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Emphasizes the unique character of the nervous system and the biological attributes that it shares with other tissues.
NS – the most complex structure in the body
Interconnected with different organs & capable of rapid communications
CENTRAL NERVOUS SYSTEM
CELLS OF THE NERVOUS SYSTEM DEMYELINATING DISEASE CONGENITAL MALFORMATION TRAUMA CIRCULATORY DISORDERS CSF INFECTIOUS DISEASE SPONGIFORM ENCEPHALOPATHIES NEURONAL STORAGE DISEASE METABOLIC NEURONAL DISEASES VITAMIN DEFICIENCIES DEGENERATIVE DISEASES NEOPLASIA
NEURONS Mature neurons do not divide The human body loses neurons – aging process Neurons cannot regenerate axons Not efficiently remyelinated after injury ANATOMY OF NEURONS Nuclei – centrally located. contain nucleolus Cytoplasm .abundant and the ribosome-studded endoplastic reticulum forms prominent basophilic granules – Nissl bodies Cytoplasmic pigment Substantia nigra Locus ceruleus Rich in neurofilaments . I. round.CELLS OF THE Nervous System I.
CELLS OF NERVOUS SYSTEM ANATOMY OF NEURONS Dendrites – branching projections in the cell body Best demonstrated by Silver impregnation Axon – may or may not have myelin sheath REACTIONS OF NEURONS Some are reversible Others forecast cell death .
CHROMATOLYSIS Swell – Imbibe fluid Nissl substance is displaced centrifugally and becomes marginated near the plasma membrane Nucleus assumes eccentric position Reversible except when the axonal transection closely approximated the body May signal serious metabolic disturbance poliovirus .NEURONAL REACTIONS TO INJURY 1.
NEURONAL REACTION TO INJURY 2.disappear . NEURONOPHAGIA Gross: reduction in brain Injuries that kill neurons weight or selective decrease abruptly create cellular debris in mass of specific region which elicits phagocytosis Huntington disease – Process of aggregation of caudate nucleus inflammatory cells about a dead neuron coupled with Cell shrivels & become phagocytosis hyperchromatic . ATROPHY 3.
INTRANEURONAL INCLUSIONS Nuclear & Cytoplasmic inclusions appear in neurons : viral encephalitides and degenerative diseases .NEURONAL REACTION TO INJURY 4.
CELLS OF THE NERVOUS SYTEM II. also neuroectodermal in origin ANATOMY Fibrillary astrocytes – white matter Protoplasmic astrocytes the gray matter Rounded nucleus 7-10 μm in diameter Homogenous chromatin pattern . ASTROCYTES ‘Star-shaped cells.
ASTROCYTIC REACTION TO INJURY ATROGLIOSIS (GLIOSIS) Multiply in and about localized sites of tissue injury Proliferation of fibrillary astrocytes is induced over a period of several days Glial scar – cell processes Astrogliosis marks certain generalized disease states Capricious Gliosis General Paresis Tertiary syphilis Pick disease Disease that progress with little attention by astrocytes Creutzfeldt-Jakob disease Alzheimer disease .
.ASTROGLIOSIS This section of a brain with Krabbe's disease shows severe This section of a brain with Krabbe's disease shows severe astrogliosis (black arrows) and globoid cells around blood vessels (blue arrows).
ASTROCYTIC REACTION TO INJURY Fibrillary astrocytes Prone to neoplastic transformation Responsible for dominant family of gliomas Protoplasmic astrocytomas uncommon antecedents of cancer .
5-20 nm amorphous structures with basophilic and argentophilic staining affinities. which are composed of carbohydrate and protein Light microscope: extracellular ‘E’ microscope: within glial processes of astrocytes .ASTROCYTIC REACTION TO INJURY Corpora amylacea Appear within the brains of all aged persons with predilection for the subpial and subependymal regions Spherical.
CELLS OF NERVOUS SYSTEM III. OLIGODENDROGLIA Myelin-producing cells of the CNS and are related to astrocytes – both are neuroectodermal in origin Have dark rounded nuclei which resembles those of lymphocytes Thin rim of cytoplasm surrounds the nuclues .
lines: the four ventricular chambers Aqueducts of sylvius Central canal of the spinal cord Filum terminale Modulate fluid transfer between the CSF and the cells of nervous system .CELLS OF THE NERVOUS SYSTEM IV. EPENDYMAL CELLS Single layer of ependymal cells –cuboidal or flat.
some viral infections target the ependymal cells: Aquiductal stenosis Congenital hydrocephalus Ependymomas – exophytic masses protruding into a ventricle (4th ) Also constitute a common intramedullary tumor of the spinal cord and filum terminale .EPENDYMAL CELLS During gestation.
& accounting for 5% of all glial multivesicular bodies cells Gray matter: appear as isolated cells or as neuronal or vascular satellites White matter: predominantly perivascular .CELLS OF NERVOUS SYSTEM V. MICROGLIAL CELLS Microglia often contains Phagocytic elements of the CNS lipofuscin. dense bodies.
With Silver: linear form appears with fine lateral projections . elongated nuclei surrounded by a thin rim of cytoplasm.MICROGLIAL CELLS ANATOMY: By H&E: hyperchromatic.
rickettsial and protozoal infection REACTIVE MICROGLIA – exhibit a prominent elongated nuclues: rod cells With necrosis. they become distended by lipid droplets and other cellular debris: gitter cells .MICROGLIAL REACTION TO INJURY PATTERNS OF REACTIONS: Focal microglial nodules Diffuse microgliosis MICROGLIAL NODULES – formed by microglia and astrocytes and characterize viral.
CONGENITAL MALFORMATIONS A congenital anomaly is the result of an interruption in the proper completion of a single developmental sequence .
CONGENITAL MALFORMATIONS I. NEURAL TUBE DEFECTS (DYSRAPHIC STATE) -Refers to the defective closure of the dorsal aspect of the vertebral column .
A. SPINA BIFIDA An NTD that is most common in the lumbosacral region Spina Bifida occulta: restricted to the vertebral arches. asymptomatic. whereas the apex is usually ulcerated . dimple or small tuft of hair Meningocoele: more extensive bony and soft tissue defect permits protrusion of the meninges as a fluid-filled sac. The lateral aspect of the sac are characteristicaly covered by skin.
SPINA BIFIDA Meningomyelocoele: refers to a more extensive defect that exposes the spinal canal and causes the nerve roots. the spinal cord appears as flattened. often without a recognizable spinal cord . ribbon-like structure Rachischisis: the spinal column is converted into a gaping canal. particularly those of the cauda equina to be entrapped in subcutaneous scar tissue Characteristically.
meningomyelocoele .SPINA BIFIDA PATHOGENESIS: Failure of closure of the neural tube Maternal Folic acid deficiency CLINICAL FEATURES: Absence of symptoms – occulta Lower limb paresis or paralysis Sensory loss Rectal & vesicle incontinence .
NEURAL TUBE DEFECTS B.5 – 2.0 / 1000 births with Female predominance Stillborn or die within 1st few days of life . ANENCEPHALY Congenital absence of all or part of the brain 0.
cerebrovasculosa .ANENCEPHALY PATHOGENESIS: Closure of the anterior neuropore Disturbed angiogenesis PATHOLOGY: Absence of the cranial vault & the cerebral hemispheres are represented by a discoid mass or highly vascularized poorly differentiated neural tissue .
MALFORMATION OF SPINAL CORD SYRINGOMYELIA: Pathology: A Tubular cavitation (syrinx) extends for variable distances along the entire length of the spinal cord which may or may not communicate with the central canal damage to the spinal cord due to the formation of a fluid-filled area within the cord Cause: Trauma. tumors Syringobulbia – Variant where slit-like cavities are located in the medulla . ischemia.
ARNOLD-CHIARI MALFORMATION The brainstem & cerebellum are compacted into a shallow. bowl-shaped posterior fossa with a low positioned tentorium Usually associated with lumbosacral meningomyelocoele PATHOGENESIS: Meningomyelocoele serves to anchor the lower end of the spinal cord and that the downward growth of the vertebral column creates traction on the medulla .
often reaching the level of C3 to C5 The herniated tissue is bound in position by thickened meninges and shows pressure atrophy with depletion of Purkinje and granular cells The brainstem is also displaced caudally .ARNOLD-CHIARI MALFORMATION PATHOLOGY: The caudal aspect of the cerebellar vermis is herniated through an enlarged foramen magnum and protrudes as a tongue on the dorsal aspect of the cervical cord.
CONGENITAL HYDROCEPHALUS Excessive amount of CSF in varied location and have many causes Congenital Atresia of Aqueduct of sylvius – most c0mmon cause Midbrain – multiple atretic channels Aqueduct stenosed by periaqueductal gliosis : transplacental transmission of viruses known to induce ependymitis .
Associated with mental retardation Polymicrogyria – presence of small and excessive gyri Pachygyria – the gyri are reduced in number and unusually broad Lissencephaly – The cortical surface of the cerebral hemispheres is smooth or only lightly furrowed Almost all patients with Lissencephaly (92%) shows deletion in the region of LIS1 gene on chromosome 17p13.DISORDERS OF CEREBRAL GYRI .3 .
a highly patterned event of the trimester of embryonic development Primitive neurons move centrifugally from the germinal mantle to populate the cortex Number of neurons and their positions in the cortex determine factors in the redundancy of the cortical mantle which initiates the infolding that creates sulci .DISORDERS OF CEREBRAL GYRI PATHOGENESIS Gyral malformations arise from disturbances in neuronal migration.
DISORDERS OF CEREBRAL GYRI Heterotopia – a focal disturbance in neuronal migration that leads to nodular collections of ectopic neurons … white matter Associated with: mental retardation seizures Migrational disturbances is associated with: Maternal alcoholism .
CONGENITAL DEFECTS ASSOCIATED WITH CHROMOSOMAL ABNORMALITIES Derangements of larger chromosomes Incompatible with sustained intrauterine life Affected fetuses are aborted .
DOWN SYNDROME Trisomy 21 – mental retardation. with disproportionately slender superior temporal gyri . and the organ is shortened in its anteroposterior dimension Simple gyral pattern. and a variety of anomalies Weight of the brain is moderately reduced. distinctive facial features.
and cleft palate Extremities exhibit polydactyly and “rocker bottom” feet . cyclopia. microphthalmia. harelip. and extremities The complex is dominated by holoprosencephaly. > female Congenital deformities involve: brain.TRISOMY 13-15 1 per 5000 births. low-set ears. facial features. arrhinencephaly.
TRISOMY 13-15 HOLOPROSENCEPHALY – refers to a microcephalic brain that features an absence of the interhemispheric fissure Horse-shoe shaped cerebral hemispheres Common ventricular chamber The base of the ventricular chamber is formed by the bilobed structures of the caudate nuclei and thalami Rarely compatible with life beyond a few weeks or months .
TRISOMY 13-15 ARRHINENCEPHALY – The absence of the olfactory tracts and bulbs (rhinencephalon) is associated with holoprosencephaly or occurs as a solitary malformation .
CAUSE: disruption to development of the fetal brain which may be related to chromosome errors. genetic factors. ABSENCE OF CORPUS CALLOSUM – regular feature of holoprosencephaly Associated with seizures Its absence permits the lateral ventricles to drift outward and upward – radiographically diagnostic . prenatal infections.Agenesis of the corpus callosum is a birth defect in which this structure in the brain is either partially or completely missing. or other factors related to prenatal environment.
abnormal motor activity or sensory or mental disturbances Idiopathic – sporadic. cerebellum. hereditary PATHOLOGY: neuronal loss & reactive gliosis Affected areas: hippocampus. Brain scar from penetrating wound . transient disturbances in brain function that are expressed as impairment in or loss of consciousness. AV mal.EPILEPSY Paroxysmal. thalamus and cerebral neocortex Acquired Seizures: Intracranial tumor.
" The "go" messages are triggered by a different type of neurotransmitter that promotes message transfer (B). The charged signals they set off are positive. which tells the receiving neuron to pass on the message. When there is not enough GABA a person can have a seizure because receiving neurons can be flooded with signals that say "pass on this message. the neurotransmitter GABA does its part to make sure the system stays in synch by triggering signals in the form of charged particles (A). This tells the neuron to not pass on the message. It causes a large concentration of negatively charged chloride particles (Cl-) to enter the receiving neuron. more positively charged sodium particles (Na+) enter the neuron. . This time.EPILEPSY A seizure occurs when the message delivery system becomes unbalanced. Under normal circumstances.
A result of a blow to the side of the head that fractures the temporal bone Must be treated promptly . EPIDURAL HEMATOMA Accumulation of blood between the calvarium & the dura.TRAUMA I.
EPIDURAL HEMATOMA PATHOGENESIS: Fracture of the temporo-parietal bone causing the transection of the branches of the middle meningeal artery (occupy the space between the dura & the calvarium) Temporal bone . .one of the thinnest bones of the skull The initial 4-8 hrs : asymptomatic The earliest volumetric adjustment – displacement of CSF through the aperture in the tentorium Symptoms: volume of the hematoma 30-50ml.
The heart slows down to increase ventricular filling & myocardial contraction become forceful > BP systolic is increased .EPIDURAL HEMATOMA PATHOLOGY When the increased ICP exceeds the venous pressure the large venous sinuses are compressed creating cerebral ischemia & hypoxia Clinical: confusion & disorientation CUSHING REFLEX: Protective response that augment cerebral circulation and increased oxygenation.
EPIDURAL HEMATOMA Continued Bleeding > Decline in the level of consciousness > hge & necrosis appear > the regional injury to the reticular formation becomes irreversible >> Death Epidural Hematomas are invariably progressive & when not recognized early & evacuated. . becomes fatal in 24-48 hrs.
vehicular accidents.SUBDURAL HEMATOMA Accumulation of blood in the subdural space as a consequence of bleeding from torn bridging veins Significant cause of death after head injuries from falls. assaults. and sporting mishaps Cerebral hemispheres are immersed in CSF Blood vessels and cranial nerves Free to float in an anteroposterior direction .
SUBDURAL HEMATOMA Venous drainage from the cerebral hemispheres flows upward through veins in the pia Parasagittal region Subarachnoid space Arachnoid Traverse the theoretical subdural space Dura sinus .
SUBDURAL HEMATOMA Arachnoid applied to the dura Dural border cell (DBC) Arachnoid barrier cell (ABC) Intercellular junctions .
SUBDURAL HEMATOMA Hematomas and hygromas separate the meninges along the path of least resistance Frontal or occipital portion/stationary head Cerebral hemispheres are displaced Soft cerebral tissues become compact and then recoil. rippled movement in the cerebral parenchyma .
SUBDURAL HEMATOMA Dura – skull Arachnoid – cerebrum Disparate movement of membranes produces shearing effect localized to the Dura Border Cell layer Cortical veins are torn Compression of severed bridging veins initiates thrombosis .
SUBDURAL HEMATOMA Bleeding from outer membrane Vulnerable to minor trauma Hyperosmotic state Diaphanous arachnoid Contiguous fibroblastic proliferation Absence of blood in the CSF does not negate the presence of a subdural hematoma .
SYMPTOMS: SUBDURAL HEMATOMA Protean Stretching of meninges – headaches Pressure on motor cortex – contralateral weakness Focal irritation of cortex – seizures Impair cognitive function Dementia Enlarge mass and lethal transtentorial herniation .
SUBARACHNOID HEMORRHAGE Bleeding into the subarachnoid space of any cause Traumatic head injuries. Laceration 2/3 of cases reflect a pre-existing arterial aneurysm 10% AV Mal is demonstrated . Cerebral contusion .
The position of a contusion is determined by the direction of the force & the intracranial anatomy .CEREBRAL CONTUSION A bruise of the cortical surface of the brain as a result of head trauma MECHANISM OF CEREBRAL CONTUSION: The cerebral hemispheres float in the CSF Rapid deceleration or less commonly acceleration of the skull cause the cortex to impact forcefully into the anterior & middle fossae.
A cerebral contusion is basically a bruise of the brain. With trauma, the tissue can become damaged and swollen and blood vessels within the tissue can break, leading to oozing of blood into the tissue. When a traumatic brain injury occurs, the brain moves around inside the skull. Direct impact or the sloshing of the brain and hitting the inner part of the skull can cause this type of injury to the brain. The brain tissue itself is quite fragile and easily injured. With enough force applied to the head, the brain can hit the side of the skull, leading to a cerebral contusion.
coup is the primary impact on the head, caused by whatever hit the head during the trauma. When this force is applied, the brain slides back and forth inside the skull, frequently hitting the bone on the other side of the head. contra coup is opposite the side of the initial impact. the most common location for these contusion injuries is in the area of the temporal lobes and lower frontal lobes.
PENETRATING WOUNDS Causes: Bullets / knives enter the cranium with variable velocities Seizures – threat Collagenous tissue Fibroblasts .
subluxation of spine HYPEREXTENSION INJURY – tears spinal ligament HYPERFLEXION INJURY – impact forces on vertebral body down upon the underlying one . fracturedislocations.SPINAL CORD INJURIES Morbidity – paraplegia or quadriplegia Penetrating wounds – stab wounds. bullets Indirect injury – vertebral fractures.
the person may be able to feel parts of the body that cannot be moved and there may be more functioning on one side of the body than the other.complete and incomplete. A complete injury means that there is no function below the level of the injury (no sensation and no voluntary movement) and both sides of the body are equally affected. An incomplete injury means that there is some functioning below the primary level of the injury.SPINAL CORD INJURY We can divide SCI into two categories . . One limb may be able to be moved more than the other.
SPINAL CORD INJURIES .
SPINAL CORD INJURIES Concussion of spinal cord – mildest injury Transient and reversible disturbance of spinal cord Contusion of spinal cord – more severe trauma Myelomalacia Hematomyelia Lacerations and transections of the spinal cord – penetrating wounds Irreversible. complete loss of function .
SPINAL CORD INJURIES The vertebral column in an adult typically consists of 33 vertebrae arranged in five regions: Seven (7) cervical vertebra twelve (12) thoracic vertebra five (5) lumbar vertebra five (5) fused sacral vertebrae four (4) fused coccyx vertebrae In adults the vertebral column is approximately 72-75cm in length and serves to: Protect the spinal cord and spinal nerves Support the weight of the body Provides a partly rigid and flexible axis for the body and a pivot point for the head Play an important role in posture and motion (movement from one place to another) .
CIRCULATORY DISORDERS VASCULAR MALFORMATION FOUR MAJOR CATEGORIES: AV-MAL – most common & w/ greatest significance Evolves during embryonic dev as a result of a focal absence of a capillary bed which direct communication between cerebral arteries an veins Located in the cerebral cortex & the contiguous underlying white matter Enlarges – recruitment of the tributary vessels .
Epilepsy focal neurological disturbances dilated. thickened blood vessels lacking elastic lamina and without intervening brain parenchyma .VASCULAR MALFORMATION CAVERNOUS ANGIOMA: Less common Formed by large vascular spaces compartymentalized by prominent fibrous walls Asymptomatic Intracranial bleed.
VASCULAR MALFORMATION TELANGIECTASIA : Focal aggregate of uniformly small vessels with intervening neural parenchyma may initiate seizures but rarely ruptures VENOUS ANGIOMA: Focus of a few enlarged veins distributed randomly in the spinal cord or brain asymptomatic .
ANEURYSMS Weakness in arterial walls exploited by intravascular pressure CAUSES: Developmental Defects – gives rise to Berry Aneurysm (saccular medial defect) Atherosclerosis Hypertension – associated with lipohyalinosis of cerebral arterioles and induces Charcot-Bouchard aneurysm Bacterial infection – leads to mycotic aneurysm Trauma – causes Dissecting Aneurysm .
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BERRY ANEURYSM PATHOGENESIS: The consequence of arterial defects that originate during the embryonic development when the bifurcation of the artery creates a Y-shaped configuration The muscle layer of the parent vessel & that of the 2 branches are separate and may fail to interdigitate adequately across the notch of the Y. the internal elastic membrane & a slender coating of adventitia Increase Pressure > internal elastic membrane degenerates & fragments > endothelium yields >Saccular aneurysm formed by adventitia . PATHOLOGY: a point of muscular weakness bridged only by endothelium.
Communicating A Complex of the int.Ant. carotid .Carotid system: At the union of Ant. Cerebral & ant.ant. Choroidal A Trifurcation of the middle cerebral A CLINICAL: Rupture – results in life threatening subarachnoid hge with a 35% mortality during the initial hge . Cerebral..post comm.BERRY ANEURYSM > 90% .
BERRY ANEURYSM .
BERRY ANEURYSM CLINICAL: Rupture – results in life threatening subarachnoid hge with a 35% mortality during the initial he Sudden severe headache – heralds the onset of subarachnoid he & maybe followed by coma Patients who survive for 3-4 days – manifest progressive decline in consciousness – attributed to arterial spasm & consequent cerebral ischemia & infarction Survivors – re-bleed & prognosis is worse .
ATHEROSCLEROTIC ANEURYSM Caused by atherosclerosis localized in the major cerebral vessels (vertebral. basilar. the vessel elongates Rarely ruptures Major complication is Thrombosis Pontine infarction – often sequelae of aneurysm in the basilar A .& internal carotids) Fibrous replacement of the media & destruction of the internal elastic membrane weakens the arterial wall & permits aneurysm dilatation Characteristically fusiform & as they enlarge.
MYCOTIC ANEURYSM Infections of arterial walls result from septic emboli with origins in an infected heart valve Emboli - Carotid circulation - lodges in a branch of Middle Meningeal Artery at the origin of the short penetrating carotid vessel -- bacteria proliferate inflammation - destroys the integrity of the arterial wall - aneurysm - rupture (seen as intracerebral or subarachnoid hge) - bacteria / microorganism released - cerebral abscess or suppurative meningitis .
CEREBRAL HEMORRHAGE Spontaneous – no trauma / vascular anomaly / consequence of long-standing hypertension Strokes or apoplexy – include occlusive cerebrovascular lesions ( infarcts) HYPERTENSIVE INTRACEREBRAL HEMORRHAGE ORDER OF FREQUENCY: Basal ganglia-thalamus 65% Pons 15% Cerebellum 8% .
CEREBRAL HEMORRHAGE HYPERTENSIVE INTRACEREBRAL HEMORRHAGE Charcot-Bouchard aneurysm – formed by the weakening of the wall Small fusiform aneurysms located on the trunk of a vessel rather than at the bifurcation & are disposed to rupture & he Onset of symptoms – abrupt & weakness dominates When hge is progressive. Death occurs within period of hours or several days .
CEREBRAL HEMORRHAGE INTRAVENTRICULAR HEMORRHAGE Rupture of a vessel into a ventricle rapidly distends the entire ventricular system with blood. Death : Distension of the 4th ventricle & compression of the vital centers of the medulla PONTINE HEMORRHAGE Loss of consciousness reflects damage to the reticular formation – overshadows all other specific cranial nerve deficits Patients rarely survives .
CEREBRAL HEMORRHAGE CEREBELLAR HEMORRHAGE Abrupt ataxia. accompanied by severe occipital headache and vomiting Compression of medulla – herniation of cerebellar tonsils into the foramen magnum OTHER CAUSES: Leakage from AV-Mal Erosion of vessels by a 1o or 2o neoplasm Bleeding diathesis – thrombocytopenic purpura Endothelial injury by microorganism: rickettsia Embolic infarction .
ISCHEMIA & INFARCTION Inadequate perfusion of the brain .
.STROKE cerebrovascular accident (CVA). It may be due to either a prolonged lack of oxygenrich blood (cerebral ischemia or cerebral infarction) or bleeding into or around the brain (cerebral hemorrhage). a stroke is a potentially fatal event in which part of the brain does not get enough oxygen.
and it accounts for about 80% of all strokes. .CEREBRAL ISCHEMIA (INFARCTION) The most common type of stroke occurs when a blood vessel becomes plugged. The plug can originate in an artery of the brain or it can originate somewhere else in the body.emboli Strokes caused by emboli from the heart are often seen in: people with an irregular heartbeat -atrial fibrillation after a heart attack or heart surgery Ischemic strokes are largely preventable if risk factors are recognized early and managed. until it lodges in a blood vessel. where it breaks off and travels up the arterial tree to the brain. "traveling clots" . often the heart.
This is when an aneurysm.CEREBRAL HEMORRHAGE Rupture of a blood vessel can produce a bleeding type of a stroke. The main thing you can do to prevent a cerebral hemorrhage is to control high blood pressure. but they are the most deadly. of a blood vessel in the brain ruptures. . Account for about 15-20% of all strokes. or an out-pouching.
PART II .
a consequence of contiguous infection: Chronic sinusitis / Mastoiditis Dura – substantial barrier to infection & inflammation is usually restricted to the outer surface .INFECTIOUS DISEASES MENINGITIS Leptomeningitis – denotes an inflammatory process that is localized to the interfacing surfaces of the pia and arachnoid CSF – excellent culture medium for most microorganisms Pachymeningitis – Inflammation of the dura.
SUPPURATIVE MENINGITIS Purulent meningitis (suppurative meningitis) is a type of meningitis characterized by a purulent exudate within the subarachnoid space Most definitive index of meningitis .BACTERIAL MENINGITIS 1.PMNs .
SUPPURATIVE MENINGITIS .
SUPPURATIVE MENINGITIS E. influenza – maximal in 3mos – 3 yrs Strep pneumoniae Pts w/ basilar skull fracture. coli – prime cause in NBs Cross-placental transfer: requires IgM H. malaise. the 2nd most frequent cause of purulent meningitis. Neisseria meningitides – frequents the nasopharynx Airborne – transmission Initial phase – bacteremia: fever. petechial rash Maybe associated with lethal adrenal hges (WaterhouseFriderichsen syndrome .
2nd peak in elderly Neonate & Children Group B Strep.ACUTE SUPPURATIVE MENINGITIS Severe infection. headache. almost always caused by bacterial infection Highest peak in Children . E. gm – rods Very ill. pneumoniae. N. neck stiffness & photophobia . Young Adults Strep. Children. coli. with fever. Listeria Older infants. prostration. meningitidis Older Adults S. Pneumonia.
Paranasal Sinuses Leak.SUPPURATIVE MENINGITIS PATHOGENESIS: Hematogenous dissemination (Most Common) From bacteremia Near organ infected Sinusitis. Otitis media. Brain Trauma From Congenital Developmental Malformation Spinal Meningocoele. Mastoiditis. Sinus Tract Cerebral surgery & lumbar puncture Iatrogenic .
hydrocephalus (impaired CSF Flow) Brain abscess .GROSS: Subarachnoid space contains cream colored purulent exudate Secondary thrombosis of the superficial vessels & cerebral ischemic damage.
TUBERCULOUS MENINGITIS .
TB MENINGITIS .
POTT DISEASE – TB OF SPINAL COLUMN .
Inclusion bodies in viral encephalitides
Herpes simplex (Cowdry Type A)
Cytomegalovirus Rabies Negri bodies Progressive multifocal leukoencephalopathy Subacute sclerosing panencephalitis
Neuron or astrocyte Neuron Oligodendroglia
Cryptococcus neoformans (Fungal) Inhalation of contaminated particulates
Birds excreta – inhaled- pneumonitis
– bloodstream – intracranial compartment Gelatinous cysts – brain parenchyma
Amoebic Meningoencephalitis Naegleria & Acanthamoeba – olfactory nerves to cribriform plate – intracranial compartment after swimming .
enters the bloodstream from the primary chancre .SYPHILITIC MENINGITIS Treponema pallidum .
SPIROCHETAL.CSF PROFILE PROFILE COMMON CAUSES PURULENT PMNs LOW GLUCOSE INCREASED CHON LYMPHOCYTIC LOW GLUCOSE LYMPHOCYTIC NORMAL GLUCOSE MOD. INCREASED CHON BACTERIAL TB. FUNGAL. SARCOIDOSIS. CA VIRAL (ASEPTIC) .
Dermoid & Epidermoid cysts. Dysgerminomas Retained Embryonal Structures – Paraphyseal cysts Metastasis .NEOPLASIA Nueroectoderm – Gliomas Mesenchymal Structures – Meningiomas & Schwannomas Ectopic Tissues – Craniopharyngiomas. Lipomas.
Astrocytomas Oligodendroglia.oligodendrogliomas Ependyma .ependymomas Meningiomas – 20% All the others – 20% Difficulty: Well-diff – Normal Tissue Anaplastic tumors – Not resemble nervous tissue .NEOPLASIA 2 % of all aggressive tumors Frequent in childhood Gliomas – 60% Astrocytes .
Malignant Requires Qualification when used in reference to gliomas Age of the Patient & Location Predictable geographic location Astrocytic tumors : Cerebral hemispheres. middle life & old age Cerebellum & pons – Childhood Spinal cord – in young adults .NEOPLASIA: REMINDERS Benign Vs.
NEOPLASIA Oligodendrogliomas Predominantly involve the cerebrum – Adults Ependymomas Highest incidence in the 4th ventricle Intramedullary lesion derived from the lining of the spinal canal & filum terminale Lowest incidence – Lateral ventricle Meningiomas – Arise from widely distributed arachnoid villi but with preferred sites of origin .
NEOPLASIA: SYMPTOMS: Neurological deficit – sensory or motor Cognitive functions Seizures Meningiomas Well-diff Gliomas: Astrocytomas Oligodedrogliomas Gangliomas Increase intracranial pressure – Edema + Mass Headache Vomiting .
TRANSTENTORIAL HERNIATION Medial aspect of the hippocampus (uncus) herniates into the aperture of the tentorium Interferes with the circultory dynamics of the midbrain & causes a decline in the level of consciousness – result of the impaired function of the reticular formation Compresses the 3rd nerve against the edge of the tentorium – 3rd nerve palsy – FIXED DILATED PUPIL Irreversible Midbrain necrosis & hemorrhage – permanent loss of consciousness then DEATH .
FORAMEN MAGNUM HERNIATION Cerebellar tonsils herniate into the Foramen magnum due to increase pressure in the posterior fossa Compresses the cardiac & respiratory centers Death .
SUBFALCINE HERNIATION The cingulate gyrus herniates beneath the falx – results in infarction of areas supplied by the pericallosal vessels >> Weakness or sensory loss in the legs .
pons & cerebellum – 1st 2 decades of life Spinal cord – pred in the thoracic & cervical regions – young Adults .TUMORS FROM ASTROCYTES 1. walls of the 3rd ventricle. ASTROCYTOMA A glioma composed of well-differentiated astrocytes 20% of primary intracranial tumors Frequent location: Cerebral hemispheres in adults Optic nerve. midbrain.
GFAP immunostain -The protein of these filaments. glial fibrillary acidic protein .FIBRILLARY ATROCYTOMA Cerebral hemispheres in adults Intermediate dense glial processes The pivotal event in the transformation of normal to neoplastic astrocytes is mutation of the tumor supressor gene p53 on 17p.
and it has a higher and more rapid rate of progression to glioblastoma . Gemistocytic is the other common subtype.ASTROCYTOMA The fibrillary astrocytoma is the most common histologic subtype of diffuse astrocytoma.
or plump with a large eosinophilic cytoplasmic mass (gemistocytic astrocytomas). spindle-shaped with fiber like processes. They spread in a diffuse fashion but may also form microcysts and other tissue patterns. .GEMISTOCYTIC ASTROCYTOMA Abundant eosinophilic cytoplasm the tumor cells can be stellate.
PILOCYTIC ASTROCYTOMA GROSS: Circumscribed & Cystic Hypothalamus Cerebellum Pons .
JUVENILE PILOCYTIC ASTROCYTOMA Sparsely cellular .biphasic pattern. consisting of cellular and Characterized by abundant fibrillary perivascular areas. without anaplasia or mitoses. alternating with hair-like glial processes & loose microcystic zones. . Occurs in children typically contains the Rosenthal fibers and eosinophilic granular bodies. .
GLIOBLASTOMA MULTIFORMEWHO GRADE IV Varriegated appearance Necrosis & hemorrhage .
GBM anaplsia Necrosis and pseudopalisading .
GBM Vascular endothelial proliferation Densely cellular arrays of tumor cells are often arranged in a perpendicular (pseudopalisading) fashion around serpiginous necrotic areas. GBM is one of the most highly vascular solid tumors. . It has been proposed that these tumor cells are migrating away from a central hypoxic area.
mitoses Grade IV-Glioblastoma Same as Grade III plus microvascular proliferation and necrosis .Anaplastic astrocytoma Cellularity. anaplasia.WHO GRADING SYSTEM Grade I-Pilocytic astrocytoma Benign cytological features Grade II-Low-grade astrocytoma Moderate cellularity-no anaplasia or mitotic activity Grade III.
slowgrowing tumors and have a mean survival of five years. They are insidious. . the tumor cells are uniform and have round central nuclei surrounded by a clear space or halo (unstained cytoplasm) which is an artifact of processing.OLIGODENDROGLIOMA Arise in the cerebral hemispheres of middle-aged adults. Oligodendrogliomas are more circumscribed than astrocytomas.
the tumor cells produce abundant plasma membrane that tends to form concentric layers mimicking myelin Some oligodendrogliomas have an astrocytic component. and necrosis.OLIGODENDROGLIOMAS Infiltrate the cortex diffusely Traversed by delicate capillaries and have a tendency to calcify. vascular endothelial proliferation. Can be classified: as lowgrade or high-grade based on cellularity. . which is helpful in radiological and histological diagnosis EM examination. mitotic activity. Such mixed tumors are called oligoastrocytomas.
They show losses of chromosomes 1p and 19q which correlate with increased sensitivity to PVC and temozolomide chemotherapy and longer survival .OLIGODENDROGLIOMAS Oligodendrogliomas are among the most chemosensitive solid tumors.
protruding into and out of the fourth ventricle.EPENDYMOMAS Predominantly tumors of children and adolescents. Arise most frequently in the 4th ventricle and cause hydrocephalus by blocking CSF flow. Well demarcated from the surrounding brain and spinal cord Grow in an exophytic fashion. Spinal ependymomas are circumscribed intra-axial masses. Occur anywhere in relation to the ventricular system or central canal The most common primary intra-axial tumors in the spinal cord and filum terminale. .
EPENDYMOMAS Perivascular pseudorosettes Tubular formation – true rosettes .
EPENDYMOMA Microscopically: The tumor cells resemble normal ependymal cells and are arranged in: perivascular formations tubular structures like the central canal of the spinal cord papillary formations An anaplastic version of ependymoma. is seen infrequently in young children. Most ependymomas are histologically and biologically low-grade. . but surgical resection of fourthventricle ependymomas is difficult. called ependymoblastoma.
All PNET tumors of the brain are invasive and rapidly growing tumors that.MEDULLOBLASTOMA 10-yr survival rate = 50% Medulloblastoma is a highly malignant primary brain tumor that originates in the cerebellum (infratentoria) or posterior fossa in the external granular layer of the neurons Another term for medulloblastoma is infratentorial PNET. unlike most brain tumors. Medulloblastoma is the most common PNET originating in the brain. spread through the CSF & freq metastasize to different locations in the brain & spine .
External granular layer
Second most frequent BT in children after pilocytic astrocytoma. Most medulloblastomas occur in the 1st decade of life. There is a second peak in the early 20s. Its embryonal nature is underlined by its high incidence in infants and children and by its undifferentiated, immature appearance, which resembles developing neural tissue. The term primitive neuroectodermal tumor (PNET), which has been applied to medulloblastoma and other "small blue cell tumors" of the brain, reflects the embryonal nature and undifferentiated appearance of these tumors and their potential for neuronal and glial diffferentiation
Gross : medulloblastomas are soft, pink-red, and well demarcated. They can block the fourth ventricle and the aqueduct, causing hydrocephalus.
Infrequent mature neurons may also be found in medulloblastomas. . undifferentiated oval or round cells. Glial differentiation in some tumors is reflected by GFAPpositive cells.MEDULLOBLASTOMA Microscopically: classical medulloblastoma is a highly cellular tumor composed of diffuse masses of small. Some medulloblastomas show neuronal. glial and other differentiation. Rosettes are groups of tumor cells arranged in a circle around a fibrillary center. Neuronal differentiation is manifested by neuropil and rosette formation.
Supratentorial or systemic spread Intracranial pressure may be controlled with corticosteroid or VP shunt This combination: 5-yr survival > 90% Gamma knife radiosurgery – for recurrent .MEDULLOBLASTOMA Treatment : Prognosis: begins with maximal resection of the tumor The addition of Radiation to the entire neuraxis and chemotherapy may increase the disease-free survival Presence of desmoplastic featres – better prognosis Prognosis is worse < 3 yrs. Spinal. Old Inadequate resection CSF.
NEOPLASM OF MESENCHYMAL ORIGIN MENINGIOMA Intracranial tumor that arise from the arachnoid villi and produce symptoms by compressing adjacent brain tissue .
spinal cord or orbit. In association with a genetic disorder esp neurofibromatosis type 2 . PATHOGENESIS: Arise in one of the 3 settings: 1.MENINGIOMA A meningioma is benign neoplasm that arises from the meninges. Sporadic cases (most common) 2. The tumor can arise within the intracranial cavity. Iatrogenic cases caused by prior radiation therapy to the cranium 3.
partial deletion or mutation of chromosome 22 involving the NF2 locus (22q12) Suggests that inactivation of the putative NF2 tumor-suppressor gene is involved in the genesis of many meningiomas and schwannomas arising sporadically Seizures – parasagittal & over the convexity Post-Radiation – dose related .MENINGIOMA Sporadic: loss.
GROSS: MENINGIOMA Meningiomas are circumscribed. Usually. . Some meningiomas grow flat on the surface of the brain. though they do not arise from the dura per se. they displace brain tissue without invading it. They may be attached to the dura.
.have no prognostic significance. Meningothelial meningiomas are composed of diffuse masses of arachnoidal-like cells.Meningioma: HISTOLOGIC the most common histological subtypes of meningiomas . Transitional meningiomas. tumor cells are arranged in whorls with hyalinized and calcified centers that are called psammoma (sand) bodies because they resemble tiny grains of sand. Fibroblastic meningiomas are composed of fascicles of fiber-like cells with abundant interstitial collagen.
MENINGIOMA Fibroblastic meningiomas Transitional meningiomas w/ whorls .
This tumor either arises from the meningeal coverings of the optic nerve or from direction extension from the cranial vault. mild proptosis. They display overt histological anaplasia and increased mitoses and invade the brain. chordoid. These atypical meningiomas grow more rapidly and are more prone to recur after surgical resection. Meningiomas of the optic nerve typically affect middleaged women (female: male ratio = 5: 1). such as papillary. also have a more aggressive behavior and are associated with a higher rate of recurrence. and clear cell meningioma.MENINGIOMA Malignant meningiomas are relatively infrequent. . rhabdoid. Some histological types. Manifestations include slowly progressive vision loss. optic atrophy & optociliary shunt vessels.
Arise most often in cranial and spinal nerve roots and peripheral nerves but can occur anywhere, including in the brain and in the ventricles. 90% arise in the 8th nerve root (acoustic Schwannoma, cerebellopontine angle tumor) The preferential involvement of the 8th nerve may have to do with chronic exposure to loud noise (acoustic trauma) Most Schwannomas are solitary. Bilateral acoustic or multiple Schwannomas are the hallmark of NF2.
Pons is deformed & pushed laterally
Palisading tissue pattern
Microscopically they consist of fascicles of spindle cells that are arranged in palisades. Less frequently they form a loose reticular pattern. They are benign, slowgrowing tumors, and cause symptoms by compression. Gross: Schwannomas are extraaxial, circumscribed and encapsulated and range from small and solid to large, irregular, cystic, and hemorrhagic masses. They do not invade, but rather displace the brainstem and spinal cord as they grow
neurofibromas) are characteristic of NF1 They cause a fusiform enlargement of the nerve in which they arise.NEUROFIBROMA Peripheral nerve tumors composed of a mixture of Schwann cells and fibroblasts. their cells are loosely arranged in a wavy pattern. Microscopically. . Multiple neurofibromas that involve long segments of peripheral nerves (plexiformfrom a Greek word that means braid.
they show a mixture of solid and cystic areas. .NEOPLASM DERIVED FROM ECTOPIC TISSUES CRANIOPHARYNGIOMA Grossly.
creating an appearance that resembles adamantinoma. FNA – CHOLESTEROL CRYSTALS Islands of keratin often calcify.CRANIOPHARYNGIOMA Microscopically composed of sheets of squamous epithelial cells and keratin. set in a loose connective tissue stroma. . Water accumulating in the central portion of the epithelial islands causes them to loosen.
Young & middle aged group Found in the cerebellum as a mural nodule within a cyst Benign Tumor which consists of numerous delicate capillaries set in a background of clear foamy cells.TUMORS OF GERM CELL ORIGIN HEMANGIOBLASTOMAS are sporadic or familial. The latter are associated with the von Hippel Lindau disease. .
CEREBRAL LYMPHOMA Spreading across the corpus callosum Large cell lymphoma with perivascular infiltration .
affect immunosuppressed individuals such as patients with AIDS Microscopically. like their extracerebral high-grade counterparts. most of them are large. Meningeal spread is very common. and some cerebral lymphomas arise in the subarachnoid space. Cerebral lymphomas.LYMPHOMAS Primary cerebral lymphomas are thought to arise from indigenous brain histiocytes (microglia) or from rare lymphocytes that are normally present in the meninges and around vessels. B-cell lymphomas. The tumor cells form dense perivascular sheaths or diffuse masses. . are highly malignant.
Brain metastases are found at autopsy in 14% to 37% of malignant tumors. In men. the most common primary is carcinoma of the lung. . which shows brain metastases in 35% of the cases in women. it carcinoma of the breast. which metestasizes in 21% of the cases.METASTATIC TUMORS Metastatic tumors account probably for the majority of BT.
Cytological examination of CSF reveals tumor cells. especially if the primary tumor is too small to be detected.METASTATIC TUMORS The tumor with the highest rate of metastasis is melanoma. The CSF in meningeal carcinomatosis shows: high protein. carcinoma of the breast. The often insidious onset of symptoms and the CSF findings suggest mycobacterial meningitis. low glucose. Meningeal carcinomatosis (diffuse spread of tumor in the subarachnoid space) is seen in 4% to 8% of metastatic BT and is more common with carcinoma of the lung. and acute lymphoblastic leukemia. . and a few lymphocytes.
i. accumulation of fluid in the interstitial space around the tumor.. Increased intracranial pressure is caused by: a) the mass of tumor added to the brain b) hydrocephalus due to obstruction of CSF circulation and c) cerebral edema.e. The general effects of tumors have to do mainly with increased intracranial pressure. .THE EFFECTS OF BRAIN TUMORS The local effects of BT are loss of function (focal deficits) and seizures.
A T & TUMORS ???? .
Only 4 is true E. Meningioms are common tumors in infants and children. 1. and 3 are true. They are more likely to behave more aggressive and recur more frequently. B. 3. intraventricular. Which of the following(s) is(are) true about childhood meningiomas? 1. 4. 2 and 4 are true. D. or intraparenchymal locations. 2.1. All of the Above C. . They are more likely to be found at infratentorial. A. 1 and 3 are true. They are associated with neurofibromatosis 2 (NF2). 2.
The most likely diagnosis is: A. Ependymoma. D.2. C. Medulloepithelioma. E. Pilomyxomoid astrocytoma. Choroid plexus papilloma. Medulloblastoma. This primary cerebral tumor was removed from an 18 month-old boy. B. .
D. Secretory meningioma. Chordoid meningioma.3. Fibrous meningioma. C. Transitional meningioma. Which type of meningioma is most likely to be found in patients under 20 years of age? A. Psammomatous meningioma. E. B. .
E. Spontaneous regression has been described in childhood cases of optic nerve gliomas. Optic nerve gliomas tend to grow outside the optic nerve and expand the subarachnoid and subdual space. C. . slowing growing fashion. Optic nerve gliomas are associated with neurofibromatosis 1 (NF1). D. Optic nerve gliomas in children tend to behave in a indolent. Which of the followings is not true about optic nerve glioma? A. B. Optic nerve gliomas in adults tend to be non-familial and behave in a benign fashion.4.
None of the above. D. Deletion of chromosome 22q. . The most likely molecular changes that would associate with this tumor is: A. E. C.q12) translocation. Isochromosome 17.22)(q24. B. This primary tumor is removed from the cerebellum of a 2 year-old boy. t(11. Human homologue of the Drosophilia segment polarity gene (PTCH gene) on chromosome 9q22.3.5.
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