D’YOUVILLE COLLEGE
BIOLOGY 307/607 - PATHOPHYSIOLOGY
Lecture 20 - PATHOPHYSIOLOGY OF NERVOUS SYSTEM I
Chapters 20 & 21
1.
Review of Nervous System A&P:
• skull (includes cranium and face) & contents:
- identifiable landmarks of skull (figs. 20 - 1, 20 - 2 & ppts. 1 & 2) bear
useful relationship to important vascular and neural contents of cranial cavity
- scalp includes five layers (acronym 'SCALP') (fig. 20 - 5 & ppt. 3); loose
connective tissue layer (dangerous space) has vascular connections to intracranial
circulation (fig. 20 - 8 & ppt. 4)
- face also has a danger zone (dangerous triangle) that may facilitate
invasion of intracranial circulation (fig. 20 - 6 & ppt. 5)
- meninges (dura mater, arachnoid mater, & pia mater) enclose brain (fig.
20 - 11a & ppts. 6 & 7); subarachnoid space (within meninges) contains
cerebrospinal fluid (CSF) that forms within brain ventricles (fig. 20 - 10 & ppt. 8);
CSF returns to blood via arachnoid villi that penetrate dural venous sinus;
obstructions that prevent normal circulation of CSF may cause swelling of brain
(hydrocephalus) and must be corrected promptly
- fractures that involve only inner table (fig. 20 - 8 & ppt. 9) of skull bone
(comminuted or depressed) need to be checked by X-ray for bone fragments in
meninges or in brain tissue
- basal skull fractures may tear meninges over cribriform plate & crista
galli (fig. 20 - 9 & ppt. 10), causing CSF to leak into nasal cavity (check for glucose
content), or driving crista galli into soft brain tissue
- fractures may also cause infections of meninges (meningitis) involving the
more delicate inner layers (arachnoid & pia), or may cause hemorrhage and/or
hematoma (epidural, subdural or subarachnoid)
Bio 307/607 lec 20
- p. 2 -
• vertebral column & contents:
- consists of 26 bones (24 vertebrae + sacrum & coccyx) (fig. 20 - 3 & ppt. 11)
- spinal cord extends only to L1/L2 or L2/L3 interspace becoming cauda
equina inferiorly
- spinal taps performed at L3/L4 level (fig. 20 - 4 & ppt. 12) reduce risk of
impaling neural structures
- cord is enclosed in meninges and bathed in CSF, similar to brain (20 11b & ppt. 13)
- 31 pairs of spinal nerves extend from cord, exiting via intervertebral
foramina
- normal curvatures (2 primary -- thoracic & sacral, & 2 secondary -- cervical
& lumbar) may become exaggerated (kyphosis or lordosis), or abnormal -- scoliosis
(fig. 20 - 13 & ppt. 14); these distortions may cause nerve entrapments or cord
damage
- vertebrae are separated by intervertebral disks (fig. 20 - 14 & ppt. 15)
consisting of fibrous outer layer (annulus fibrosus) enclosing a soft center (nucleus
pulposus); shrinkage of disks with age or herniations may cause nerve entrapments
or cord damage
- fractures or dislocations may also cause entrapments or cord damage, e.g.,
the odontoid process (dens) of the axis (fig. 20 - 14b & ppt. 16) may be fractured &
driven into the cord by hyperextension of the neck (whiplash)
Bio 307/607 lec 20
2.
- p. 3 -
Cerebral Circulation & Cerebrovascular Accident (Stroke) (CVA):
• circle of Willis: arterial anastomosis supplied by vertebral arteries (30%) and
internal carotid arteries (70%); derivative arteries are middle cerebrals, anterior
cerebrals, posterior cerebrals & communicating branches (fig. 20 - 15a - c & ppt. 17);
areas supplied by anastomosis of arterial branches are known as watershed zones
and are more protected from circulatory disruptions
• dural sinuses: collection vessels for cerebral veins; include superior sagittal
sinus, inferior sagittal sinus, straight sinus, cavernous sinuses, transverse sinuses
& sigmoid sinuses (that drain into internal jugular veins outside cranium) (fig. 20 15d, e & ppts. 18 & 19)
• aneurysms: berry aneurysms develop at vulnerable bifurcations of arteries
(fig. 20 - 28& ppt. 20); distensions (fusiform aneurysms) may also occur; aneurysms
may burst provoking sudden CVAs
• transient ischemic attack (TIA): brief episode of disrupted cerebral function (5
min. to an hour or up to a day) caused by microthrombi or embolisms that resolve, or by
vasospasm downstream from plaque; often precedes full-blown CVA
• strokes are caused by poor perfusion (ischemia) of cerebral tissue, which
may be transitory with minimum functional loss or severe, resulting in necrosis of
brain tissue & even death; occlusive & hemorrhagic mechanisms are recognized
- occlusive (thrombotic) CVA: develops slowly (over many months to years)
while the thrombus grows until ischemia becomes damaging; most vulnerable areas
are the tissues at ends of arterial branches that have no anastomosis (fig. 20 - 30 &
ppt. 21)
- resulting dead tissue presents a liquefaction necrosis
- occlusive (embolic) CVA: thromboembolisms, fat embolisms (from bone
fractures), tumor or vegetation embolisms constitute usual causes
- hemorrhagic CVA: from trauma to circulation or burst aneurysm,
hemorrhage disrupts perfusion of downstream tissues
Bio 307/607 lec 20
- p. 4 -
- formation of hematoma may cause more serious and widespread
brain damage (including elevated intracranial pressure with resulting compression
damage)
Bio 307/607 lec 20
3.
- p. 5 -
Meningitis - Encephalitis - Myelitis:
• spinal tap (ppt. 22) reveals bacterial infection: cloudy CSF that is low in
glucose (consumed by bacteria), high in protein and reveals elevated white cell
count (5000/mm3); viral infection features CSF rich in lymphocytes
• infections may be confined to inner meninges (meningitis) or spread to
neighboring brain (encephalitis) or to neighboring spinal cord (myelitis); blood-brain
barrier may interfere with some therapies because of exclusion of drugs or
antibiotics, e.g., penicillin (fig. 20 - 16 & ppt. 23)
- acute bacterial forms are severe and have high mortality rate; require
immediate intervention with appropriate antibiotics
- viral is less severe, most cases resolving without problems
4.
Intracranial pressure (ICP):
- causes of elevated ICP include:
- edema (vasogenic or cytotoxic) -- vasogenic edema results from poor
drainage of cerebral circulation; cytotoxic edema is cellular swelling due to hypoxia
of brain tissue (impaired sodium pump)
- hematoma -- pooling of blood due to hemorrhage from circulatory
trauma or burst aneurysm (fig. 20 - 23a & ppt. 24)
- increased CSF volume -- overproduction, impaired drainage, occlusion
of passages (hydrocephalus)
- tumors -- swelling mass from rapidly growing neoplasm (fig. 20 - 38)
- effects include localized damage to compressed areas, damage due to
herniations (fig. 20 - 12a & 25)