11.8.b.Meninges and Ventricular system.txt

• Development of meninges
• The meninges develop from a single menbrane, the “PRIMARY MENINX”, which differentiates into two layers: the external pachymeninges (Dura); and the leptomeninges (arachnoid and pia)

• Dense fibrous connective tissue, tightly attached to the periosteum of the skull
• Within the dura see meningeal arteries which are tightly attached to the dura: they supply the blood to the calvarium
• Middle meningeal artery enters the scull through: foramen spinosum

• Falx cerebri: between hemispheres
• Tentorium cerebelli: between cerebrum and cerebellum
• Gives rise to terms: supratentorial and infratentorial

• Subfalcine: side to side beneath the falx cerebri; also called the CINGULATE herniation
• Transtentorial: through the opening in the tentorium cerebelli; also called UNCAL herniation
• Tonsillar (medulla) or brain stem (cerebellar) herniation: through the foramen magnum

• To form venous sinuses.
• Cerebral veins drain into the venous sinuses
• Veins cross the potential subdural space

• Superior and inferior sagittal sinuses
• Straight sinus
• Transverse sinuses, and sigmoid sinuses

• Epidural
• Subdural
• Subarachnoid
• Intraventricular
• Intracerebral

• Surgical emergency!
• A hemorrhage between the dura and the inner table of the skull
• Caused by injury to a meningeal artery following trauma with skull fracture
• Most often affects the middle meningeal artery or one of its branches
• Since it’s high arterial pressure – causes hemorrhage to enlarge very rapidly: surgical EMERGENCY!

• The arachnoid closely underlies the dura
• Bleeding between the dura and the arachnoid: subdural hematoma

• bridging” veins: connect the cerebral veins with the dural venous sinuses
• They may be damaged by minor trauma, especially in the elderly
• Almost always result from trauma, but don’t need a scull fracture here to cause a bleed
• Often develop slowly, so are usually not a surgical emergency.

• Blood between the dura and arachnoid
• Usually related to closed head injury
• Bleeding is due to tearing of small veins
• Hematoma enlarges slowly: b/c of low pressure
• Gradually displaces brain
• Often bilateral

• Is often asymptomatic, until it becomes very large
• Layer of organizing hematoma is adherent to dura; it can be peeled off as a “membrane”

• Blood accumulates in the space normally occupied by CSF
• Trauma – most frequent cause
• Spontaneous SAH is usually due to rupture of a “berry” aneurysm

Rupture of a “berry” aneurism

Trauma

• Invaginations of the arachnoid membrane into the overlying dural venous sinuses
• CSF is reabsorbed into the venous system through the arachnoid villi

• Light microscopy – many nuclei appear to occupy a cytoplasmic mass
• E.M. of two adjacent arachnoid cells: their cytoplasm interdigitates so intimately, that the light microscope can’t resolve the cell membrane

Tumor of arachnoid cells

• Sinuses and middle ear
• Hematogenous dissemination
• Direct extension
• Peripheral nerve

• Inflammation in the subarachnoid space
• Subarachnoid fluid supposed to be clear, but it’s not
• Inflammatory cells are distributed throughout the subarachnoid space
• Collection of pus and congestion of vessels is apparent, vessels are seen though a thin layer of pus, so appear “out of focus”

the lower lumbar region below the conus medullaris: so CSF may safely be sampled by lumbar puncture

• Normally: clear, colorless, no cells seen
• In acute meningitis: proteinacious material, neutrophils can be seen and other inflammatory cells, and may see an organism

• Provides mechanical buoyancy and cushioning
• Removes brain metabolites and acts as a chemical reservoir to buffer local changes
• Average person has 80-150 ml of CSF in subarachnoid space and ventricular system
• Choroid plexus makes ~500 ml per day

Flows through the ventricular system into subarachnoid space and is absorbed into the venous system through arachnoid villi (granulations)

• Cavities within the brain derived from the neural canal
• Contiguous with the central canal of the spinal cord
• Lined by ependymal cells

• Line the ventricles and the central canal of the spinal cord
• Simple columnar epithelial cells many are ciliated

• Frontal (anterior) horn
• Central part
• Temporal (inferior) horn
• Occipital (posterior) horn

• Left interventricular foramen
• Aka foramen of Monro

• Vascular organ that produces CSF
• Present in body and temporal horns of lateral ventricles
• Also present in roofs of 3rd and 4th ventricles:

• Thalamus and hypothalamus: form the lateral walls
• Choroid plexus forms the roof

• Aka aqueduct of Sylvius: passage through the midbrain
• Narrowest part of the system and most vulnerable to occlusion

• Cerebellum: forms the roof
• Pons and medulla: form the floor
• Choroid plexus: lies in the roof and extends to the lateral apertures

• In the fourth ventricle
• Allow the CSF to flow from the ventricles into the subarachnoid space surrounding the brain and spinal cord

• Enlarged “reservoirs” of CSF in the subarachnoid space
• Named for anatomical locations, e.g:
• Cerebello-medullary cistern (cisterna magna)
• Suprachiasmatic
• Interpeduncular
• Quadrigeminal
• Paramesencephalic
• Pontine
• Lumbar
• Etc.

• Results from either blockage of flow or impaired reabsorption
• Symptoms: may include headache, nausea, vomiting, and/or bradycardia
• Due to pressure on the vagal centers on the floor of the 4ths ventricle: !

Papilledema: swelling of the optic disk by increased CSF pressure surrounding the optic nerve which impedes the venous drainage from the eye

• Increased volume of CSF within the cranial cavity with or without an increase in pressure
• Enlarged ventricles
• Caused by blockage of CSF flow and/or decreased resorption

• CSF flow is blocked within the ventricular system
• e.g. by aqueductal stenosis
• Reabsorption of CSF is blocked outside ventricles, e.g. due to scarring from meningitis

The skull can expand, so this may lead to enlargement of the head

Treated by inserting a shunt from ventricle to jugular vein or peritoneum

• (Hycrocephalus ex vacuo)
• occurs in brain atrophy as CSF fills space of lost brain tissue volume
• no increase in CSF pressure: !
• Can be gross or focal enlargement of ventricles following tissue destruction by infarct (stroke)