Central Nervous System Flashcards by Jamaira Belmes

changes seen following acute CNS hypoxia/ischemia, severe hypoglycemia,
and other acute insults

THE EARLIEST MORPHOLOGIC MARKERS OF NEURONAL DEATH

evident by 6 to 12 hours after an irreversible hypoxic/ischemic insult

Acute neuronal injury (“red neurons”)

shrinkage of the cell body
pyknosis of the nucleus
disappearance of the nucleolus
loss of Nissl substance
intense cytoplasmic eosinophilia

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refers to neuronal death that occurs as a result of a progressive
disease of months to years duration, as is seen in slowly evolving
neurodegenerative diseases such as amyotrophic lateral sclerosis
and Alzheimer disease.

Subacute and chronic neuronal injury (“degeneration”)

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change observed in the cell body during regeneration of the axon

Axonal reaction

best seen in ANTERIOR horn cells of the spinal cord when motor axons are cut or seriously damaged

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refers to degeneration of axons after disruption of nerve fibers

Wallerian degeneration

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The most important histopathologic marker of CNS injury, regardless of etiology

characterized by hypertrophy and hyperplasia of ASTROCYTES

GLIOSIS

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occurs when unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the falx.

compression of the anterior cerebral artery and its branches –>
secondary infarcts.

SUBFALCINE (CINGULATE) HERNIATION

herniating part: CINGULATE
herniation through: UNDER THE FALX CEREBRI

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occurs when the medial aspect of the temporal lobe is compressed
against the free margin of the tentorium

COMPRESSED STRUCTURES:
CN III
PCA
contralateral cerebral peduncle

DURET HEMORRHAGES - brainstem and pons

TRANSTENTORIAL (UNCAL, MESIAL TEMPORAL) HERNIATION

herniating part: MEDIAL ASPECT OF TEMPORAL LOBE
herniation through: TENTORIUM CEREBELLI

KERNOHAN PHENOMENON

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refers to displacement of the cerebellar tonsils through the foramen magnum

life-threatening because it causes brainstem compression and
compromises vital respiratory and cardiac centers in the medulla

COMPRESSED STRUCTURES:
brainstem

TONSILLAR HERNIATION

herniating part: CEEBELLAR TONSILS
herniation through: FORAMEN MAGNUM

cardiac and respiratory depression

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MC CNS malformations

NEURAL TUBE DEFECTS

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malformation of the anterior end of the neural tube that leads to absence of most of the brain and calvarium

Forebrain development is disrupted at approximately
28 days of gestation

all that remains in its place is the area cerebrovasculosa - flattened remnant of disorganized brain tissue with admixed ependyma, choroid plexus, and
meningothelial cells

ANENCEPHALY

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extrusion of malformed brain tissue through a midline defect in the cranium

ENCEPHALOCELE

OCCIPUT - common location

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MC neural tube defects may be an asymptomatic bony defect (spina bifida occulta)

SPINAL DYSRAPHISM OR SPINA BIFIDA

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spectrum of malformations characterized by incomplete separation of the cerebral hemispheres across the midline

midline facial abnormalities - cyclopia
absence of the olfactory cranial nerves and related structures

HOLOPROSENCEPHALY

ASSOCIATIONS:

Trisomy 13

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Absence of white matter bundles that carry cortical projections from one hemisphere to another

Agenesis of the corpus callosum

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POSTERIOR FOSSA ANOMALIES

less severe disorder

low-lying CEREBELLAR TONSILS extend down into the VERTEBRAL CANAL

may be a silent abnormality or may become symptomatic
because of impaired CSF flow and medullary compression

Chiari type I malformation

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POSTERIOR FOSSA ANOMALIES

SMALL POSTERIO FOSSA
misshapen midline cerebellum with downward extension of vermis through the foramen magnum
hydrocephalus
lumbar myelomeningocele

Other associated changes may include
caudal displacement of the medulla, malformation of the tectum,
aqueductal stenosis, cerebral heterotopias, and hydromyelia

Arnold-Chiari malformation (Chiari type II malformation)

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POSTERIOR FOSSA ANOMALIES

SMALL POSTERIOR FOSSA
misshapen midline CEREBELLUM with downward extension of vermis through the foramen magnum
hydrocephalus
lumbar myelomeningocele

Arnold-Chiari malformation (Chiari type II malformation)

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POSTERIOR FOSSA ANOMALIES

enlarged posterior fossa
ABSENCE or HYPOPLASIA of cerebellar vermis
CYSTIC DILATATION of the 4th ventricle

Dandy Walker Malformation

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Neurons sensitive to ischemia

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Pyramidal layer of hippocampus (CA1: Sommer sector)
Cerebellar Purkinje cells
Pyramidal cells of cerebral cortex

Common sites of hypertensive intraparenchymal hemorrhage

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PUTAMEN
thalamus
pons
cerebellar hemispheres

MC clinically significant vascular malformations

10-30 y/o
MALES

SEIZURE
intracerebral hemorrhage
SAH

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ARTERIOVENOUS MALFORMATION

posterior branches of MCA

(+) neutrophils
DECREASED sugar
INCREASED protein
(+) culture

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ACUTE PYOGENIC MENINGITIS

(+) lymphocytic - viral
(+) neutrophils - chemical

NORMAL sugar
INCREASED protein
(-) culture

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ACUTE ASEPTIC MENINGITIS

(+) mononuclear
N or DECREASED sugar
MARKED INCREASED protein
(+) MTB

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TUBERCULOUS MENINGITIS

Signs of meningeal irritation

Nuchal rigidity (+) Brudzinski sign (+) Kernig sign

chronic meningitis involving the base of the brain and more variably the cerebral convexities and spinal leptomeninges

MENINGOVASCULAR NEUROSYPHILIS

caused by invasion of the brain by T. pallidum manifests as insidious but progressive cognitive impairment associated with mood alterations (DELUSIONS OF GRANDEUR) that terminate in severe dementia (general paresis of the insane)

PARETIC NEUROSYPHILIS

the result of damage to the sensory axons in the dorsal roots impaired joint position sense and ataxia (locomotor ataxia) loss of pain sensation --> skin and joint damage (Charcot joints) “lightning pains” absence of deep tendon reflexes

TABES DORSALIS

Neuronophagia of the anterior horn motor neurons of the spinal cord

POLIOMYELITIS

widespread neuronal degeneration and an inflammatory reaction that is most severe in the BRAINSTEM basal ganglia, spinal cord, and dorsal root ganglia may also be involved

RABIES

Pathognomonic microscopic findings in RABIES cytoplasmic, round to oval, eosinophilic inclusions found in:

NEGRI BODIES PYRAMIDAL NEURONS OF THE HIPPOCAMPUS PURKINJE CELLS OF THE CEREBELLUM

autoimmune demyelinating disorder characterized by distinct episodes of neurologic deficits that are separated in time and are attributable to patchy white matter lesions that are separated in space the MC of the demyelinating disorders CD4+ hypersensitivity to myelin sheath

MULTIPLE SCLEROSIS CSF: moderate pleocytosis mildly elevated protein increased IgG OLIGOCLONAL IgG bands MORPHOLOGY: multiphasic sclerotic plaques

Common initial manifestation of multiple sclerosis

unilateral involvement of the OPTIC NERVE (OPTIC NEURITIS)

The MC prion disease rare disorder that manifests clinically as a rapidly progressive dementia dementia startle myoclonus

Creutzfeldt-Jakob Disease (CJD) SPONGIFORM transformation of the cerebral cortex and deep gray matter structures (caudate, putamen) KURU PLAQUES - extracellular deposits of aggregated abnormal PrP Congo red– and PAS-positive and usually occur in the cerebellum

the most common cause of dementia in older adults, with an increasing incidence as a function of age AB generation - critical event accumulation of two proteins (Aβ and tau) APP (Ch21) - Down syndrome region ApoE (Ch 19) - strong influence

Alzheimer Disease (AD) TAU - triggers stress response -- neuronal injury AB - forms PLAQUES and TANGLES -- elicits inflammatory response PNEUMONIA - usual terminal event

Brain in patients with Alzheimer shows variable CORTICAL ATROPHY marked by GYRAL NARROWING and SULCAL WIDENING that is most pronounced in

frontal temporal parietal lobes

focal, spherical collections of dilated, tortuous, axonal or dendritic processes (dystrophic neurites) often around a central amyloid core, which may be surrounded by a clear halo deposits of aggregated AB peptides in the neuropil SPECIFIC FOR AD

NEURITIC PLAQUES

tau-containing bundles of filaments in the cytoplasm of the neurons that displace or encircle the nucleus NOT specific for AD correlate better with DEGREE OF DEMENTIA

NEUROFIBRILLARY TANGLES

Basis for cognitive impairment in patients with AD

DECREASED choline acetyltransferase loss of synaptophysin immunoreactivity INCREASED amyloid burden

neurodegenerative disease marked by a hypokinetic movement disorder that is caused by loss of dopaminergic neurons from the substantia nigra PALLOR OF SUBSTANTIA NIGRA

PARKINSON DISEASE tremor rigidity bradykinesia

neurodegenerative disease marked by a hypokinetic movement disorder that is caused by loss of dopaminergic neurons from the substantia nigra

PARKINSON DISEASE tremor rigidity bradykinesia

Diagnostic hallmark of PD

LEWY BODY (a synuclein)

AD disease caused by degeneration of striatal neurons characterized by a progressive movement disorder and dementia jerky, hyperkinetic, sometimes dystonic movements involving all parts of the body (chorea) are characteristic affected individuals may later develop bradykinesia and rigidity

HUNTINGTON DISEASE CAG repeats atrophy of the caudate nucleus and the putamen

AR disease characterized by progressive ataxia, spasticity, weakness, sensory neuropathy, and cardiomyopathy generally begins in the first decade of life with gait ataxia, followed by hand clumsiness and dysarthria Deep tendon reflexes are depressed or absent, but an extensor plantar reflex is typically present

FRIEDREICH ATAXIA GAA repeats - FRATAXIN

progressive disorder in which there is LOSS OF UMN in the cerebral cortex and LMN in the spinal cord and brainstem denervation of skeletal muscles --> weakness and atrophy SOD1 (Ch21) mutation

Amyotrophic Lateral Sclerosis (ALS) UPPER MOTOR - cerebral cortex; atrophic BA 4,6 (precentral gyrus) LOWER MOTOR - thinned anterior roots loss of motor neurons and CN motor nuclei BUNINA BODIES - PAS (+) cytoplasmic inclusions seen in remaining neurons corticospinal tract degeneration

Central Nervous System Flashcards

(45 cards)