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MINISTRY OF THE PUBLIC HEALTH OF THE REPUBLIC UZBEKISTAN TASHKENT MEDICAL ACADEMY CHAIR OF THE NERVIOUS DISEASES The Subject to lectures: Lecture 7 Infectioninflammatory diseases of the nervous system. The meningitis’s, chronic leptomeningitis, chronic chorioepindimitis, categorization, etiology, clinic, therapy. For student of 5 courses medical and physician-pedagogical faculty It Is Approved: 25.08.2012 Tashkent 2012 Лекция № 7 Lecture 7 Infection-inflammatory diseases of the nervous system. The meningitis’s, chronic leptomeningitis, chronic chorioepindimitis, categorization, etiology, clinic, therapy. The Purpose to lectures. Tell the students about importance sanitary-educational work amongst populations in preventive maintenance of that diseases (the sharp infectious diseases, festering will cast, tuberculosis, parotitis and others), which in the following can be a reason of the development of the meningitis or leptomeningitis. The Problems to lectures and short motivation of the subject: Acquaint the student about notion meningismus, meningitis and leptomeningitis. Train the student ethiopatogenezis,, clinic, diagnostics, preventive maintenance and principle treating different forms of the meningitis and leptomeningitis. Infectious-inflammatory diseases of the nervous system are a wide-spread diseases and undue or wrong diagnostics can bring about lethal upshot or is a reason deep invality. 4. The analysis following questions subjects to on lectures: 4.1. The Categorization infectious-inflammatory diseases of the nervous system (the meningitides and leptomeningitis). 4.2. The сonstruction shell cerebrum. The notion about meningitis and leptomeningitis. 4.3. Ethiopatogenez, clinic, diagnostics and principles treating different forms (the serous, tuberculosis, meningoccus) meningitis. 4.4. Ethiopatogenez, clinic, current, potomorphogy, diagnostics and principles treating different forms of leptomeningitis. Localization CNS infection may involve the leptomeninges and CSF spaces (meningitis), the ventricular system (ventriculitis), the gray and white matter of the brain (encephalitis), or the spinal cord (myelitis). A focus of bacterial infection of the brain is called a brain abscess, or cerebritis in the early stage before a frank abscess is formed. Pus located between the dura mater and the arachnoid membrane is called a subdural empyema, while pus outside the dura is called an epidural abscess. Course The clinical manifestations may be acute (purulent meningitis, CNS listeriosis, herpes simplex encephalitis), subacute (cerebral abscess, focal encephalitis, neuroborreliosis, neurosyphilis, tuberculous meningitis, actinomycosis, nocardiosis, rickettsiosis, neurobrucellosis), or chronic (tuberculous meningitis, neurosyphilis, neuroborreliosis, Whipple encephalitis, Creutzfeldt–Jakob disease). The epidemiological pattern of infection may be sporadic, endemic or epidemic, depending on the pathogen. Clinical Manifestations Meningitis and encephalitis rarely occur as entirely distinct syndromes; they usually present in mixed form (meningoencephalitis, encephalomyelitis). CSF examination establishes the diagnosis. These disorders may present in specific ways in certain patient groups. Neonates and children commonly manifest failure to thrive, fever or hypothermia, restlessness, breathing disorders, epileptic seizures, and a bulging fontanelle. The elderly may lack fever but frequently have behavioral abnormalities, confusion, epileptic seizures, generalized weakness, and impairment of consciousness ranging to coma. Immunodeficient patients commonly have fever, headache, stiff neck, and drowsiness in addition to the manifestations of their primary illness. Meningitic syndrome is characterized by fever, severe, intractable headache and backache, photophobia and phonophobia, nausea, vomiting, impairment of consciousness, stiff neck, and hyperextended posture, with opisthotonus or neck pain on flexion. Kernig’s sign (resistance to passive raising of leg with extended knee) and Brudzinski’s sign (involuntary leg flexion on passive flexion of the neck) are signs of meningeal involvement. Painful neck stiffness is due to (lepto)meningeal irritation by infectious meningitis, septicemia, subarachnoid hemorrhage, neoplastic meningitis, or other causes. Isolated neck stiffness not caused by meningitis (meningism) may be due to cervical disorders such as arthrosis, fracture, intervertebral disk herniation, tumor, or extrapyramidal rigidity. Papilledema is usually absent; when present, it indicates intracranial hypertension Encephalitic syndrome is characterized by headache and fever, sometimes accompanied by epileptic seizures (often focal), focal signs (cranial nerves deficits, especially of CN III, IV, VI, and VII; aphasia, hemiparesis, hemianopsia, ataxia, choreoathetosis), behavioral changes, and impairment of consciousness (restlessness, irritability, confusion, lethargy, drowsiness, coma). The neurological signs may be preceded by limb pain (myalgia, arthralgia), a slight increase in body temperature, and malaise. For acute cerebellitis, see Brain stem encephalitis produces ophthalmoplegia, facial paresis, dysarthria, dysphagia, ataxia, and hearing loss. Myelitic syndrome. Myelitis presents with severe local pain, paraparesis, paresthesiae, or some combination of these. Incomplete or complete paraplegia or quadriplegia develops within a few hours (acute) or days (subacute). The differential diagnosis may be difficult. Pathogenesis Pathogens usually reach the CNS by local extension froma nearby infectious focus (e. g. sinusitis, mastoiditis) or by hematogenous spread from a distant focus. The ability of pathogens to spread by way of the bloodstream depends on their virulence and on the immune status of the host. They use special mechanisms to cross or circumvent the blood–brain barrier. Some pathogens enter the CNS by centripetal travel along peripheral nerves (herpes simplex virus type I, varicella-zoster virus, rabies virus), others by endocytosis (Neisseria meningitidis), intracellular transport (Plasmodium falciparum via erythrocytes, Toxoplasma gondii via macrophages), or intracellular invasion (Haemophilus influenzae). Those that enter the subarachnoid space probably do so by way of the choroid plexus, venous sinuses, or cribriform plate. Having entered the CSF spaces, pathogens trigger an inflammatory response characterized by the release of complement factors and cytokines, the influx of leukocytes and macrophages, and the activation of microglia and astrocytes. Disruption of the blood–brain barrier results in an influx of fluids and proteins across the vascular endothelium and into the CNS, causing vasogenic cerebral edema, which is accompanied by both cytotoxic cellular edema and interstitial edema due to impaired CSF circulation. Cerebral edema causes intracranial hypertension. These processes, in conjunctionwith vasculitis, impairment of vascular autoregulatory mechanisms, and/or fluctuations of systemic blood pressure, lead to the development of ischemic, metabolic, and hypoxic cerebral lesions (focal necrosis, territorial infarction). Treatment The immune system is generally no longer able to hold pathogens in check once they have spread to the CNS, as the immune response in the subarachnoid space and the neural tissue itself is less effective than elsewhere in the body. Having gained access to the CNS, pathogens meet with favorable conditions for further spread within it. Prophylaxis. The occurrence and spread of CNS infection can be prevented by mandatory reporting (as specified by local law), prevention of exposure (isolation of sources of infection, disinfection, sterilization), and prophylaxis in persons at risk (active and passive immunization, chemoprophylaxis). Treatment. Patients with bacterial or viral meningoencephalitis must be treated at once. The treatment strategy is initially based on the clinical and additional findings. Antimicrobial therapy is first given empirically in a broadspectrum combination, then specifically tailored in accordance with the species and drug sensitivity pattern of the pathogen(s) identified. Causative organisms may be found in the CSF, blood, or other bodily fluids (e. g., throat smear, urine or stool samples, bronchial secretions, gastric juice, abscess aspirate). Bacterial Infections ! Meningitis/Meningoencephalitis For an overview of the most common pathogens, cf. Table 29. Immune prophylaxis:Vaccines are available against Haemophilus influenzae type B infection (for infants, small children, and children over 6 years of age at increased risk), Pneumococcus (children over 2 years of age and adults with risk factors such as immunosuppression or asplenia), and meningococcus (travel to endemic regions, local outbreaks). Chemoprophylaxis is indicated for close contacts of persons infected with Haemophilus influenzae (rifampicin) or meningococcus (rifampicin, ciprofloxacin, or ceftriaxone). Brain Abscess Brain abscess begins as local cerebritis and is then transformed into an encapsulated region of purulent necrosis with perifocal edema. The pathogenic organisms may reach the brain by local or hematogenous spread (mastoiditis, otitis media, sinusitis, osteomyelitis; endocarditis, pneumonia, tooth infection, osteomyelitis, diverticulitis), or by direct inoculation (trauma, neurosurgery). The clinical manifestations include headache, nausea, vomiting, fever, impairment of consciousness, and focal or generalized epileptic seizures, neck stiffness, and focal neurological signs. The diagnosis is made by MRI and/or CT (which should include bone windows, as the infection may have originated in bony structures) and confirmed by culture of the pathogenic organism. Bacterial Vasculitis Arteries. Vessel wall inflammation in association with sepsis. Bacterial endocarditis causes cerebral abscess formation or infarction by way of infectious thromboembolism (! focal inflammatory changes in the cerebral parenchyma ! metastatic or embolic focal encephalitis). The syndrome is characterized by headache, fever, epileptic seizures, and behavioral changes in addition to focal neurological signs. Meningoencephalitis may cause arteritis by direct involvement of the vessels. Embolization of infectious material may lead to the development of septic (“mycotic”) aneurysms. Veins. Bacterial thrombophlebitis of the cerebral veins or venous sinuses may arise as a complication of meningitis or by local spread of infection from neighboring structures. Ventriculitis Infection of the ventricular system (perhaps in connection with an intraventricular catheter for internal or external CSF drainage). The clinical findings are often nonspecific (somnolence, impairment of concentration and memory). Abdominal complaints (peritonitis) may predominate if the infection has spread down a ventriculoperitoneal shunt to the abdomen. Diagnosis: CSF examination and culture. Septic Encephalopathy Bacteremia leads to the release of endotoxins, which, in turn, impair cerebral function. Septic encephalopathy can produce findings suggestive of meningoencephalitis such as impairment of consciousness, epileptic seizures, paresis, and meningismus, despite the absence of CSF inflammatory changes and a sterile CSF culture. Diagnosis: EEG changes consistent with the diagnosis (general changes, triphasic complexes, burst suppression) in the setting of known systemic sepsis with sterile CSF. CT and MRI are normal. Tuberculous Meningitis Pathogenesis. Mycobacterium tuberculosis transmission in man is usually by transfer of droplets fromand to the respiratory tract (rarely orally or through skin lesions). The pathogen replicates in the lungs (primary infection), either in the lung tissue itself or within alveolar macrophages. Macrophages can only destroy tubercle bacilli after they have been activated by T cells; the course of the infection thus depends on the state of the immune system, i.e., on the ability of activated macrophages to hold the bacilli in check. The stage of primary infection lasts 2–4 weeks, is not necessarily symptomatic (if it is, then with nonspecific symptoms such as fever, anorexia, and lethargy), and cannot be detected by immune tests performed on the skin. The inflammatory process may also involve the regional (hilar) lymph nodes (primary complex). Calcified foci in the primary complex are easily seen on plain radiographs of the chest. The bacilli may remain dormant for years or may be reactivated when the patient’s immune defenses are lowered by HIV infection, alcoholism, diabetes mellitus, corticosteroid therapy, or other factors (reactivated tuberculosis). Spread from the primary focus to other organs (organ tuberculosis) can occur during primary infection in immunocompromised patients, but only after reactivation in other patients. The bacilli presumably reach the CNS by hematogenous dissemination; local extension to the CNS from tuberculous bone (spinal cord, base of skull) is rare. Symptoms and signs. The type and focus of CNS involvement (neurotuberculosis) vary, depending mainly on the age and immune status of the host. Tuberculous meningoecephalitis. The prodromal stage lasts 2–3 weeks and is characterized by behavioral changes (apathy, depression, irritability, confusion, delirium, lack of concentration), anorexia, weight loss, malaise, nausea, and fever. Headache and neck stiffness reflect meningeal involvement. Finally, cerebral involvementmanifests itself in focal signs (deficits of CN II, III, VI, VII, and VIII; aphasia, apraxia, central paresis, focal epileptic seizures, SIADH) and/or general signs (signs of intracranial hypertension, hydrocephalus). The focal signs are caused by leptomeningeal adhesions, cerebral ischemia due to vasculitis, or mass lesions (tuberculoma). Chronic meningitis most likely reflects inadequate treatment, or resistance of the pathogen, rather than being a distinct form of the disease. Diagnosis: CSF examination for initial diagnosis and monitoring of disease course. The diagnosis of tuberculous meningitis can only be confirmed by detection of mycobacteria in the CSF with direct microscopic visualization, culture, or molecular biological techniques. As the prognosis of untreated tuberculous meningitis is poor, treatment for presumed disease should be initiated as soon as the diagnosis is suspected from the clinical examination and CSF findings; the latter typically include high concentrations of protein (several grams/liter) and lactate, a low glucose concentration (!50% of blood glucose), a high cell count (over several hundred), and a mixed pleocytosis (lymphocytes, monocytes, granulocytes). Tuberculoma is a tumorlike mass with a caseous or calcified core surrounded by granulation tissue (giant cells, lymphocytes). Tuberculomas may be solitary or multiple and are to be differentiated from tuberculous abscesses, which are full of mycobacteria and lack the surrounding granulation tissue. Diagnosis: CT or MRI. Spinal tuberculosis. Transverse spinal cord syndrome can arise because of tuberculous myelomeningoradiculitis, epidural tuberculous abscess associated with tuberculous spondylitis/ discitis, or tuberculoma. Diagnosis: MRI. Antibiotic treatment. One treatment protocol specifies a combination of isoniazid (with vitamin B6), rifampicin, and pyrazinamide. After 3 months, pyrazinamide is discontinued, and treatment with isoniazid and rifampicin is continued for a further 6–9 months. The treatment for HIVpositive patients includes up to five different antibiotics. 5. The Text of lectures. Cerebrospinal Fluid System Survey The CNS is completely surrounded by cerebrospinal fluid. This also fills the internal cavities of the brain, the ventri cles, so that it is possible to distinguish internal and external cerebrospinal fluid spaces, which communicate in the region of the IVth ventricle. Internal cerebrospinal fluid spaces. The ventricular system consists of four ventricles: two lateral ventricles (I and il) A1 in the telencephalic hemispheres, the Mlrd ventricle ABC2 in the diencephalon, and the IVth ventricle ABC 3 in the hindbrain (pons and medulla oblongata). The two lateral ventricles communicate with the lllrd ventricle through the interventricular foramen (Monro) AC 4, which lies on each side in front of the thalamus. The lllrd ventricle in turn communicates with the IVth ventricle by a narrow opening, the cerebral aqueduct (aqueduct of Sylvius) ABC 5. Corresponding to the rotation of the hemisphere the lateral ventricle is semicircular in shape, with a caudally directed spur. We distinguish several regions: the anterior horn BC6 in the frontal lobe, bordered laterally by the head of the caudate nucleus, medially by the septum pe lucid urn and dorsally by the corpus callosum; the narrow central part (cella media) BC7 above the thalamus; the temporal horn BC8; and the occipital horn BC9 in the occipital lobe. The lateral wall of the lllrd ventricle is formed by the thalamus with the in-terthalamic substance C10 and the hypothalamus. The optic recess C11 and the infundibular recess C12 project anteriorly, and the suprapineal recess C13 and the pineal recess C14 caudally. The IVth ventricle forms a tent-shaped space over the rhomboid fossa between the cerebellum and the medulla and extends as a long lateral recess BC15 on both sides. Each recess ends in the foramen of Luschka. the lateral opening of the IVth ventricle. At the attachement of the inferior medullary velum lies the median aperture of Magendie. External cerebrospinal fluid spaces. The external cerebrospinal fluid space lies between the two layers of the leptomeninges. It is limited inter-nelly by the pia mater and externally by the arachnoid. It is narrow over the convexity of the brain and only becomes enlarged at the base of the brain in certain areas, where it forms the cerebrospinal fluid cisterns. While the pia rnater adheres closely to the outer surface of the CNS. the arachnoid membrane spans the sulci, indentations and fossae so that over deeper indentations larger spaces are formed, the subarachnoid cisterns, filled with cerebrospinal fluid. The largest space is the cerebellomedullary cistern A16 between the cerebellum and the medulla. The interpeduncular cistern A17 lies in the angle between the floor of the diencephalon, the cerebral peduncles and the pons, and in front of it, in the region of the chiasm lies the chiasmatic cistern A18. The surface of the cerebellum, the quadrigeminai plate and the epiphysis border the cisterna ambiens A19 (superior cistern) traversed by a wide-meshed network of connective tissue. Cerebral fluid circulation. The cerebrospinal fluid is produced by the choroid plexus. It flows from the lateral ventricles into the lllrd ventricle and from there through the aqueduct into the IVth ventricle. There it enters the external cerebrospinal fluid space through the median and lateral foramina of the IVth ventricle. Drainage of CSF into the venous circulation occurs partly via the arachnoid villi, which protrude into the venous sinus, and partly at the point of exit of the spinal nerves, where there is a transition into the dense venous plexus and into the nerve sheaths (a route into the lymphatic circulation). Cerebrospinal Fluid System Choroid Plexus Lateral Ventricle The choroid plexus consists of convoluted vascular villi which invaginate from certain parts of the ventricular wall and protrude into the cavity of the ventricle. The part of the wall (lamina choroidea) A1 which lies on the medial surface of the hemisphere becomes thinner during embryonic development and is pushed out into the lumen of the ventricle A2 by vascular loops lying in the external pia mater. At the beginning of development all the vascular convolutions are covered by a thin layer of the hemisphere wall. This changes ultimately into a layer of epithelial cells, the plexus epithelium. Thus, the adult choroid plexus consists of two components: the vascular connective tissue derived from the pia, and an epithelial layer of transformed hemisphere wall cells. It has become invaginated into the ventricular cavity and is only connected to the outer pia via the small choroidal fissure A3. When the choroid plexus is removed, the thinned parts of the wall of the hemisphere tear off at this fissure. The lines of the tear are called the taeniae choroKtoae. One line is attached to the fornix and the fimbria, and is called the taenia for-nicis C4 and the other extends along the lamina affixa . as the taenia choroidea C 5. In accordance with the rotation of the hemisphere, the plexus on the medial wall of the ventricle describes a semicircle which extends from the interventricular foramen across the pars centralis C6 into the inferior horn C7. The anterior horn C8 and the posterior horn C9 do not contain a plexus; they are developmentally secondary formations. Tela Choroidea When the hemispheres grow over the diencephalon, the pia and arachnoid of the two parts of the brain come to lie upon one another, causing a kind of duplication A10, the tela choroidea B, a connective tissue plate stretched out between the hemispheres and the diencephalon. On its lateral margins the pia forms vascular villi for the plexus of the lateral ventricle, and medially the tela covers the roof of the third ventricle, the tela choroidea of the Hlrd ventricle BC11. In this region two rows of vascular villi invaginate into the lumen of the third ventricle and form the choroid plexus of the third ventricle. When the roof of the ventricle is removed, the line of the tear, which is called the taenia thalamiC\ 2, remains along the medullary stria over the thalamus. Fourth Ventricle The tela choroidea of the IVth ventncle forms over the IVth ventricle, again as a duplication of the pia mater, because of the apposition of the undersurface of the cerebellum to the upper surface of the hindbrain E. The roof of the hindbrain is reduced to an epithelial layer which is pushed inward into the ventricle by the vascular loops arising in the tela. The tela choroidea of the IVth ventricle only consists of pia, as the arachnoid does not adhere to the surface of the cerebellum, but is stretched across the cerebromedul-lary cistern. At the attachment of the tela, above a narrow myelinated lamella, the obex D13, lies the median foramen of Magendie D14. The lateral apertures of Luschka. through which protrudes the lateral end of the choroid plexuses, open from the IVth ventricle on both sides (Bochdalek's flower basket D15). Cerebrospinal Fluid System Histology of the Choroid Plexus The treelike branching of the plexus A produces a very large free surface. Each branch contains one or more vessels, arteries, capillaries and thin-walled venous cavities. The vessels are surrounded by a loose network of collagen fibers B1 and this, in turn, is covered by the plexus epithelium B. The plexus epithelium consists of a single layer of finely ciliated cuboid cells. The cytoplasm of the cells contains vacuoles and coarse granules, lipid and glycogen inclusions. The choroid plexus is considered to be the site of cerebrospinal fluid production. A transfer of fluid from the vascular system of the plexus occurs through its epithelium into the ventricles. It is not certain whether the cerebrospinal fluid is secreted by the plexus epithelium or is dialyzed by it. i. e, a type of selective filtration. Like the pia-arachnoid and dura, the plexus is richly innervated (branches from the trigeminal and vagus nerves and autonomic fibers). The plexus and the meninges, therefore, are sensitive to pain, while the substance of the brain is largely insensible. Ependyma The walls of the ventricular system are covered by a single layer of cells, the ependyma C. Each ependymal cell has a process that runs radially into the brain substance, the ependymal fiber. The free surface, which is directed toward the ventricle, often carries a few cilia. The cell bodies contain small granules blepharoblasts C2, which usually are arranged in a row beneath the surface. An electron micrograph shows irregular, vesicle-containing evaginations D3 on the ventricular surface of the ependymal cells. The cilia D4 contain a central fiber D5, around which a number of peripheral fibers D6 are arranged in a circle The base of each cilia is surrounded by a granular zone D7, into which radiate numerous small roots D8. On one side is the basal foot D9, which may be of importance in controlling the direction of the ciliary beat. Ependymal cells are connected with each other laterally by zonulae adherentes D10 and zonulae oc-cludentes D11, which separate the CSF space imperviously from the brain tissue. Nerve cell processes D12. Beneath the ependyma lies a sparsely cellular layer of radially or horizontally running glial fibers C13, and adjacent to it is the subependymal glial cell layer C14. In addition to astrocytes, it contains transitional forms between ependymal cells and astrocytes and clusters of small dark cells. The subependymal zone, in which the continuous replenishment of glial cells is thought to occur, contains therefore mainly undifferentiated types of glia. The structure of ventricular walls differs markedly in different regions. In certain areas the ependymal covering or the subependymal glial fiber layer may be completely absent. The subependymal glial cell layer is best developed over the head of the caudate nucleus and at the base of the anterior horn, but is absent over the hippocampus. Cerebrospinal Fluid System Circumventricular Organs In the lower vertebrates, the ependy-ma has secretory and probably also receptor functions. This has led to the development of specialized structures, which are still demonstrable in mammals. To these so-called circumventricular organs belong the vascular organ of the lamina terminalis. the subfornical organ, the paraphysis, the subcommissural organ, and the area postrema. The epiphysis and hypophysis, which really should be included with these organs, are not discussed here. In man these organs are regressive and some are only present temporarily during embryonic development. Their function is unknown, although there are hypotheses concerning their importance for the regulation of CSF pressure and composition and about their relationships to the neuroendocrine system of the hypothalamus. Their position at narrowings in the ventricular system, their marked vascularity and the presence of cavities (so-called 'fluid clefts') is striking Vascular Organ of the Lamina Terminalis AD 1 This lies in the lamina terminalis, the rostral end of the llird ventricle, between the rostral commissure and the chiasma. There is an outer, very vascular zone beneath the pia and an inner zone consisting mainly of glia. The vessels form a dense plexus with sinuslike dilatations. Nerve fibers from the supraoptic nucleus, which contain Gomori-positive material, run in the inner zone. In addition it receives peptidergic fibers from the hypothalamus. Subfornical Organ BD2 The subfornical organ lies as a small pinhead-sized nodule between the two foramina of Monro in the roof of the iilrd ventricle, at the oral end of the tela choroidea. Besides glial cells and isolated nerve cells it contains large round elements, whose neuronal character is disputed. Electron microscopy has demonstrated ependymal canaliculi, which extend inward from the outer surface and are connected to the intercellular spaces. Vascular loops from the tela choroidea penetrate into the interior of the subfornical organ. Peptidergic nerve fibers (somatostatin, luliberin) terminate on the capillaries and in the region of the ependymal canaliculi. Area Postrema CD3 The area postrema consists of two slender, symmetrical structures on the floor of the rhomboid fossa, which lie at the funnel shaped entrance to the central canal. The loose tissue in this region contains many small cavities. It consists of glia and so-called parenchymal cells, which are now generally regarded as neuronal elements. The tissue contains many convoluted capillaries, which appear extensively fenestrated in electron micrographs. The area postrema is, therefore, one of the few areas of the brain in which the blood brain barrier is readily permeable. Paraphysis and Subcommissural Organ In man these two structures only appear transitorily during embryonic development. The paraphysis forms a small saclike evagi-nation in the root of the llird ventricle caudal to the foramina of Monro The subcommissural organ D4 consists of a complex of cylindrical ependymal cells beneath the epithalamic commissure. They produce a secretion which does not disperse in the cerebrospinal fluid but thickens to form a long, thin thread. Reissner"s fiber In animals, in which the central canal is not obliterated, this fiber extends into the lower spinal cord. Cerebrospinal Fluid System Meninges The brain is enclosed by mesodermal coverings, the meninges. The outer layer is the tough pachymeninx or dura mater A1 and the inner, the lep-tomeninx, is divided into the arachnoid A2 and the pia mater A3. Dura Mater The dura covers the inner surface of the skull and also forms the periosteum. Sturdy septa extend from it deep into the cavity of the skull. Between the two hemispheres invaginates the falx cerebri B4. Its attachment begins at the crista galli and extends over the crista frontalis backward to the internal occipital protuberance, where it merges into the tentorium cerebelli B5, which extends to both sides. The falx divides the superior part of the cranial cavity in such a way that each hemisphere is secured in its own space. The tentorium cerebelli stretches like a tent over the cerebellum lying in the posterior cranial fossa. It is attached along the transverse sulcus of the occipital bone and the upper margin of the petrous bone. Orally it leaves a wide opening for the passage of the brain stem B6. The falx cerebelli projects into the posterior cranial fossa from the lower surface of the tentorium and the occipital crest. The large venous channels, the sinuses of the dura mater, are embedded in the two laminae of the dura. Section through the superior sagittal sinus B8 and the trans verse sinus B 9. Certain structures lie in dural pockets and are separated from the remainder of the cranial cavity. Thus, the dia-phragma sellae B10 stretches over the sella turcica, and is penetrated by the hypophysial stalk through the diaphragmatic hiatus B11. On the anterior surface of the petrous bone, the trigeminal ganglion is enclosed in a dural pocket, the trigeminal cave (of Meckel). The Arachnoid The arachnoid membrane A 2 adheres closely to the inner surface of the dura and is only separated from it by a potential space, the cavum subdurale A12. It encloses the subarachnoid space, which contains the cerebrospinal fluid, the cavum subarachnoidal A13, and is connected to the pia by trabeculae A14 and septa, which form a dense network in which there is a system of communicating cavities. Pedunculated, mushroomlike protrusions of the arachnoid project into the principal venous sinuses, the Pac-chioni's granulations (granulations arachnoideales) A15. They consist of an arachnoid network and are covered by mesothelium. The dura, which still encloses them, is reduced to a membrane. The majority of arachnoid villi are present around the superior sagittal sinus A16, in the lateral lacunae A17, and less commonly at the points of exit of the spinal nerves. It is thought that cerebrospinal fluid enters the venous circulation through the villi. In older people the villi may penetrate into the bone (foveolae granulans) and invaginate into the diploic veins A18. Scalp A19, Bones A 20, Diploe A 21. Pia Mater The pia A3 is the covering that carries the blood vessels. It borders directly on the brain substance and forms the mesodermal side of the pia glial barrier Vessels leave the pia to enter the brain and are accompanied by a thin sheath of pia for some distance. The List of the used literature. 1. An introductions to clinical neurology: path physiology, diagnosis and treatment 1998 2. Parkinsons diseas and Movement Disorders. 1998 3. Neuroscience: Exploring the Brain. 1996 4. Anatomical Science. Gross Anatomy. Embryology. Histology. Neuroanatomy. 1999 5. Headache. Diagnosis and Treatment. 1993 6. Rohkamm, Color Atlas of Neurology © 2004 Thieme 7. Color Atlas of Human Anatomy Sensory organs And Nervous System (Werner Kahle) - 1986 http://www.medmedia.ru/pediatrics/Detskieinfekcionnyebolezni/a3800382 http://alexmorph.narod.ru/atlas/cns/cns.htm http://fanat-nevro.narod.ru/mening/treat.htm