CENTRAL NERVOUS

SYSYTEM
INTRODUCTION
• Made up of the brain & spinal cord are covered by a triple layered
membrane called meninges; altogether,they are encased in d bony
skull & vertebrae
• The brain weighs averagely 1400g in males & 1250g in females
• The CNS serves to coordinate the activities of the entire body by
combining information from all body parts
• Cells & tissues of the CNS:
NEURONS :
- the functional unit of the CNS;
- receives and transmits information;
- can not divide after birth
GLIA: 2 types
- macroglia:
o astrocytes, oligodendrocyte, ependyma
o they are involved in repair
- Microglia:
o member of d mononuclearphagocyte system
MENINGES: include dura, arachnoid and pia
Dura: closely attached to the skull bone
- Epidural space(between dura and skull bone)
- Subdural space(between dura and arachnoid)
Arachnoid
Sub arachnoid space(between arachnoid and pia)
- Pia
Pia and arachnoid also known as leptomeninges
Developmental Anomalies
• Could be Inherited or acquired(infections , drugs and chemicals,
radiation)
• Examples include
NEURAL TUBE DEFECTS(NT): due to failure of a portion of d NT to
close or reopening of region after closure
Anencephaly:
- due to malformation of d anterior part of the NT
- absence of the brain and calvarium
- Encephalocele: herniation of neural tissue thru a defect in d cranium
Encephalocele
Spina bifida: failure of d dorsal portion of d NT to fuse→defect in d
vertebral column. Types include
Spina bifida occulta:
- no obvious defect
- May be represented by a dimple or tuft of hair at site of defect
Spina bifida cystica: swelling containing meninges &/or Spinal cord
tissues. It may be a:
• Meningocele: contains only meninges
• Meningomyelocele: meninges & neural tissues
• Myelocele: neural tissues are exposed with leakage of CSF
FORE BRAIN ANOMALIES
• Megalencephaly/microencephaly: large brain or small brain
• lissencephaly/agyria : reduced number of gyri or absence gyri leaving
a smooth- surfaced brain
• Polymicrogyria: small, numerous, irregularly formed cerebral
convolutions
• Holoprosencephaly: incomplete separation of the cerebral
hemisphere across the midline
POSTERIOR FOSSA ANOMALIES
• Dandy-Walker malformation: characterized
- enlarged posterior fossa
- with a large midline cyst
- and absent cerebellar vermis
• Arnold-Chiari malformation characterized by
- small posterior fossa
- with abnormally shaped cerebellum
- and downward extension of the vermis thru the foramen magnum
HYDROCEPHALUS
• Refers to accumulation of CSF within the ventricular system
• CSF is normally produced by the choroid plexus in the lateral and 3rd
ventricles
• It then flows into the 3rd ventricles through the foramen of Monro
• Then into the 4th ventricle through the acqueduct of silvius
• And then into the sub arachnoid space through the foramens of
Luschka and Magendie from where it is absorbed into venous sinuses
via the arachnoid granulations
classification
• Its classified into primary and secondary hydrocephalus
Primary:
- there is actual increase CSF volume
- associated with raised ICP
Causes of primary include
- obstruction to CSF flow
- overproduction of CSF(choroid plexus papilloma)
- deficient resorption(meningitis)
Obstruction is d commonest cause.
Primary hydrocephalus is therefore classified into 2 types based on
where obstruction is
o Communicating: obstruction in d subarachnoid space
o Non communicating: obstruction is before the subarachnoid space
most commonly in d 3rd ventricle due to acqueduct stenosis
Secondary:
- compensatory increase in CSF due to loss of brain substance
- no raised ICP
CEREBRAL OEDEMA
It means accumulation of excess fluid within the brain parenchyma. 2 types
• Vasogenic:
- fluid accumulates in the extracellular space
- results from disturbance of the BBB making fluid to leave intravascular
compartment into the extracellular space;
• Cytotoxic:
- an increase in intracellular fluid due to neuronal and glial injury
- results from generalized hypoxic or ischemic injury
• Morphology:
- The brain is heavier and softer than normal
- The brain sags on its axis
- flattened gyri
- narrowed sulci
RAISED INTRACRANIAL PRESURE
AND HERNIATIONS
• Increased ICP usually occurs because the brain is encased within a rigid bony skull
• Causes include
- increased CSF volume
- cerebal oedema
- intracranial mass lesions
• Because the cranial vault is partitioned by the rigid falx and tentorium, localized
brain expansion displaces the brain in relation to these partitions. This may lead
to a herniation syndrome eg
- Subfalcine(cingulate) herniation: due to assymetric expansion of the cerebral
hemisphere→displacement of cingulate gyrus under the falx cerebri;
→compression of branches of anterior cerebal artery
- Transtentorial(uncinate) herniation: d medial aspect of d temporal
lobe is compressed against the free margin of the tentorium;
→compression of 3rd cranial is compressed → pupillary dilation
impairment of ocular movement on the side of the lesion
- Tonsilar herniation: displacement of d cerebellar tonsils through d
foramen magnum → brain stem compression which affects
respiratory and cardiac centers
TRAUMA TO THE CNS
• Causes: common causes include RTA, falls, violence
• Consequences:
epidural hematoma:
usually due to rupture of middle meningeal arteries
its associated with a lucid interval
Subdural hemorrhage:
usually due to rupture of bridging veins
most commonly encountered elderly & infants
Types of Subdural hemorrhage
. Acute: freshly clotted blood along d contours of d brain
. Chronic: fresh blood due to repeat bleeding from thin-walled bld vess
Parenchymal injuries: can take any of the following forms
Concussion: clinical syndrome of altered consciousness caused by sudden
change in momentum of d head
Contusion:
- results from blunt trauma to d head leading to damage to brain tissue & bld
vessel causing hemorrhage & oedema.
- Can be a coup injury: injury on the side of impact
- or countre coup injury: injury on the opposite side of impact
Laceration: caused by penetrating objects leading to tearing of tissue
Diffuse axonal injury:
- Occurs when the brain shifts rapidly within the skull during the course of
injury
- Leads to widespread injury to axons in the deep white matter characterized
by axonal swelling & focal hemorrhage
CEREBROVASCULAR DISEASES
• Abnormality of d brain resulting from disorder of blood vessels
• Manifest usually with transient ischemic attack(TIA) or stroke(sudden
development of focal neurologic deficit ranging from trivial neurologic
disorder to hemiplegia and coma)
• Two types: Ischaemic brain damage & Intracranial haemorrhage
 Ischaemic brain damage: caused by
- Generalized reduction in blood flow. may result in selective neuronal
damage, lacunar necrosis or border zone infarction
- Local vascular obstruction. May result in cerebral infarction
 Intracranial haemorrhage: usually due to blood vessel abnormality
and rupture
Types include(epidural and subdural hemorrhage are excluded because
they are primarily traumatic in origin)
- Intraparenchymal haemorrhage (hypertension, vasculitis, coagulation
disorders, aneurysm)
- Sub-arachnoid haemorrhage (berry aneurysm, hypertension)

HYPERTENSIVE CEREBROVASCULAR DISEASE

The effects of hypertension on the brain include formation of lacunar
infarcts, slit hemorrhages, intraparenchymal hemorrhage and
development of encephalopathy
 Lacunar infarcts:
- single or multiple, cavitory, lake-like spaces found in the brain of
hypertensives
- Lacunar infarct are most commonly in the lenticular nucleus followed
by thalamus, internal capsule, deep white matter, caudate nucleus,
and pons in that order
- Lacunar infarct is caused by arteriolosclerosis and occlusion affecting
the deep penetrating arterioles
 Slit hemorrhages:
- results from rupture of small caliber penetrating vessels giving rise to
small hemorrhages
- The hemorrhages resorb with time leaving behind slit-like cavities
 Hypertensive encephalopathy:
- acute hypertensive encephalopathy is a clinicopathologic syndrome
arising in the setting of malignant hypertension and characterized by
diffuse cerebral dysfuntion including headaches, confusion, vomiting,
convulsions, and sometimes coma
- Post mortem examination shows edematous brain with or without
trans-tentorial or tonsillar herniation
- Individuals who over the course of many months and years suffer
multiple bilateral gray matter and white matter infarcts may develop a
distinctive clinical syndrome characterized by dementia, gait
abnormalities, pseudobulbar signs and neurologic deficits
 Intraparenchymal hemorrhage:
- hypertension is the most common risk factor associated with deep
brain parenchymal hemorrhages
- Hypertension is associated with weakening of vessels making them
prone to rupture;
- sometimes the weakened vessels develop minute aneurysms termed
Charcot-Bouchard aneurysms which may be the site of rupture
- The hemorrhages typically occur in the deep white matter or deep
grey structures, followed by the brain stem and cerebellum
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