perivascular cuffing by lymphocytes and plasma cells

neuronal necrosis

inclusion bodies

microglial proliferation

microglial nodules

hemorrhagic necrosis (specific to)

Viral Encephalitis

(HSV-1)

alterations in mood, memory and behaivior

neuronal necrosis

hemorrhagic necrosis

abscesses

encephalitis

granulomatous inflammation

central liquefactive necrosis

surrounded by zone of fibrous tissue with

proliferation of small vessels

vasogenic edema

reactive gliosis

Chronic meningitis

perivascular inflammatory rxn rich in plasma cells and lymphocytes

invasion of the brain by treponema pallidum

progressive mental deficits

mood alterations progressive to severe dementia

parenchymal damage in the cerebral cortex

loss of neurons

proliferation of microglia

gliosis

damage to the sensory nerves in dorsal roots

impaired joint position sense --> ataxia

loss of pain sensation

lighting pains

absence of deep tendon reflexes

loss of axons and myelin in the dorsal roots --> pallor and atrophy in the dorsal columns

Argyll-Robertson pupils

affects mainly subcortical areas

diffuse white matter pallor

perivascular infiltrates of lymphocytes and macrophages

foci of necrosis, gliosis and/or demyelination

microglial nodules, macropahges and multinucleated giant cells

inclusion bodies in oligodendroglia nuclei

transformed bizarre astrocytes

gliosis

PML - progressive multifocal leukoencephalopathy

(virus infects oligodendrocytes)

Subacute Sclerosing Panencephalitis

inclusion bodies in oligodendroglia, neurons and astrocytes

chronic inflammation (perivascular cuffing by lymphocytes and plasma cells)

resting tremor

bradykinesia

rigidity

Mood disorder, later dementia and dysautonomia

gait instability

Parkinson's Disease

remember ASYMMETRY

nausea

orthostatic hypotension

hallucinations

dyskinesias

pramipexole

early falls

down-gaze paralysis

axial rigidity

truncal apraxia

wide-eyed, unblinking face

CST & CBT signs

early falls

nocturnal stridor

cerebellar signs

CST signs

prominent dysautonomia

no response to levadopa

shy-drager

SND

OPCA

progressive asymmetric rigidity

apraxia

myoclonus

alien limb (dystonia)

Gaze palsy -rare

levadopa unresponsive

wet, wobbly and wacky

urinary incontinence, gait ataxia, dementia

deficient copper excretion

basal ganglia -akinetic- rigid, wing beating tremor, dystonia, chorea

high serum/urine copper

low ceruloplasmin

sustained and/or phasic contraction of muscle causing abnormal posture or repetetive movements

co-contraction of antagonist and agonist muscles

DYT-1 gene mutation

A Dominant

GTP cyclohydrolase mutation

A Dominant

degenerative

autoimmune

drugs

metabolic

polycythemia vera

Autosomal Dominant

gain-of-function of the mutant protein huntingtin

atrophy of the caudate nucleus

ventricular dilatation

lesion in liver

putamen and globus pallidus

Autosomal recessive

Chromosome 13

SOD1 gene

Autosomal Dominant

Familial in only 10% cases

loss of anterior horn cells in spinal cord and

motor neurons in the motor strip

Wallegerian degeneration

GAA trinucleotide repeat expansion in the first intron of FRDA

Lesion in the DRG and cerebellum

loss of axons and myelin in posterior columns, spinocerebellar tracts, corticospinal tracts.

gliosis

loss of DRG cells and Purkinje cerebellar cells

Degeneration of the cerebellar dentate nucleus

excessive daytime sleepiness and

disordered regulation of REM sleep

pervasive iron metabolism abnormality

brain iron deficiency

abnormalities in subcortical CNS dopaminergic systems

Hyperdopaminergic state

REM ON neurons use this neurtransmiter

astrocytes have very dense fibers

rosenthal fibers

cuboidal

well circumscribed cells

true ependymal rosettes

perivascular pseudorosettes

looks well circumscribed but it infiltrates widely

areas of hemorrhage, necrosis and cysts

marked edema

mild increase in glial cellularity

astrocytic processes

astrocytes w/ PLEOMORPHIC NUCLEI

negligible mitotic activity

dense cellular regions

greater nuclear pleomorphism

MITOTIC FIGURES

gemistocytic astrocytes

NECROSIS AND/OR ENDOTHELIAL

PROLIFERATION

Perinecrotic palisading

nuclear pleomorphism

mitosis

glomeruloid body

central nuclei and halo of clear cytoplasm "fried egg appearance"

may be lo grade or high grade (anaplastic, necrosis, mitotic act.)

perivascular cuffing of tumor cells

diffuse inflitration of surrounding neural tissue

scant cytoplasm and large pale nuclei

wholrs of cells

psammoma bodies (concentrical calcifications produced by mineral deposition in whorls of cells)

not exclusive to this type of tumor but

central necrosis, hemorrhage and widespread edema

paresthesias of the circumoral area, hands and feet

visual field constriction

ataxia

12-36 hrs  after nausea and dyr mouth

difficulty swallowing and speaking

double vision

weakness

symmetrical flaccid paralysis

inactivates synaptobrevin

blocks synaptic transmission that would inhibit motor neurons

leads to generalized contractions

opisthotonos

toxin that causes:

extra-pyramidal and cerebellar signs

mental fatigue

polyneuropathy

neuronal necrosis and apoptosis

neuronal necrosis in cerebral cortex, hippocampus, cerebellum, and globus pallidus

toxin that causes degeneration of retinal ganglion cells

degeneration of motor and sensory nerves

distal region affected first

degeneration of both myelin and axons (anterior horn and posterior root deg)

confusion

opthalmoplegia

ataxia

W encephalopathy

Wernicke-Korsakoff syndrome

mammillary bodies

periaqueductal gray matter

alcoholic polyneuropathy

WK syndrome

deficiency that causes degeneration of white matter in the CNS

primary lesion appears to be in myelin

sensory and motor UMN signs

high ammonia levels

astrocytes clear ammonia

abnormal astrocytes with a very large nucleus (Alzheimer type II)

high ammonia

brain edema

behaivoral and neurological disturbances

consciousness and motor abnormalities