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25 Cards in this Set
- Front
- Back
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Cell body
Acute ischemic or hypoxic damage |
Produces a shrinkage of the cell body and a hypereosinophilia. The nucleus becomes pyknotic. These are thought to be irreversible and lethal changes
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Cell body
Atrophy |
A non-eosinophilic shrinkage of the cell body, is the hallmark of many neurodegenerative disorders (eg Alzheimers, Parkinson, Huntington). The neuron may be involved directly or indirectly, through retrograde or anterograde transneuronal or transynaptic degeneration
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Cell body
Chromatolysis |
Results from axon damage (including axon transection). The cell body becomes hypertrophic and loses its Nissl substance (rough ER). Chromatolysis may be followed by regrowth of the axon from teh point of damage, a pehnomenon more often seen int eh peripheral than in the central nervous system.
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Cell body
Inclusions |
Represent abnormal nuclear or cytoplasmic structures. SOme reflect the focal storage of metabolites, some the presence of viral proteins or nucleoprotines and some the abnormal accumulation of structural proteins (eg. neurofibrillary tangles, Lewy bodies)
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Cell body
Lipofuscin |
Insoluble mix of proteins, lipids, and minerals that accumulates in neurons and astrocytes during the normal aging process.
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Cell body
Neuronophagia |
Phagocytosis of degenerating neurons, usually by macrophages. This is commonly seen after hypoxic or ischemic insults or during viral infections
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Hydrocephalus
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Enlargement of ventricles
Overproduction of CSF Obstructive, or Non-communicating Block of Resorption |
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Hydrocephalus
Overproduction of CSF |
Rare, choroid plexus papillomas
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Hydrocephalus
Obstructive, or non-communicating |
Block of CSF flow through the ventricles
Aqueductal stenosis Masses in ventricle system and foramina Malformation (e.g. Arnold Chiari) |
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Hydrocephalus
Communicating |
Block of resorption
Meningitis Subarachnoid hemorrhage Dural sinus thrombosis |
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Brain edema
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Rapid expansion
Increase in volume and weight due to accumulation of fluid |
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Vasogenic edema
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Edema due to increased cerebrovascular permeability. May be due to:
a) destruction of vessels (e.g. trauma, hemorrhage) b) increased pinocytic activity c) growth of capillaries that do no have a competent BBB (e.g. vessels in tumors, either CNS or metastatic, or granulation tissue) Progression and extent depend upon: 1. Level of systolic blood pressure 2. Duration of BBB incompetence BBB breakdown due to: Trauma Infarction Hemorrhage Neoplasms Infections Inflammation |
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Uncal herniation
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Midbrain level
1. CN III - pupil dilates (ipsilateral to herniation, and eventually to ipsilateral oculomotor palsy) 2. PCA/SCA - visual cortex (the ipsilateral posterior cerebral artery may be compressed) 3. Cerebral peduncles - ipsi- or contralateral hemiparesis (Ipsilateral peduncular compression leads to hemiparesis or hemiplegia on the side opposite the lesion, while contralateral peduncular compression leads to hemiparesis or hemiplegia, ipsilateral to the original lesion) 4. AP compression - aqueductal compression hydrocephalus |
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Duret hemorrhage
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Compresses midline midbrain and pons caudally
Blood vessel are arterial, and hemorrhages result from stretching of perforating vessels of the stem. |
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Cerebellar tonsillar herniation
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Compression of medulla (contains respiratory and CV sychronicity) in foramen magnum
Herniating cerebellar tonsils squeeze the medulla, producing medullary paralysis and death (loss of consciousness, bradycardia, irregular respirations or apneic periods, and hypotension). Cerebellar masses may produce signs of lower midbrain and of pontine compression also. Fatal |
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Sequelae of rapidly expanding supratentorial lesions
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1. Uncal, hippocampal herniation
2. Compression of ipsilateral CN III 3. A-P compression of midbrain 4. Obstructive hydrocephalus 5. Cerebral peduncle compression (ipsi- or contralateral hemiparesis) 6. PCA compression (ischemia of visual cortex and thalamus) 7. Duret hemorrhages (central stem) 8. Tonsillar herniation - compression of medulla |
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Cytotoxic edema
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Swelling of cellular elements in the presence of an intact BBB
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Edema and ischemic infarcts
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Early changes include an increase in water content, then swelling of astrocyte processes. After several hours breakdown of the BBB occurs. Thus the early edema after ischemic injury is cytotoxic, whereas the later edema has a vasogenic component
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Generalized increase in intracranial volume leading to increased ICP
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e.g. pseudotumor cerebri
Signs and symptoms include headache, nausea, vomiting, papilledema, and rarely a sixth nerve palsy (false localizing sign). In pseudotumor cerebri, there is no obstruction to CSF flow nor is regulation of cerebral blood flow disturbed. Brain volume is increased diffusely. Consequently, shifts in brain substance usually do not occur. |
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Cingulate herniation
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A laterla hemispheric lesion will shift that hemisphere medially, pushing the ipsilateral cingulate gyrus under the free edge of the falx cerebri. This may compress the internal cerebral vein and the ipsilateral anterior cerebral artery.
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Herniation of the brain stem
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Clinical signs referable to brain stem compromise during herniation progress in a rostral to caudal fashion. Ipsilateral pupillary dilatation usually occurs first (midbrain). Disappearance of oculocephalic and oculovestibular reflexes indicating pontine dysfunction. Coma develops as midbrain and pontine reticular formation is compromised. In late stages, the eye signs and pyramidal tract signs may become bilateral.
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Signs of diencephalic dysfunction
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Decreasing alertness progressing to stupor or coma, small pupils, Babinski reflexes, Cheyne-Stokes breathing, and decorticate posturing.
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Signs of midbrain dysfunction
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Moderate pupillary dilatation, dysconjugate eye movements, hyperventilation, and decerebration
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Signs of pontine and upper medullary dysfunction
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Loss of oculocephalic and oculovestibular reflexes, shallow, irregular breathing, and flaccidity of limbs. Pupils are midposition and unresponsive.
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Signs of medullary dysfunction
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Irregular respiration, apneic periods, tachy- or bradycardia, and hypotension. This is terminal stage
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