CYST-MURAL NODULE
Differential diagnosis:
 Pilocytic astrocytoma
 Pleomorphic xanthoastrocytoma
 Ganglion cell tumors
 Hemangioblastoma
FREQUENTLY CALCIFIED
TUMORS
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Oligodendroglioma
Pilocytic astrocytoma
Subependymal giant cell astrocytoma
Ependymoma/ subependymoma
Choroid plexus papilloma
Ganglion cell tumor
Central neurocytoma
Pineal cyst
Meningioma
Craniopharyngioma
Vascular malformations
Retinoblastoma
NEOPLASTIC CYSTIC LESIONS
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Pilocytic astrocytoma
Ganglion cell tumors
Desmoplastic infantile ganglioglioma
Ependymoma
Hemangioblastoma
Pleomorphic xanthoastrocytoma
Craniopharyngioma
Meningioma (occasional)
Schwannoma (usually large ones)
INTRAVENTRICULAR TUMORS
 Ependymoma (lateral, 3rd, 4th)
 Subependymoma (lateral, 4th)
 Subependymal giant cell astrocytoma
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(lateral)
Choroid plexus tumors (lateral, 3rd, 4th)
Pilocytic astrocytoma (lateral, 3rd, 4th)
Central neurocytoma (lateral, 3rd)
Papillary craniopharyngioma (3rd)
Colloid cyst (3rd)
Meningioma (lateral, 3rd, 4th)
REACTION OF NEURON TO INJURY
Acute neuronal injury:
 Shrinkage of cell body, pyknosis of nucleus, disappearance
of the nucleolus, loss of Nissl substance, intense eosinophilia
of cytoplasm Red Neuron
Subacute & chronic neuronal injury:
 Degeneration- cell loss often selective, reactive gliosis
Axonal reaction:
 Regeneration of the axon- enlargement & rounding up of cell
body, peripheral displacement of nucleus, dispersion of nissl
substance to the periphery of cell
Subcellular alterations:
 Neuronal inclusions, neurofibrillary tangles.
NEURON-NISSL STAINED-CENTRAL
CHROMATOLYSIS
REACTION OF ASTROCYTES TO
INJURY
 Gliosis: hypertrophy & hyperplasia of astrocytes.
 Gemistocytic astrocyte: Nucleus of astrocyte
enlarges, prominent nucleolus, cytoplasm expands
becomes bright pink and irregular displacing nucleus to
periphery
 Rosenthal fibers: thick elongated brightly eosinophilic
structures with irregular contours, within astrocytic
processes
 Corpora amylacea: polyglucosan bodies faintly
basophilic PAS positive concentrically lamellated
BRAIN PARENCHYMAL INJURIES
 CONCUSSION
 CONTUSIONS-coup and countrecoup
 LACERATION
INFLAMMATORY DISEASES
 DEMYELINATING DISEASES-multiple
sclerosis
 IDIOPATHIC INFLAMMATORY & REACTIVE
DISORDERS
 XANTHOMATOUS LESIONS
 HISTIOCYTOSES
MULTIPLE SCLEROSIS
Presentation:
May present as space occupying tumors with mass effect, edema
and disruption of blood brain barrier, neurological deficit due to
involvement of cranial nerves, spinal cord lesion cause
sensory/motor impairement
 CT MRI : diffuse / ring-like enhancement
 Gross: Lesions sharply delineated from adjacent white matter.
 Microscopy: Diffuse infiltration of foamy macrophages,
reactive astrocytosis, perivascular aggregates of small
lymphocytes and plasma cells
 Pathogenesis: Cellular immune response against components of
myelin sheath, demyelination casused by activated macrophages
 CSF EXAM- mild elevation of protein , moderate pleocytosis,
gamma globulin increased most patient shows oligoclonal bands
MULTIPLE SCLEROSIS
Brown plaque
MULTIPLE SCLEROSIS
CEREBROVASCULAR DISORDERS
INFARCTION
 Cerebral blood flow—50 ml/min per 100 gm of
tissue.
 Two principal types of ischemic injury
 GLOBAL CEREBRAL ISCHEMIA
 FOCAL CEREBRAL ISCHEMIA
GLOBAL CEREBRAL ISCHEMIA
 Cause: (diffuse ischemic encephalopathy) generalized
reduction of cerebral perfusion e.g. shock cardiac arrest,
severe hypotension
 Morphology: Swollen brain, widened gyri, narrowed sulci,
little demarcation b/w white and gray matter
 Early changes12-24 hrs: acute neuronal cell change- red
neurons, microvacuolization, cytoplasmic eosinophilia,
nuclear pyknosis and karyorhexis. These changes later
appear in astrocytes and glial cells. infiltration of
neutrophils
 Subacute changes 24hrs-2wks: necrosis, influx of
macrophages, reactive gliosis and vascular proliferation.
 Border zone (water shed) infarct: wedge shaped , lie at most
distal fields of arterial irrigation
FOCAL CEREBRAL ISCHEMIA
Cerebral arterial occlusion resulting in ischemia and infarction
in a specific region within the territory of distribution of
the compromised vessel
Causes:
Thrombosis
CADASIL
Cerebral amyloid angiopathy
Embolism
1. THROMBOSIS: majority due to atherosclerosis,
• Sites : carotid bifurcation, origin of middle cerebral
artery, basilar artery
• Predisposing factors: Arteritis due to syphilis and
tuberculosis, polyarteritis nodosa and primary angitis of
CNS; hypercoagulable states, dissecting aneurysm and
drug abuse are other causes.
1.
2.
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4.
THROMBOSIS
FOCAL CEREBRAL ISCHEMIA
2.
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CADASIL: cerebral autosomal dominant arteriopathy
with subcortical infarcts and leukoencephalopathy
Morphology: concentric thickening of adventitia and
media of cerebral and leptomeningial arteries.
Basophilic PAS positive granules in walls of vessels also in
other sites like skin or muscle biopsies.
3.
CEREBRAL AMYLOID ANGIOPATHY:
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deposits of amyloidogenic peptides Aβ40 in walls of small
and medium sized vessels
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EMBOLISM :
Predisposing factors: cardiac mural thrombi, MI ,
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valvular disease, atrial fibrillation, atherosclerotic thrombi,
paradoxical emboli.
Site: Territory of middle cerebral artery is most frequently
affected
Focal infarction with punctate
hemorrhages caused by an embolus