Download 2. Parkinsons diseas and Movement Disorders. 1998

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