Showing papers on "Nervous system published in 1977"

Pathology of Tumours of the Nervous System

Abstract: Incidence pathogenesis and other general aspects experimental tumours of the nervous system tumours of central neuroepithelial origin tumours of specialized tissues of central neuroepithelial origin the growth of dissemination of central neuroepithelial tumours tumours of the meninges and related tissues tumours of the cranial, spinal and peripheral nerve sheaths nervous system involvement by lymphomas, histiocytoses and leukaemias tumours of vascular origin tumours and tumour-like lesions of maldevelopmental origin dysgenetic syndromes (phacomatoses) associated with tumours and hamartomas of the nervous system secondary tumours of the nervous system deformations and other structural changes produced by intercranial tumours effects of radiation and other forms of therapy on intracranial and spinal tumours and their surrounding tissues tumours of peripheral neuroblasts and ganglion cells paragangliomas.

Ultrastructural studies of the dying-back process. III. The evolution of experimental peripheral giant axonal degeneration.

Abstract: The spatio-temporal evolution of peripheral giant axonal degeneration has been studied in rats during the development of concurrent peripheral (PNS) and central (CNS) nervous system dying-back disease after chronic intoxication with the neurotoxic hexacarbons n-hexane (CH3CH2CH2CH2CH2CH3), methyl n-butyl ketone (MBK) (CH3COCH2CH2CH2CH3), or 2,5-hexanedione (CH3COCH2CH2CHOCH3), a neurotoxic metabolite of MBK. Each compound caused animals insidiously to develop identical, symmetrical peripheral neuropathies characterized by eversion and drop of hindfeet, inability to extend hindlimbs and upper extremity weakness. Teased fiber studies demonstrated that giant axonal swellings first developed on the proximal sides of multiple paranodes sited in distal, non-terminal regions of large myelinated fibers. Later, swellings developed at internodal sites. Smaller myelinated and unmyelinated fibers also underwent multifocal, giant axonal swelling. In affected myelinated fibers, swollen nodal and paranodal axons were frequently associated with retracted paranodal myelin sheaths. Adjacent distal internodes were attenuated and corrugated. Demyelinated paranodes apparently underwent local shrinkage and remyelination before complete distal fiber breakdown commenced. The proximal limits of chains of homogeneous myelin ovoids were interfaced with proximal, preserved regions at sites of giant axonal swellings. Regeneration of myelinated axons also occurred during intoxication. Regenerating fibers wre composed of multiple, short, branched internodes which sometimes appeared multifocally swollen. Interfaces between regenerating and preserved portions of fibers were unswollen. Thick section studies showed that pronounced endoneurial edema accompanied fiber degeneration in peripheral nerve trunks. Ultrastructural studies revealed multifocal, giant axonal swellings containing masses of 10 nm neurofilaments and sometimes, clustered mitochondria, neurotubules and smooth endoplasmic reticulum. Enlarged granular mitochondria, interdigitated Schwann cell/axon networks and corrugated myelin sheaths were common findings. Dense granules, vesicles and hexagonal particles were also noted in the axoplasm. These findings provide new insights into the nature of the dying-back process: although there was a retrograde, temporal spread of axonal swelling up affected nerve trunks, axonal degeneration neither began in the nerve terminal nor spread seriatim centripetally along individual nerve fibers. The dying-back process was further examined in a companion study in this issue (32) which analyzed some of the factors determining the differential vulnerability of PNS and CNS fibers in animals intoxicated either with these neurotoxic hexacarbons or with acrylamide.

Neurological differential diagnosis

Abstract: 1. History Taking and Physical Examination 2. The Pupils and their Reactions 3. Vision, the Visual Fields and the Olfactory Nerve 4. Examination of the Optic Fundus 5. The Third, Fourth and Sixth Cranial Nerves 6. The Cerebellopontine Angle and Jugular Foramen 7. Conjugate Eye Movements and Nystagmus 8. The Cerbral Hemispheres: The Lobes of the Brain 9. The Cerbral Hemispheres: Vascular Diseases 10. The Cerbral Hemispheres: Disorders of the Limbic System and Hypothalamus 11. The Brain Stem 12. The Extrapyramidal System and the Cerebellum 13. The Anatomy, Physiology and Clinical Features of Spinal Cord Diseases 14. Metabolic Infective and Vascular Disorders of the Spinal Cord 15. The Spinal Cord in Raltion to the Vertebral Column 16. Diagnosis of Cervical Root and Peripheral Nerve Lesions Affecting the Arm 17. Nerve Root and Peripheral Nerve Lesions Affecting the Leg 18. Diseases of Muscle and the Muscle End-Plate 19. Peripheral Neuropathy and Diseases of the Lower Motor Neuron 20. Headache 21. Facial Pain 22. Attacks of Altered Consciousness 23. Trauma and the Nervous System 24. Neurological Complications of Systemic Disorders Suggestions for Further Reading and Study Index

Azorean Disease of the Nervous System

Abstract: We studied a family of Portuguese ancestry from the Azores who suffered a progressive neurologic disease characterized by gait ataxia, features similar to Parkinson's disease in some patients, limitation of eye movements, widespread fasciculations of muscles, loss of reflexes in the lower limbs, followed by nystagmus, mild cerebellar tremor and extensor plantar responses. Two post-mortem examinations revealed loss of neurons and gliosis in the substantia nigra, nuclei pontis (and in the putamen in one case) as well as in the nuclei of the vestibular and other cranial nerves, columns of Clarke and anterior horns, in the spinal cord there were also loss of fibers in the fasciculi gracilis and mild changes in the pyramidal tracts. Comparison of the disease in this family with the findings reported in three families of similar ancestry, previously thought to have different disorders, suggests that they may all represent a single genetic entity with variable expression.

Substance P: localization in synaptic vesicles in rat central nervous system

Abstract: SUBSTANCE P (SP) was originally isolated from brain and gut extracts (VON EULER & GADDUM, 1931) and has been characterized as an undecapeptide (CHANG & LEEMAN, 1970). It is highly concentrated in the dorsal horn of the spinal cord of mammals where it appears to be localized mainly in the terminals of primary sensory neurones (TAKAHASHI & OTSUKA, 1975; HOKFELT et al., 1975a; CUELLO et al., 1976). In addition, dorsal root stimulation causes the release of SP-like immunoreactive material from the neonatal rat spinal cord in uitro (OTSUKA & KONISHI, 1976). SP is a potent excitant of spinal cord motoneurones (KONISHI & OTSUKA, 1974a, b) and of dorsal horn neurones which respond specifically to nociceptive stimuli (HENRY, 1976). There is thus convincing evidence that SP may be the neurotransmitter released by certain primary afferent terminals in the spinal cord. In addition SP-containing neurones occur in many parts of the brain (HOKFELT et al., 1975b; CUELLO & KANAZAWA, in preparation; BROWNSTEIN et al., 1976; KANAZAWA & JESSELL, 1976) and a stimulus-evoked release of SP has been demonstrated from rat hypothalamic slices and from synaptosome preparations in uitro (JESSELL et al., 1976; SHENKER et al., 1976). If SP acts as a neurotransmitter in CNS it might be expected to occur in high concentrations in synaptic vesicle storage sites within nerve terminals, as is the case for other neurotransmitters (DE ROBERTIS, 1964; ECCLES, 1964; KATZ, 1971). Previous studies have shown that SP is concentrated in synaptosomal fractions from brain homogenates (WHITAKER, 1964; LEMBECK & HOLASEK, 1960), and there is suggestive evidence for its association with synaptic vesicles in the brain (RYALL, 1962 & 1964; DUFFY et al., 1975) and in peripheral nerves (VON EULER & LISHAJKO, 1961). The present experiments provide a direct demonstration of such vesicular storage sites.

Immunofluorescence studies of neurofilaments in the rat and human peripheral and central nervous system

Abstract: Localization of antisera to neurofilament antigens derived from rat peripheral nerve was carried out in tissues of rat and human peripheral and central nervous systems by indirect immunofluorescence. Unfixed and chloroform-methanol-fixed frozen sections of tissues were incubated in purified IgG of the experimental rabbit antisera and subsequently exposed to goat anti-rabbit IgG conjugated with fluorescein isothiocyanate. Control studies were conducted on identical tissue preparations incubated in the same concentrations of nonspecific rabbit IgG or in experimental rabbit IgG absorbed with extracts of rat peripheral nerve containing neurofilament antigen. Extensive immunofluorescence was observed in rat and human peripheral and central nervous systems. The distribution and configuration of immunofluorescence corresponded to neurofilament-rich structural components of these tissues. Prominent immunofluorescence was also noted in neuronal cell bodies of spinal sensory ganglia, especially in perikarya of the large neuronal type. Immunofluorescence of the central nervous system was located predominantly in myelinated axons of the white matter in cerebrum, cerebellum, brain stem, and spinal cord. Less intense immunofluorescence was also seen in neuronal perikarya and in short thin linear processes of grey matter.

Development of the nervous system of Aplysia californica.

Abstract: The ability to grow the marine molluse Aplysia under laboratory conditions allows a detailed study of the formation of the nervous system and of the development of specific identified cells. I have found that the ganglia develop in a specific temporal order. Cerebral and pedal ganglia develop at hatching, the abdominal, pleural, and osphradial ganglia 3 weeks after hatching, and the buccal ganglia at 4 weeks. The origin of the abdominal ganglion is complex; its anlage forms at 3 weeks from three larval ganglia that fuse to form the abdominal ganglion. Individual cells cannot be distinguished from one another by their location within the ganglion or by their appearance alone until metamorphosis at 5 weeks. After metamorphosis, the identified neuron, R2, suddenly becomes recognizable because of a significant increase in its size.

Neuroendocrine neoplasms and their cells of origin.

Abstract: The body's homeostasis depends on the co-ordinated activity of the nervous system and the endocrine system. Although the physiologic co-operation of these two systems has long been recognized, neurons and endocrine cells are generally regarded as developmentally and functionally distinct. Neurons are thought to be of ectodermal origin and to function mostly as elongated conducting structures that directly control the behavior of other cells by transmission of electrical impulses and localized release of transmitter substances. Endocrine cells are thought to be mostly of nonectodermal origin and to control the behavior of other cells indirectly, by releasing hormones into the blood. . . .

Pathogenesis of spontaneous hypertension as a model for essential hypertension.

Abstract: Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...

Eye-Tracking and Optokinetic Nystagmus Results of Quantitative Testing in Patients with Well-Defined Nervous System Lesions

Abstract: Eye-tracking and optokinetic nystagmus (OKN) abmormalities in patients with focal lesions of the nervous system are reviewed. Patients with peripheral labyrinthine lesions can have deficits in smooth pursuit and OKN, but they are rapidly compensated after an acute lesion. By contrast, patients with large, cerebellopontine angle tumors have progressive impairment of pursuit and OKN as the tumor enlarges. Abnormalities of saccadic eye movements suggest intrinsic central nervous system (CNS) dysfunction. Saccade accuracy is severely impaired with cerebellar lesions, while brain stem disease frequently results in a slowing of saccade maximum velocity. Smooth pursuit and OKN abnormalities are common with all types of CNS lesions. The pattern of eye-tracking and OKN abnormality can be useful in anatomically localizing nervous system lesions.

Toxic Effects of Adriamycin on the Ganglia of the Peripherial Nervous System: A Neuropathological Study

Abstract: Rats were injected intravenously with 10 mg/kg of adriamycin (doxorubicin). All the treated animals developed severe posterior limb ataxia on days 11 and 12 following the injection. Mild ataxia of the forelimbs was noted later. The animals were killed between days 10 and 50. Light microscopy revealed changes in ganglion cells of the peripheral nervous system with sparing of neurons in the central nervous system. In the spinal, paravertebral and trigeminal ganglia, necrosis of neurons was followed by mild lymphocytic infiltration, and ultimate loss of ganglion cells, and a marked proliferation of nerve sheath cells. Electron microscopic study revealed increased numbers of neurofilaments and the presence of membrane-bound cisterns in the affected dorsal root ganglion cell bodies. It is concluded that adriamycin, an important anticancer therapeutic agent, has neurotoxic properties and that it selectively damages the ganglia of the peripheral nervous system.

Normal and Abnormal Development of the Human Nervous System

Abstract: Normal and Abnornml De the Human Nervous Syste Lemire, J. D. Loeser, R. VN -.E. C. Alvord. (Pp. 421 $27.50.) Harper and Row USA. 1975. 'Fills a long-felt gap' is a viewers but the phrase is ii this book. In a clear an way it gathers together a of information about the and growth of the hun system and gives a brief the major developmental Standardised graphs pres formation in a manner rapid reference so that can assess the probable t life at which abnormalities so much detail compreE reasonable space and so n A versial material-even in syndromes such as the Ar it is not surprising that th( errors and omissions or tha pretations do not appeal ti The wonder is that it has well.

Seasonal monoamine changes in the central nervous system ofMytilus edulis (Bivalvia)

Abstract: The levels of serotonin, dopamine and norepinephrine exhibit seasonal changes in the central nervous system of Mytilus edulis. These monoamines were higher during the summer and lower during the winter.

GABA in Nervous System Function

Abstract: symposia was held in October 1974 in New Delhi and considered growth and development of the brain, and the prcceedings are now presented under the editorship ef Dr. Mary Brazier. Contributions include a number from wellknown research workers from Europe and North America, as well as less well-known, including some from India and Iran. Topics include very full and helpful reviews of morphological, biochemical and neurophysiological aspects of brain maturation, as well as a detailed account ef the effects of human malnutrition. It is these reviews rather than the accounts of contributors' original work which are most valuable to those seeking a recent perspective of this very important field. Rajalakshuni is rather cautious in his poper on 'Factors affecting psychelogical development in man' in extrapolating from the intellectual deficits seen as a result of extreme malnutrition (for example, kwashiorkor) to populations where nutritional intake is thought to be sufficiently inadequate to influence birth weight. He concludes that, in India, the evidence studied so far does not suggest that the mental development of well children differs significantly according to their nutritional status. In a final provocative paper with a title more like a banner headline from a daily tabloid 'U.S. poverty impact on brain development' a group from the Universities of California (San Diego and Berkeley) conclude that as many as 10% of the population of San Diego County 'are seriously undernourished according to our criteria relating to brain jeopardy'. (Symbionese Liberation Army, please note.)

A cannabinoid with cardiovascular activity but no overt behavioral effects

Abstract: Abnormal-Δ8-tetrahydrocannabidiol (ABN-Δ8-THC) failed to elicit central nervous system and cardiovascular effects in laboratory animals. Abnormal-cannabidiol (ABN-CBD) was also devoid of overt behavioral effects but produced marked hypotension with only slight bradycardia in anesthesized dogs.

Quaking mouse: an ultrastructural study of the peripheral nerves.

Abstract: Ultrastructural study of the peripheral nervous system of quaking mice has revealed several unusual features in the pattern of myelination in addition to hypomyelination.

The Anatomy Coloring Book

Abstract: Orientation to the Body. Cells and Tissues. Integumentary System. Skeletal and Articular Systems. Skeletal Muscular System. Nervous System. Central Nervous System. Central Nervous System: Cavities and Coverings. Peripheral Nervous System. Autonomic Nervous System. Special Senses. Cardiovascular System. Lymphatic System. Immune (Lymphoid) System. Respiratory System. Digestive System. Urinary System. Endocrine System. Reproductive System. Human Development.

Spontaneous phagocytosis of boutons on spinal motoneurons during early postnatal development. An electron microscopical study in the cat

Abstract: The boutons making synaptic contact with different regions of spinal motoneurons have been studied during the early postnatal period. The observations suggest that a spontaneous glial phagocytosis of boutons of different types occurs mainly during the second postnatal week. This finding is discussed in relation to the previously demonstrated disappearance of boutons from the initial axon segment of spinal motoneurons during the same period of development and also in relation to other degenerative and eliminatory phenomena associated with the normal development of the nervous system.