Sweep 1 Flashcards
c. cytoplasmic eosinophilia (red neurons), observed in
hematoxylin and eosin stained sections.
- Astrocytes (astroglia)
b. in response to brain injury, the astrocytes react by producing a dense network of cytoplasmic processes surrounding the area of injury. This is somewhat analogous to a ———- occurring elsewhere in the body, and is known as ———–.
fibrous scar
reactive gliosis
- Microglia (phagocytes, macrophages)
a. Microglia derived from ————
b. serve as
circulating monocytes
antigen presenting cells in inflammatory conditions
- Types of neuronal injury-share pathology with other cells.
a. Acute “red neurons” see
12-24 h after irreversible hypoxic/ischemic insult.
See shrinkage of the cell body, pyknosis of the nucleus, loss of nucleolus, loss Nissl substance, red cytoplasm, break down in bloodbrain barrier with acute injuries.
- Types of neuronal injury-share pathology with other cells.
a. Astrocytes and injury: Often show
astrogliosis (repair and/or scar formation).
Increased bright pink cytoplasm, cytoplasmic swelling, formation Rosenthal fibers (thick eosinophilic protein aggregates seen in chronic gliosis)
- Types of neuronal injury-share pathology with other cells.
a. Ependymal cells: Certain pathogens (e.g. CMV) cause
extensive ependymal injury with viral inclusions.
- Types of neuronal injury-share pathology with other cells.
a. Microglia: Fixed macrophages in CNS are ———— positive. Can also note blood borne ————-
CD68 and CR3
macrophages with inflammation.
- Hydrocephalus
a. Choroid plexus produces CSF. In continuity with ependyma, ————- lined by epithelial cells.
intraventricular fibrovascular cores
- Hydrocephalus
3 main types
Subfalcine
Uncinate
Tonsilar herniation
- Hydrocephalus
• Subfalcine (cingulated):
Unilateral or asymmetric expansion of the cerebral hemisphere displaces cingulated gyrus under falx cerebri-may compress anterior cerebral artery.
- Hydrocephalus
• Uncinate (transtentorial):
Medial aspect temporal lobe compressed-CN III compromised-pupils dilate and impairment ocular movements-may also compress posterior cerebral artery-affecting visual cortex-Duret Hemorrhage-midbrain bleeds.
- Hydrocephalus
• Tonsillar herniation:
Displacement cerebellar tonsils through foramen magnum-life threatening as the brain stem becomes compromised as the breathing and cardiac regulatory centers are located in the medulla oblongata.
- Epidural hematomadural arteries most frequently the
mid-meningeal artery
• Usually associated with a skull fracture
• Dura separates from blood accumulation. Rupture of a meningeal artery- arterial bleeding
• “Lucid interval”, then progressive loss of consciousness
• Neurosurgical emergency Need PROMPT DRAINAGE as this is a life-threatening condition.
Brain Infarction: evolution
- Grossly & histologically normal: first 12 hours
- 24-36 hours (acute): Red neurons and neutrophil infiltration into the brain parenchyma
- 3rd – 5th day (subacute): Involved tissue becomes softer in consistency. Macrophages with foamy cytoplasm begin to infiltrate
- 1 month: Soft, irregular, cavitated lesion, loss of brain tissue.
- 6 months (chronic): Smooth walled cavity
- Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
a. ———— is the most common underlying cause of primary parenchymal hemorrhage.
Hypertension
- Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
b. ———— in larger vessels and ————– in smaller vessels weakens the vessel walls.
Accelerated atherosclerosis
hyaline arteriolosclerosis
- Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
c. Subsequently note wall rupture and hemorrhage, which is most common in the regions of the
basal ganglia, followed by pons, thalamus and cerebellum.
- Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
Symptoms:
e. Severe headache, hemiparesis, hemisensory loss
- Subarachnoid hemorrhage
a. Defined as abrupt onset
extravasation of blood in space between arachnoid and pia (arterial bifurcations of the circle of Willis) matter due to rupture of vessels in arachnoid space.
- Subarachnoid hemorrhage
a. Often are ———, but could also be precipitated by ————-.
spontaneous
traumatic injury
- Subarachnoid hemorrhage
a. Chief complaint of patient
“Worst headache of my life”.
- Subarachnoid hemorrhage
a. ————- is the most common cause of non-traumatic hemorrhage.
Ruptured berry (saccular) aneurysm (of major brain arteries)
- Subarachnoid hemorrhage
a. Most aneurysms arise from branches of the
middle cerebral, internal carotid and the junction between the anterior cerebral and anterior communicating arteries.
- Subarachnoid hemorrhage
a. Probably represents an acquired, degenerative process, aggravated by
hypertension.
- Subarachnoid hemorrhage
a. Subarachnoid hemorrhage i.e. blood in CSF may be seen together with
intraparenchymal hemorrhage.
- Vascular malformations.
a. Etiology: most commonly from ——— in developing brain.
abnormal angiogenesis
- Vascular malformations.
b. Types are
arteriovenous malformation (AVM), cavernous angioma, capillary telangiectasias and venous angioma.
- Vascular malformations.
c. AVMs
(Collection of abnormal blood vessels of variable caliber) are most common and most likely to result in intraparenchymal and/or subarachnoid bleeds.
- Acute bacterial meningitis
a. Infections resulting in inflammation of the
leptomeninges and subarachnoid space.
- Acute bacterial meningitis
Brain is swollen. Purulent exudate under
subarachnoid space, over the cerebral hemispheres. Purulence within the ventricles
- Acute bacterial meningitis
c. Chronic leptomeningitis is caused by both
bacterial e.g Mycobacterial tuberculosis and fungal e.g. Cryptococcus neoformans organisms.
Acute bacterial meningitis
e. Symptoms include
neck stiffness, neurologic impairment, headache, photophobia.
- Tuberculous Meningitis (chronic meningitis)
a. > 2-3 weeks of
headache, lethargy, nausea & vomiting
- Tuberculous Meningitis (chronic meningitis)
Path:
b. Cranial nerve palsies, epilepsy
c. Gelatinous exudate, may appear nodular.
- Tuberculous Meningitis (chronic meningitis)
d. Histology:
Lymphocytes, macrophages, and multinucleated giant cells form granulomas.
- Tuberculous Meningitis (chronic meningitis)
Mycobacteria may be demonstrable by
acid fast stain
- Cryptococcal Meningitis (chronic meningitis)
a. —————, found in ————-
Spherical budding yeast
soil and bird excrement
- Cryptococcal Meningitis (chronic meningitis)
symptoms
b. Low grade fever, debility, headache
- Cryptococcal Meningitis (chronic meningitis)
Path
c. Slimy exudate, capsular material
- Encephalitis.
a. Diffuse inflammation of the ———- caused by a number of
brain parenchyma
viral agents e.g. HSV most common, HIV, cytomegalovirus and also many arthropod-borne encephalitis viruses.
- Encephalitis.
b. Clinical symptoms:
headache, neck stiffness, pyrexia (fever) and focal seizures.
- Encephalitis.
c. Without treatment,
usually fatal.
- Encephalitis.
d. Microscopically can note
perivascular lymphocytosis, microglial nodules and neuronophagia.
Encephalitis
May also note
viral inclusions e.g. Cowdry A and Negri bodies.
Huntington’s Disease
e. Microscopically note severe ——- in the
neuronal loss
basal ganglia, accompanied by fibrillary gliosis.
- Gliomas
a. ———- (infiltrating) comprise 80% of adult tumors.
Astrocytomas
- Gliomas
Symptoms include
seizures, headaches and focal neurologic deficits.
- Gliomas
b. In adults, mostly affects the
cerebral hemisphere
- Gliomas
c. Pilocytic astrocytoma (Grade I) →
Astrocytoma (Grade II) → Anaplastic astrocytoma (Highly cellular with mitotic figures, Grade III) → Glioblastoma (Necrosis and microvascular proliferation, Grade IV). Glioblastoma → note endothelial cell proliferation.
- Gliomas
d. Clinical features-may remain “silent” until
increase in growth.
Gilomas
Treatment consists of
surgical resection, then radiation and chemotherapy. ~ 15 month survival.
Gilomas
e. Pilocytic astrocytoma:
Less aggressive, often in pediatric patients, usually located in the cerebellum.
