary observations suggested that arterial and arteriolar necrosis in vasculitis of the peripheral nerve leads to local haemorrhage and subsequent deposition of haemosiderin. This pigment is more readily recognized in the nerve by the sensitive Perls' test for iron than by relying on recognizing its yellow colour. To support the use of iron staining as an index of vasculitis, in addition to necrosis and fibrin deposition, we obtained the following results from nerve biopsy and autopsy nerve specimens: vasculitis confined to PNS = 5/6 iron positive; polyarteritis nodosa and Wegener's granulomatosis = 4/5 iron positive; systemic lupus erythematosus 2/3 iron positive; rheumatoid disease 1/1 iron positive; acute Guillain–Barré syndrome and subacute or chronic demyelinating polyradiculoneuropathy = 12/12 iron negative; and other perivascular inflammation in the PNS (without evidence of vasculitis) = 2/2 iron negative. One case of Churg–Strauss syndrome showed no changes on nerve biopsy. Iron staining was also demonstrated in the kidneys of five or six patients with polyarteritis nodosa.
INFLAMMATORY DEMYELINATING NEUROPATHY IN C57BL/KaLwRij MICE
Authors: VITAL A. , VITAL C. , RADL J. , ZURCHER C.
Published: May 2008

Neuropathies associated with monoclonal gammopathy (MG) in humans have been extensively studied in the past few years, but experimental models have proved difficult to create. C57BL mice are prone to develop benign MG and it has been reported that some of these mice with benign IgG MG present an inflammatory demyelinating neuropathy (IDN). In order to verify such findings, the serum and the sciatic nerve of the first group of 28 C57BL/KaLwRij mice were examined: none of 10 mice with normal serum showed ultrastructural abnormalities in the sciatic nerve, while lesions of IDN were present in three out of 10 mice with benign IgG MD, in two out of seven with benign IgM MG, and in a mouse with Waldenström–like lymphoma. The second group of animals was studied in the same way; it was composed of seven C57BL mice with transplanted multiple myeloma, and six C57BL mice with Morbus Waldenstrom–like lymphoma. In none of these animals, which were younger than those of the first group, was any lesion of IDN observed.
ANTIPHOSPHOLIPID ANTIBODY SYNDROME PRESENTING WITH COMPLEX PARTIAL SEIZURES AND TRANSIENT ISCHAEMIC ATTACKS DUE TO WIDESPREAD SMALL CEREBRAL ARTERIAL THROMBOSIS
Authors: LEACH I. H. , LENNOX G. , JASPAN T. , LOWE J.
Published: May 2008

The neuropathologies findings in a young man with the antiphospholipid antibody syndrome presenting with complex partial seizures and transient ischaemic attacks are described. Whilst some of his symptoms could be attributed to large vessel thrombosis, the dominant pathological process was widespread small cerebral arterial thrombosis causing extensive microinfarcts within the cerebral cortex. These findings help to explain the neurological manifestations of the antiphospholipid antibody syndrome.
Technical communication Immunogold light and electron microscopic detection of amyloi plaques in transmissible spongiform encephalopathies
Authors: DOERR‐SCHOTT J. , KITAMOTO T. , TATEISHI J. , BOELLAARD J. W. , HELDT N. , LICHTE C.
Published: May 2008

The antigenicity of the ‘prion’ protein amyloid fibrils was shown to be preserved after glutaraldehyde/OsO4 fixation in uranyl acetate‐ stained brain tissue blocks from patients with Gerstmann‐Straussler syndrome (GSS) and from mice infected with Creutzfeldt‐Jakob disease (CJD). Amyloid plaques were demonstrated by light microscopy in immunogold silver‐intensified semithin sections. Under the electron microscope, the amyloid fibrils were labelled in immunogold‐reacted ultrathin sections using an antiserum prepared against GSS amyloid plaque cores and mouse amyloid fibrils respectively. The influence of various oxidizing agents (hydrogen peroxide, sodium metaperiodate) on the tissue preservation and the immunohistochemical detection was tested.