1-57 of 57
CSF is reabsorbed in venous circulation through a pressure gradient between the
arachnoid villi and the cerebral venous sinuses. The arachnoid villi protrude from the
arachnoid space, through the dura mater, and lie within the blood flow of the venous
sinuses. The vili function as one way valves directing CSF outflow into the blood but
preventing blood flow into the subarachnoid space.
Give this one a go later!
, Know the function of the arachnoid villi. CH 15 pg 451
Encephalocele - definition and location of defect(p. 664) a herniation or protrusion of
the brain and meninges through a defect in the skull, resulting in a sac like structure.
Encephalocele occurs during the first weeks of pregnancy. When the defect contains
only meninges, it is referred to as a cranial meningocele. Most encephaloceles occur
in the occipital area, with the remainder found in the frontal, parietal, or
nasopharyngeal regions
Meningocele - definition and location of defect(p. 664) Type of spina bifida; saclike
cyst of meninges filled with spinal fluid. It develops during the first four weeks of
pregnancy when the neural tube fails to close completely. Meningocele is a structural
anomaly of the posterior arch of the vertebra. The cystic dilation of meninges
protrudes through the vertebral defect and around the malformed tube. The dura
mater may be missing and the arachnoid layer of the meninges bulges beneath the
skin. This defect does not involve the spinal cold. Meningoceles occur with equal
frequency in the cervical, thoracic and lumbar spines. At birth the infant has a
protruding sac on the back at level of the defect.
Spina bifida - definition and location of defect(p. 664-666) When defects of the
neural tube closure occur, such as meningocele or myelomenigocele, an
accompanying vertebral defect allows the protrusion of the neural tube contents. This
defect is called spina bifida (split spine). The cause of spina bifida is unknown.
Periconceputal maternal folate deficiency and genetic alternations are commonly
associated with the defect. It is also possible for the defect to occur without any
visible exposure of meninges or neural tissue. This is referred to as spina bifida
occulta. In spina bifida occulta the posterior vertebral laminae have failed to fuse.
80% of these vertebral defects are located in the lumbosacral regions, most
commonly in the 5th lumbar vertebra and the first sacral vertebra
Myelomeningocele - definition and location of defect(p. 665) Type pf spina bifida
more common than meningocele and one of the most common developmental
anomalies of the nervous system; cystic dilation of meninges and protuberance of
various amounts of the spinal cord through the vertebral defect and assoc. w/ more
severe complications than a meningocele. D/t changes in CSF flow, they are likely to
be assoc. w/ a Chiari II malformation (downward placement of the cerebellum,
,brainstem, and fourth ventricle). The Chiari II compresses and stretches the posterior
region of the cerebellum and brainstem downward through the foramen magnum ⇒
hydrocephalus, ↑ ICP from obstructed CSF flow, syringomyelia (causes cysts at
multiple levels of spinal cord), and cognitive and motor deficits. *Location is evident
at birth as a defect on the infant's back, 80% are located on in the lumbar and
lumbosacral region, the last region to close up.
Give this one a go later!
Define encephalocele, meningocele, spina bifida, myelomeningocele.
Where is the defect located in each?
CH 20 pg 621
Parkinson Disease, where is the primary defect? (p.564) The main disease feature is
degeneration of the basal ganglia (corpus striatum, globus pallidus, subthalmic
nucleus, and substantia nigra) involving the dopaminergic nigrostriatal pathway.
Huntington Disease - where is the primary defect? (p.562) The principal pathologic
feature of HD is severe degeneration of the basal ganglia, particularly the caudate
and putamen nuclei and the frontal cerebral cortex. The degeneration of the basal
ganglia leaves enlarged lateral ventricles.
Give this one a go later!
Where is the primary defect in Parkinson's disease and Huntington's?
ICP is normally between 5 to 15 mmHG of 60- 180mm H20.
Increased ICP may occur with an increase in inter cranial content (tumor growth),
edema, excess CSF or hemorrhage. It needs an equal reduction in volume of the
other cranial contents. The most available to displace is CSF. If ICP remains high after
CSF displacement out of the cranial vault cerebral blood volume and flow are altered.
Dramatic sustained rises in ICP are not seen until all compensatory mechanisms have
, been exhausted. Dramatic rises in ICP occur over a very short period. Autoregulation,
the compensatory alteration in the diameter of the intracranial blood vessel designed
to maintain a const blood flow during changes in cerebral perfusion pressure, is lost
with progressively increased ICP. Accumulating CO2 may still cause vasodilation
locally, but without auto regulation this vasodilation causes the hydrostatic BP in the
vessels to drop and blood volume to increase. The increases pressure may obstruct
venous outflow. The brain volume is thus further enhanced, and ICP continues to rise.,
and the pressure takes much longer to return to baseline As the ICP approaches
systematic blood pressure, cerebral perfusion pressure falls and cerebral perfusion
slows dramatically. The brain tissues experiences severe hypoxia, hypercapnia, and
acidosis all of which cause cerebrovascular dilation.
Give this one a go later!
Know normal intracranial pressure. How does body compensate for
increased ICP? CH 17 pg 528
Respiratory patterns help evaluate the level of brain dysfunction and coma. Breathing
patterns can be categorized as hemispheric or brainstem.
With normal breathing, a neural center in the forebrain (cerebrum) produces a
rhythmic breathing pattern. When consciousness decreases, lower brainstem center
regulate the breathing pattern by responding only to changes in PaCO2 levels, called
post hyperventilation apnea (PHIVA)
Cheyne-Stokes respiration is an abnormal rhythm of ventilation (periodic breathing)
with altering periods of hyperventilation and apnea (crescendo-decresendo pattern).
In the damaged brain, higher levels of PaCO2 are required to stimulate ventilation,
and increased in PaCO2 lead to tachypnea. The PaCO2 level then decreases to below
normal, and breathing stops (apnea) until the CO2 accumulates again stimulates
tachypnea.
Central Neurogenic hyperventilation is a respiratory pattern of sustained
hyperventilation caused by a lesion in the central pons.
Apneustic respirations have prolonged inspiratory and expiatory phases caused by
CSF is reabsorbed in venous circulation through a pressure gradient between the
arachnoid villi and the cerebral venous sinuses. The arachnoid villi protrude from the
arachnoid space, through the dura mater, and lie within the blood flow of the venous
sinuses. The vili function as one way valves directing CSF outflow into the blood but
preventing blood flow into the subarachnoid space.
Give this one a go later!
, Know the function of the arachnoid villi. CH 15 pg 451
Encephalocele - definition and location of defect(p. 664) a herniation or protrusion of
the brain and meninges through a defect in the skull, resulting in a sac like structure.
Encephalocele occurs during the first weeks of pregnancy. When the defect contains
only meninges, it is referred to as a cranial meningocele. Most encephaloceles occur
in the occipital area, with the remainder found in the frontal, parietal, or
nasopharyngeal regions
Meningocele - definition and location of defect(p. 664) Type of spina bifida; saclike
cyst of meninges filled with spinal fluid. It develops during the first four weeks of
pregnancy when the neural tube fails to close completely. Meningocele is a structural
anomaly of the posterior arch of the vertebra. The cystic dilation of meninges
protrudes through the vertebral defect and around the malformed tube. The dura
mater may be missing and the arachnoid layer of the meninges bulges beneath the
skin. This defect does not involve the spinal cold. Meningoceles occur with equal
frequency in the cervical, thoracic and lumbar spines. At birth the infant has a
protruding sac on the back at level of the defect.
Spina bifida - definition and location of defect(p. 664-666) When defects of the
neural tube closure occur, such as meningocele or myelomenigocele, an
accompanying vertebral defect allows the protrusion of the neural tube contents. This
defect is called spina bifida (split spine). The cause of spina bifida is unknown.
Periconceputal maternal folate deficiency and genetic alternations are commonly
associated with the defect. It is also possible for the defect to occur without any
visible exposure of meninges or neural tissue. This is referred to as spina bifida
occulta. In spina bifida occulta the posterior vertebral laminae have failed to fuse.
80% of these vertebral defects are located in the lumbosacral regions, most
commonly in the 5th lumbar vertebra and the first sacral vertebra
Myelomeningocele - definition and location of defect(p. 665) Type pf spina bifida
more common than meningocele and one of the most common developmental
anomalies of the nervous system; cystic dilation of meninges and protuberance of
various amounts of the spinal cord through the vertebral defect and assoc. w/ more
severe complications than a meningocele. D/t changes in CSF flow, they are likely to
be assoc. w/ a Chiari II malformation (downward placement of the cerebellum,
,brainstem, and fourth ventricle). The Chiari II compresses and stretches the posterior
region of the cerebellum and brainstem downward through the foramen magnum ⇒
hydrocephalus, ↑ ICP from obstructed CSF flow, syringomyelia (causes cysts at
multiple levels of spinal cord), and cognitive and motor deficits. *Location is evident
at birth as a defect on the infant's back, 80% are located on in the lumbar and
lumbosacral region, the last region to close up.
Give this one a go later!
Define encephalocele, meningocele, spina bifida, myelomeningocele.
Where is the defect located in each?
CH 20 pg 621
Parkinson Disease, where is the primary defect? (p.564) The main disease feature is
degeneration of the basal ganglia (corpus striatum, globus pallidus, subthalmic
nucleus, and substantia nigra) involving the dopaminergic nigrostriatal pathway.
Huntington Disease - where is the primary defect? (p.562) The principal pathologic
feature of HD is severe degeneration of the basal ganglia, particularly the caudate
and putamen nuclei and the frontal cerebral cortex. The degeneration of the basal
ganglia leaves enlarged lateral ventricles.
Give this one a go later!
Where is the primary defect in Parkinson's disease and Huntington's?
ICP is normally between 5 to 15 mmHG of 60- 180mm H20.
Increased ICP may occur with an increase in inter cranial content (tumor growth),
edema, excess CSF or hemorrhage. It needs an equal reduction in volume of the
other cranial contents. The most available to displace is CSF. If ICP remains high after
CSF displacement out of the cranial vault cerebral blood volume and flow are altered.
Dramatic sustained rises in ICP are not seen until all compensatory mechanisms have
, been exhausted. Dramatic rises in ICP occur over a very short period. Autoregulation,
the compensatory alteration in the diameter of the intracranial blood vessel designed
to maintain a const blood flow during changes in cerebral perfusion pressure, is lost
with progressively increased ICP. Accumulating CO2 may still cause vasodilation
locally, but without auto regulation this vasodilation causes the hydrostatic BP in the
vessels to drop and blood volume to increase. The increases pressure may obstruct
venous outflow. The brain volume is thus further enhanced, and ICP continues to rise.,
and the pressure takes much longer to return to baseline As the ICP approaches
systematic blood pressure, cerebral perfusion pressure falls and cerebral perfusion
slows dramatically. The brain tissues experiences severe hypoxia, hypercapnia, and
acidosis all of which cause cerebrovascular dilation.
Give this one a go later!
Know normal intracranial pressure. How does body compensate for
increased ICP? CH 17 pg 528
Respiratory patterns help evaluate the level of brain dysfunction and coma. Breathing
patterns can be categorized as hemispheric or brainstem.
With normal breathing, a neural center in the forebrain (cerebrum) produces a
rhythmic breathing pattern. When consciousness decreases, lower brainstem center
regulate the breathing pattern by responding only to changes in PaCO2 levels, called
post hyperventilation apnea (PHIVA)
Cheyne-Stokes respiration is an abnormal rhythm of ventilation (periodic breathing)
with altering periods of hyperventilation and apnea (crescendo-decresendo pattern).
In the damaged brain, higher levels of PaCO2 are required to stimulate ventilation,
and increased in PaCO2 lead to tachypnea. The PaCO2 level then decreases to below
normal, and breathing stops (apnea) until the CO2 accumulates again stimulates
tachypnea.
Central Neurogenic hyperventilation is a respiratory pattern of sustained
hyperventilation caused by a lesion in the central pons.
Apneustic respirations have prolonged inspiratory and expiatory phases caused by
