Pathology Neurology

3.
Cerebral edema
Cerebral edema, particularly brain parenchymal edema, occurs due to increased fluid leakage
from blood vessels and injury to cells in the central nervous system (CNS). There are two
primary pathways of edema formation:
1. Vasogenic Edema: This type involves an increase in extracellular fluid due to disruption
of the blood-brain barrier and increased vascular permeability. It allows fluid to shift
from blood vessels into the intercellular spaces of the brain. The lack of lymphatics
impairs the removal of excess extracellular fluid. Vasogenic edema can be localized, such
as near areas of inflammation or tumors, or generalized, which can follow global
ischemic injury.
2. Cytotoxic Edema: This type results from an increase in intracellular fluid due to injury
to neuronal, glial, or endothelial cell membranes. It occurs with generalized
hypoxic/ischemic insults or metabolic derangements that disrupt normal membrane ionic
gradients.
In clinical scenarios, conditions associated with generalized edema often involve elements of
both vasogenic and cytotoxic edema. In generalized edema, the gyri (ridges) of the brain flatten,
the sulci (grooves) between them narrow, and the ventricular cavities are compressed. As the
brain expands, there's a risk of herniation, where brain tissue shifts from its usual position,
potentially leading to serious complications.
4. Hydrocephalus
Hydrocephalus occurs when there is an excessive accumulation of cerebrospinal fluid (CSF)

within the ventricular system of the brain. Here's a breakdown of its key points:
1. CSF Production and Circulation: CSF is produced by the choroid plexus within the
ventricular system. It circulates through the ventricles and enters the cisterna magna at
the base of the brainstem via foramina. Subarachnoid CSF bathes the brain's surface and
is absorbed by arachnoid granulations.
2. Causes: Most cases of hydrocephalus result from impaired CSF flow and resorption.
Rarely, overproduction of CSF can occur, often accompanying tumors of the choroid
plexus.
3. Presentation: In infants, hydrocephalus occurring before cranial suture closure leads to
an enlarged head. After suture closure, hydrocephalus results in ventricular expansion
and increased intracranial pressure, without a change in head size.
4. Types:
o Noncommunicating (Obstructive) Hydrocephalus: This occurs when there's a
focal obstruction in the ventricular system, such as a mass in the third ventricle or
aqueductal stenosis.
o Communicating Hydrocephalus: Here, the ventricular system remains connected
to the subarachnoid space, leading to enlargement of the entire ventricular system.
Causes include CSF overproduction from a choroid plexus tumor or arachnoid
fibrosis post-meningitis.
5. Hydrocephalus ex Vacuo: This term describes a compensatory increase in ventricular
volume due to loss of brain tissue. It's not a true hydrocephalus but rather a response to
brain atrophy or shrinkage.
Understanding hydrocephalus involves grasping its causes, presentation, and the distinction
between its various types.
5. Neural tube defects
NTDs are common malformations of the central nervous system (CNS) involving neural tissue,
meninges, and surrounding bone or soft tissue. They arise from two main pathogenic
mechanisms:
1. Failure of Neural Tube Closure: This leads to secondary defects in mesenchymal tissue
due to abnormal skeletal modeling around the malformed tube. Examples include
anencephaly (absence of most of the brain and calvarium) and myelomeningocele
(protrusion of CNS tissue through a vertebral column defect).
2. Primary Bony Defects: These are caused by abnormal axial mesoderm development,
resulting in secondary CNS abnormalities. Examples include encephalocele (extrusion of
malformed brain tissue through a cranial defect) and spina bifida (asymptomatic bony
defects or severe malformations of the spinal cord).
 Anencephaly: Forebrain development is disrupted, leaving behind a flattened remnant of

disorganized brain tissue. Posterior fossa structures may be spared depending on the
extent of the skull deficit.
 Myelomeningocele: CNS tissue protrudes through a vertebral column defect, typically in
the lumbosacral region. This condition causes motor and sensory deficits in the lower
extremities and may lead to bowel and bladder control issues.
 Encephalocele: Malformed brain tissue protrudes through a midline defect in the
cranium, often occurring in the occiput or nasofrontal region.
 Spina Bifida: It can range from asymptomatic bony defects (spina bifida occulta) to
severe malformations with disorganized spinal cord segments and overlying meningeal
outpouching. Folate deficiency during early gestation is a known risk factor, and
supplementation is recommended for women of childbearing age to reduce the risk of
NTDs.
Understanding NTDs involves recognizing their various manifestations and the importance of
preventive measures such as folate supplementation during pregnancy.

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3.

Hydrocephalus occurs when there is an excessive accumulation of cerebrospinal fluid (CSF)

5. Neural tube defects

 Anencephaly: Forebrain development is disrupted, leaving behind a flattened remnant of

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