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Pathology > Central Nervous System > Flashcards

Central Nervous System Flashcards

1
Q

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

A

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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2
Q

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.

A

Subacute and chronic neuronal injury (“degeneration”)

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3
Q

change observed in the cell body during regeneration of the axon

A

Axonal reaction

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

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4
Q

refers to degeneration of axons after disruption of nerve fibers

A

Wallerian degeneration

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5
Q

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

characterized by hypertrophy and hyperplasia of ASTROCYTES

A

GLIOSIS

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6
Q

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.

A

SUBFALCINE (CINGULATE) HERNIATION

herniating part: CINGULATE
herniation through: UNDER THE FALX CEREBRI

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7
Q

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

A

TRANSTENTORIAL (UNCAL, MESIAL TEMPORAL) HERNIATION

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

KERNOHAN PHENOMENON

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8
Q

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

A

TONSILLAR HERNIATION

herniating part: CEEBELLAR TONSILS
herniation through: FORAMEN MAGNUM

cardiac and respiratory depression

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9
Q

MC CNS malformations

A

NEURAL TUBE DEFECTS

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10
Q

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

A

ANENCEPHALY

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11
Q

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

A

ENCEPHALOCELE

OCCIPUT - common location

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12
Q

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

A

SPINAL DYSRAPHISM OR SPINA BIFIDA

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13
Q

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

A

HOLOPROSENCEPHALY

ASSOCIATIONS:

Trisomy 13

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14
Q

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

A

Agenesis of the corpus callosum

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15
Q

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

A

Chiari type I malformation

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16
Q

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

A

Arnold-Chiari malformation (Chiari type II malformation)

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17
Q

POSTERIOR FOSSA ANOMALIES

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

A

Arnold-Chiari malformation (Chiari type II malformation)

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18
Q

POSTERIOR FOSSA ANOMALIES

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

A

Dandy Walker Malformation

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19
Q

Neurons sensitive to ischemia

A

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

20
Q

Common sites of hypertensive intraparenchymal hemorrhage

A

PUTAMEN
thalamus
pons
cerebellar hemispheres

21
Q

MC clinically significant vascular malformations

10-30 y/o
MALES

SEIZURE
intracerebral hemorrhage
SAH

A

ARTERIOVENOUS MALFORMATION

posterior branches of MCA

22
Q

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

A

ACUTE PYOGENIC MENINGITIS

23
Q

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

NORMAL sugar
INCREASED protein
(-) culture

A

ACUTE ASEPTIC MENINGITIS

24
Q

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

A

TUBERCULOUS MENINGITIS

25
Q

Signs of meningeal irritation

A

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

26
Q

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

A

MENINGOVASCULAR NEUROSYPHILIS

27
Q

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)

A

PARETIC NEUROSYPHILIS

28
Q

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

A

TABES DORSALIS

29
Q

Neuronophagia of the anterior horn motor neurons of the spinal cord

A

POLIOMYELITIS

30
Q

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

A

RABIES

31
Q

Pathognomonic microscopic findings in RABIES

cytoplasmic, round to oval, eosinophilic inclusions found in:

A

NEGRI BODIES

PYRAMIDAL NEURONS OF THE HIPPOCAMPUS
PURKINJE CELLS OF THE CEREBELLUM

32
Q

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

A

MULTIPLE SCLEROSIS

CSF: moderate pleocytosis
mildly elevated protein
increased IgG
OLIGOCLONAL IgG bands

MORPHOLOGY:
multiphasic sclerotic plaques

33
Q

Common initial manifestation of multiple sclerosis

A

unilateral involvement of the OPTIC NERVE (OPTIC NEURITIS)

34
Q

The MC prion disease

rare disorder that manifests clinically as a rapidly progressive dementia

dementia
startle myoclonus

A

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

35
Q

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

A

Alzheimer Disease (AD)

TAU - triggers stress response – neuronal injury

AB - forms PLAQUES and TANGLES – elicits inflammatory response

PNEUMONIA - usual terminal event

36
Q

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

A

frontal
temporal
parietal lobes

37
Q

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

A

NEURITIC PLAQUES

38
Q

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

A

NEUROFIBRILLARY TANGLES

39
Q

Basis for cognitive impairment in patients with AD

A

DECREASED choline acetyltransferase
loss of synaptophysin immunoreactivity
INCREASED amyloid burden

40
Q

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

PALLOR OF SUBSTANTIA NIGRA

A

PARKINSON DISEASE

tremor
rigidity
bradykinesia

40
Q

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

A

PARKINSON DISEASE

tremor
rigidity
bradykinesia

41
Q

Diagnostic hallmark of PD

A

LEWY BODY (a synuclein)

42
Q

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

A

HUNTINGTON DISEASE

CAG repeats

atrophy of the caudate nucleus and the putamen

43
Q

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

A

FRIEDREICH ATAXIA

GAA repeats - FRATAXIN

44
Q

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

A

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

Pathology (24 decks)

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