Neuro Flashcards
(270 cards)
1
Q
What may cause enlargement of lacrimal gland
A
Sacroidosis-inflammation
Neoplasm-lymphoma, pleomorphic adenoma, adenoid cystic carcinoma
2
Q
Wegener granulomatous is
A
May start in eye
Necrosis and degenerating collagen with vasculitis
3
Q
What orbital masses are encapsulated
A
Lacrimal gland
Dermoidneurliemmoma
4
Q
Non Hodgkin lymphoma eye
A
Can effect entire orbit or be confined to a compartment
5
Q
Metastatic prostic carcinoma
A
May present like idiopathic orbital inflammation
6
Q
Metastatic neuroblastoma and wilms
A
Rich vascular neoplasms
Perioculat ecchymoses
7
Q
What does an eyelid basal cell carcinoma look like
A
Pearly white with depressed central area
8
Q
Granulomatous associated with systemic sarcoidosis may be detected in __
A
Fornix
50%. Nulomas
9
Q
Primary lymphoma of conjunctiva in ___
A
Fornix
10
Q
Prob with conjunctival scarring
A
Reduce goblet cells reduced mucin
Tears don’t adhere even if production ok
XEROPTHALMIA
11
Q
Delle
A
Depression in corneal tissue from dehydration caused by pniguecula
*not enter cornea though causes uneven distribution of tear film
12
Q
How does conjunctival melanoma form
A
Phase of intraepihtelial growth called primary acquired mmelanosis with atypia
13
Q
Who gets immune complex deposition with sclera
A
RA
14
Q
Major refractive surface of the eye
A
Cornea and tear film
15
Q
Nonimmunologic grade rejection cornea
A
Loss of endothelial cells and then edema
16
Q
What causes stromal edema
A
Loss of endothelial cells and deturgence
17
Q
Descent membrane
A
Thicker with age
Where copper deposition occurs in kayser fleischer
18
Q
Corneal ulceration
A
Herpes, acanthamoebe
Bacteria fungal prozoa
Keratitis-activation of collagenases and stromal fibroblasts
19
Q
How visualize corneal ulceration
A
Exudate and cells leaking from the iris and ciliary body vessels can be seen by slit lamp or pen lite
(Hypopyon no organisms) but corneal ulcer infectious
20
Q
What is keratitis
A
Corneal inflammation
21
Q
Chronic herpes
A
Keratitis associated with granulomatous reaction involving descent
22
Q
Oil droplet keratopathy
A
Oil droplet keratopathyactinic band
Actinic band superficial corneal collagen
23
Q
Keratoconus
A
Thinning of cornea without inflammation. Or vascularization
Corneal degeneration
Descent may rupture
Corneal hydrops cause corneal scarring and vision loss
SUDDEN corneal hydrops
24
Q
Corneal hydrops
A
Keratoconus
Haab striae (infantile glaucoma)
Obstetric forceps injury
25
Fuchs
Gutatta
Stroma ground glass
Stroma vascularization from edema
26
Degenerative pants
Fuchs
Fibrous CT between epithelium and bowman
Epithelium detaches from basement membrane
27
Pseudophakic bulbous keratopathy
After cataract surgery
| Edema vision loss
28
Stromal dystrophy-discrete opacities in cornea that compromise vision
TGFB1 mutation
Keratoepithelin
Or improper folding of keratoepithelin
29
Pars plicata
Of ciliary body make aqueous humour to enter posterior chamber through pupil to anterior
30
Nuclear sclerosis
Age related opacification of lens makes brown cant see blue
| Rembrandt yellow
31
Caues of cataract
Age
| Galactosemia, diabetes, Wilson, atopic dermatitis, corticosteroids, radiation, intraocular disorders
32
Posterior subscapular cataract
Migration of lens epithelium posterior to lens secondary to enlarged or weird positioned lens epithelium
33
Phacolytic glaucoma from a morgagnin cataract
Lens cortex liquify(mortgaging cataract)
High molecular weight proteins leak thorough lens capsule)phacolysos_
Proteins or contained in macrophages can clog trabecular meshwork and cause ICP and optic nerve damage
34
What causes increased pressure in open angle glaucoma
Increased resistance to flow
35
Angle closure
Iris adhere to meshwork
36
Glaucoma
Most from IOP
| Visual field and cup of optic nerve changes
37
Primary open angle
MYOC mycolilin
OPTN optineurin
Risk-hyperopia
38
Secondary open glaucoma
Pseudoexfoliation glaucoma-deposition of fibrillation material throughout anterior segment
Lysyl oxidase 1
Get deposition around CT, liver kidney too
Clog trabecular meshwork
39
Ghost cell glaucoma
High molecular weight from phacolytic, senescent red cells after trauma
40
Pigmentary glaucoma
Iris epithelial pigment granules
41
Melanomalytic glaucoma
Necrotic tumours
42
Episcleral venous pressure
Elevations in pressure on the surface of the eye in the presence of open angle
-sturge Weber syndrome or arterialization of episcleral veins following traumatic carotid cavernous fistula
43
Primary angle closure
Hyperopia
Adhere iris to TM
Pupillary block
44
Iris bombe
Iris move forward in closed angle
| Increases pressure in posterior chamber
45
Glaukomflecken
Minute anterior subscapular opacities visible on slit lamp from unremitting elevation in IOP in primary closed angle damage to lens epithelium
46
What can IOP in closed angle primary cause
Glaukomflecken
Corneal edema
Bulbous keratopathy
47
Secondary closed angle
Contraction of pathological membranes over iris can draw it over TM, occluding flow like in neovascular glaucoma
Tumors in iris mechanically compress iris nonto trabecular mesh
Retinoblastoma can induce neovascular glaucoma
48
Chronic retinal ischemia
Upregulation of VEGF and proangiogenic factors which cause the development of thin fibrovascular membranes ont he surface of the iris
Cause secondary closed
49
What may cause neovascular glaucoma
Chronic retinal ischemia upregulated vegf and proangiogenic factors causing development of thin fibrovascular membranes on surface of the iris
Necrotic tumors like retinoblastoma can also induce neovascular glaucoma
50
Endopthalmitis
Inflammation vitreous humour
51
Anterior syenchiae
Adhesion between the iris and TM or cornea
From inflammation-vessels in ciliary body and iris become leaky and allow cells and exudate to accumulate in anterior chamber and adhere to corneal endothelium to form keratic precipitates (slit lamp)
52
Posterior synechiae
Adhesion between iris and anterior surface of lens
53
Anterior synechia can lead o what
Secondary closed angle
| IOP and optic nerve damage
54
Posterior synechiae can lead to what
Deprive lens epithelium of aqueous humour and induce fibrous metaplasia of lens epithelium (anterior subscapular character)
55
Endophthalmitis
Vitreous humour inflammation
| -damage retina
56
Exogenous endophthamitis
Originating in environment and gain access through wound
57
Endogenous endopthalmitis
Delivered to eye hematogenously
58
Panophthalmitis
Whole eye inflammation including retina, choriod, sclera and extend into orbit
59
What is uvea
Iris, choroid and ciliary body
60
What is one of the most richly vascularized sites in body
Choriod
61
Uveitis
Iris choriod ciliary inflammation
Inflammation to eye
62
Uveitis may manifest anterior segment
Juvenile RA
63
Uveitis is accompanied by what
Retinal pathology
64
What causes uveitis
Pneumocystitis carnii, autoimmune (sympathetic ophthalmia), idiopathic sarcoidosis
65
Granulomatous uveitis
Sarcoidosis
Anterior segment mutton fat keratic precipitates
Posterior segment-choroid and retina where granulomatous can develop
Retina-perivascular inflammation see candle wax dripping
Do conjunctival biopsy to detect granulomas
66
Retinal toxoplasmosis
Uveitis, scleritis
67
AIDS
CMV retinitis, pneumocystitis, mycotic choroiditis
68
Sympathetic ophthalmia
Non infections panuveitis
Bilateral granulomas inflammation
Penetrating eye injury antigens released to conjunctiva and get delayed hypersensitivity weeks to years later
Granulomatous inflammation where eosinophils seen
Give immunosuppressive agent
69
Most common site of intraocular malignancy
Uveal-choroid(5% of melanoma)
SHORT SURVIVAL palliative
85% GNAQ and GNA11 (GPCR oncogenes) gain of function
Loss chromosome 3, delete BPA1, a tumor suppressor on chromosome 2 that encodes a deubiquinating enzyme
In epigenetics-does gene silencing
70
Uveal nevi
10% caucasions
GNAQ and GNA11 (GPCR, oncogenes)
Don’t transform
71
GNAQ GNA11
MAPK promote proliferation
72
Uveal melanoma morphology
1 cell types,
Spindle-fusiform
Epithelioid cells-spherical treated cytology atypicallity
Looping slit like spaces lined by laminitis surround tumors ells that aren’t cellls but act as vessels in a process of vasculogenesis mimicry
-are conduits for nutrients allowto spread
73
How do uveal melanoma spread
HEMATOGENOUS
74
Clinical uveal melanoma
Found by chance
Lateral size of tumor big bad
Epithelial cells bad
Loss of chromosome 3 bad
75
Iris vs ciliary body and choroid melanoma
Ok vs BAD 5 yr survival 80% 10 year 40$ dead increase 1% per year after
76
Tumor dormancy
Uveal melanoma
| Metastasis appear out of the blue
77
What is special about the retina
Derivative of diencephalon and undergoes gliosis when damaged -no lymphatics like brain
78
Hemorrhage in retina nerve fiberslooks like what
Horizontal streaks or flames
79
Hemorrhage in external retina
Dots (tips of cylinders perpendicular to retinal surface)
80
Where does exudate accumulate in retinal
Outer plexiform layer, espicially macula
81
Layers of the retina
```
Optic fiber layer(light hit)
Ganglion cell layer
Inner plexiform later
Inner nuclear layer
Outer plexiform layer
Outer nuclear layer
Inner segments
Outer segments
RPE choroid
```
82
RPE derived from what
Primary optic vesicle
Helps maintain outer segments of photoreceptors
83
Retinal detachment
RPE from neurosensory retina
84
Persistent hyperplastic primary vitreous
Fetal vessels do not regress in in vitreous humor (adult in avascular)
85
What can opacity the vitreous humour
Hemorrhage from trauma or retinal neovascularization
86
Vitreous and aging
Liquify and collapse (sensation fo floaters)
Posterior vitreous detachment-posterior face separate from neurosensory retina
87
Retinal detachment
RPE from neurosensory
Rhegmatogenous or non rhegmatougenous
Need to maintain photoreceptors in outer retina
88
Rhegmatougenous retinal detachment
Full thickness tear
From collapse of vitreous and posterior hyaloid exerts traction
Or from proliferative vitreoretinopathy where there is formation of epiretinal or subretinal membranes by retinal glial cells (muller cels) or RPE
Vitreous humour leak into space between RPA and neurosensory
89
Non rhegmatougenous retinal detachment
Without retinal break
From retinal vascular disorders associated with significant exudation and any condition that damages RPE and permits fluid ear from choroidal circulation under retina
Associated with malignant HTM
90
Retinal hypertension
Vessels narrow and extra thickness causes color change from red to copper and silver this is bad bc retainal and arterioles share adventitious sheath so can compress veins when cross causing venous stasis
Damage vessels of retina and choroid with malignant hypertension
91
Elschnig spots
Infarcts of the choroid due to damage of choroid vessels
92
If there is damage to choriocapillaries I then there could be damage to __
RPE and allow exudate to enter and cause detachment
| -exudate accumulate in outer plexiform layer
93
Damage to retinal arterioles causes what
Exudate in outer plexiform layer
94
What are signs or exudate in outer plexiform layer
Macular star-spoke like arrangement of exudate in the macula in the setting of malignant hypertension, oblique rather than perpendicular to surface
95
Occlusion of retinal arterioles causes what
Infarcts of nerve fiber later (ganglion) and axons
| -axoplasmic transport interrupted, accumulation of mitochondria at swollen ends of axons causes cystic bodies
96
Characterization of infarct of nerve fiber layer
Cystoid bodies(accumulation of mitochondria at the swollen ends of damaged axons)-collections of these seen as cotton wool spots on ophthalascope
97
Besides HTN, what may cause retinal vasculopathy
AIDS
98
Diabetes eye
Thicken BM of epithelium of pars plicata of ciliary body-proliferative or non)
99
Non proliferative diabetic retinopathy
Thick BM of BV
(Decrease in pericytes to endothelial cells)
Microaneusysms and hemorrhages
VEGF makes retinal microcirculation leaky
Cause macular edema -vision loss
Vascular microocclusions can be seen with intravenous fluorescein
Exudate in outer plexiform
Non perfusion of the retina due to microcirculatory change is associated with up regulation of VEGF
100
Proliferative diabetic retinopathy new vessels from optic nerve head of retina
Extend along posterior hyaloid and retinal plane
Can get posterior vitreous detachcausing hemorrhage from ruptured neovascular membranescarring and wrinkle of retina cause vision prob and may cause retinal detachment (traction retinal detachment)
101
Retinal neovascularization may accompany
Iris neovascularization
102
Retinopathy of prematurity (retro lentil fibroplasia0
At term lateral retina is incompletely vascularized , medial is vascularized
Premature baby-immature retinal vessels in temporal constrict making ischemic here..places on O2
Upregulate VEGF and get retinal angiogenesis
Contraction of resulting peripheral retinal neovascular membrane may drag the temporal aspect of the retina toward peripheral zone and displace macula lateral or detach retina
103
Sickle retinopathy
Non proliferative SS SC
Or
Proliferative
Cause vascular occlusion form low O2 tension leading to RBC sickling
104
Vascular occlusion from sickle retinopathy
Pre retinal, intraretinal and sub retinal hemorrhage
Resolution of hemorrhages look like salmon patches, iridescent spots and black sunburst lesions
VEGF-neovascularization seen as sea fans
105
Organization fo pre retinal hemorrhage may result in retinal traction leading to what
Detachment
106
What are sea fans and why seen
Neovascularization in retina from sickle retinopathy, damage to retinal celebs, radiation
Cause ischemia trigger angiogenesis
107
Complications of retinal neovascularization
Hemorrhage, traction detachment
108
Hollenhorst plaques
Fragments of atherosclerotic plaques lodge within the retinal circulation
109
What get retinal infarct
When total retinal artery occluded
110
What happens with retinal infarct
Derived from brain
Swell and opaque which blocks view of choroid and fundus appears white instead of orange
WHITE INFARCT from arterial occlusion
111
Diffuse retinal infarct
Total occlusion of central retinal artery
Retina white opaque
Fovea thin and unaffected;cherry red spot bc red choroid is visible
112
What do we see cherry red spot in
Diffuse infarct retina
| Ray Sachs Niemeyer pick
113
Retinal vein occlusion
Without ischemia-hemorrhage, exudate, macular edema, no neovascularization
With ischemia-upregulate vegf neovascularization -of retina, optic nerve, iris (can get angle closure glaucoma)
114
AMD
Wet or dry8% over 75
115
Dry AMD
Drusen deposits in bruch and RPE atrophy
| No treat
116
Wet AMD
Choroidal neovascularization of vessels that originate from choriocapillaries and penetrates through bruch membrane beneath RPE and can fo through RPE to neurosensory retina
117
Issue with wet AMD
Vessels leak and blood organize by RPA macular scare
| Can get diffuse vitreous hemorrhage
118
Treat wet AMD
VEGF antagonist
119
What may abuse choroidal neovascularization
Myopia(fuch spot), disruption of bruch due to trauma, immmune to histoplasmosis
120
Bruch membrane
BM or RPE
121
Choriocapillaries
Innermost layer of choroidal
122
Genetic AMD
CHF complement
| Also light
123
Functional unit of AMD
RPE, bruch membrane which has BM of RPE and innermost choroidal layer, choriocapillaries
-vision loss from photoreceptor damage to any of these
124
Retinitis pigmentosa
```
Inherited rod cone RPE mutation
Non inflammatory
Total blind
Retinal degeneration
AR, X, AD (AD later in life)
```
125
What syndromes may retinitis pigmentosa be a part of
Bardet-biedl syndrome, usher syndrome, refuse disease
126
Sign of retinitis pigmentosa
Rod and cones lost to apoptosis with rode leading to night bling and cones center field blind
127
Retinal atrophy from RP
Optic nerve atrophy (waxy pallor of optic disc) and accumulation or retinal pigment around the vessels
128
Genetic mutations of RP
Transcription factors, structural genets, catabolic paths
129
Infections retinitis
Candida can get to retina via blood causing multiple retinal abscesses
CMV retinitis is a major cause of visual impairment in AIDS
HEMATOGENOUS
130
Retinoblastoma
Most common intraocular malignancy in kids
131
What recent of RB is familial
40
132
RB is __ of function
Loss
133
RB unilateral or bilateral
Bilateral
134
What is RB associated with
Pinealoblastoma (trilateral retinoblastoma) bad outcome
135
Sporadic RB
Two mutations q
136
Morphology RB
Diffferentiated0round, small cells of hyperchromic nuclei
Flexing wintersteiner rosettes and fleurettes (photoreceptor differentiation)
-focal zones of dystrophic calcification)
137
Where does RB spread
Brain and bone marrow
| Not lungs
138
What disintguishes bad prognosis of RB
Not differentiation
Extraocular extensiona Nd invasion along optic nerve and by choroidal invasion
139
Retinocytoma/retinopathy
Premalignant lesion
| -
140
Appearance of retinoblastoma in one eye and retinocytoma in other
Heritable retinoblastoma
141
Retinal lymphoma
AGGRESSIVE
| Involves RPE and neurosensory retina
142
What is special about RPE and neurosensory retina
Derived from brain
143
Who gets retinal lymphoma and what does it mimic
Old people
| Uveitis
144
How may diffuse B cell ymphma spread to brain
Optic nerve
145
Pilocytoc astrocytoma
Gloomy of optic nerve
146
Anterior ischemic optic neuropathy
Similar to stroke
| -injuries to optic nerve from ischemia /infarction
147
What does optic nerve in AOIN look Ike
Swollen pale
148
Transient AION
Vision loss comes back
149
Total occlusion infarct AION
Partial or complete vision loss
150
Does optic nerve regenerate
No
151
What causes ischemia infarct in AOIN
Embolism, thrbomtis
152
Temporal arthritis
Optic nerve bilateral infarct causes total blindness
153
Papilledema
Edema of head of ON from increased ICP
(Bilateral)
Or neoplasm (unilateral)
154
What does nerve head look like in papilledema
Swollen hype remix
155
Is acute papilledema from increased intracranial pressure associated with visual loss
No
156
Glaucoma optic nerve damage
Loss of ganglion cells and thinning of retinal nerve fiber layers
Optic nerve is cupped and strophic
157
Elevated IOP in kids
Diffuse enlargement of eye (buphthalmos) or enlargement of cornea (megalocornea)
158
IOP in adult
Thin sclera staphylococcus
159
Methanol and optic neuropathy
Sure toxic
160
Lever hereditary optic neuropathy
Inherited mitochondrial gene mutations (maternal)
Males 9:1
10-30 yr onset
Clouding of vision and progress to vision loss and optic nerve damage
161
Optic neuritis
Loss of vision secondary to optic nerve damage
| MS
162
40 yo female with vision loss
MS workup
163
Increased risk of MS is
Optic neuritis
| Evidence of brain lesions via MRI
164
Phthisis bulbi
Phthisis bulbiend stage eye shrunken and disorganized atrophy
165
Ciliochoroidal effusion
Exudate between ciliary body and scleraand choroid and sclera
Phthisis bulbi
Low IOP (hypotonic)
Square eye
166
Cyclists membrane
Membrane from ciliary body to ciliary body
167
Signs of end stage eyes
```
Phthisis bulbi which see
Ciliochordial effusion
Cyclonic membrane
Chronic retinal detachment
Optic nerve atrophy
Intraocular bone
Thickened sclera
Square eye
```
168
Red neuron
Intense eosinophilia loss of his SLE and pyknosis and shrinkage
169
Central chromatolysis
Axonal injury
170
Gemistocytic astrocytes
Injury
Nucleus enlarges becomes pink
Eccentric nucleus with ramifying processes
171
Alzheimer’s type II astrocyte
Gray matter cell pale staining LARGE intranuclear glycogen droplet and a prominent nuclear membrane and nucleolus
172
Microglial nodules
Aggregates around small foci of tissue necrosis
173
Neuropharmacologist
Microglia around cell bodies of dying neurons
174
MSA oligodendrocytes
Glial cytoplasmic inclusions with a synuclein
175
PML oligodendrocytes
Viral inclusions
176
Injury or apoptosis oligodendrocytes
Demylinating disease and leukodystrophies
177
Ependymal
Ciliated columnar cells
-CMV viral inclusions
Granulations-inflammation or disption of ependymal lining paired with subependylmal proliferation of astrocytes
178
Response of astrocytes to injury
Hypertrophy
Accumulation GFAP
Hyperplasia
179
Vasogenic edema
Disrupt BBB and increased vascular permeability
ECF
Non lymphatics in brain to reabsorbed
180
Localized vasogenic edema
Adjacent to inflammation or neoplasm
181
Generalized vasogenic edema
Ischemic injury
182
Cytotoxic edema
BB ok Na K atpas lead to retention in NA
ICF increase from neuronal, glial or endothelial cell membrane injury
183
Cause of cytotoxic edema
Generalized hypoxic or ischemic
| Components of vasogenic
184
Generalized edema
Vasogenic and cytotoxic
185
Signs of generalized edema
Gyri flat and narrow sulcu ventricular cavities compressed, herniation
186
Interstitial edema(hydrocephalus edema)
Hydrocephalus send CSF to perientricular white matter
187
Choroid plexus papilloma
Tumor in choroid hydrocephalus rare
188
Causes of genetic non communicating hydrocephalus
Aqueductal stenosis dandy walker
189
Dandy walker
Vermis aplasia
4th v big
Hydrocephalus
190
Chronic adhesive arachnoiditis
Hydrocephalus from failure of CSF resorption
191
What ind of hydrocephalus is hydrocephalus ex vacuo
Communicating
192
Subfalcine herniation
Cingulate ACA
193
Transtentorial
Medial femoral
CNIII
PCA
Contralateral cerebral peduncle (ipsilateral hemiparesis-weak)
194
Kernohan notch
Compression of peduncle in transtentorial herniation
195
Duret hemorrhage
Form transtentorial herniation
Secondary hemorrhagic linear of flame shaped lesion in midbrain and pons that often accompany transtentorial herniation
-midline and paramedian regions
Mesencephalon
196
Tonsillarr herniation
Brainstem problem
| Respiratory fail
197
Symptoms of myelomeningocele
Motor and sensory deficits in lower extremities with bowel and bladder dysfunction complicated by superimposing infection that enters thin overlying skin
198
Encephlaocele
Brain stick out
Nasal glioma
Or posterior fossa
199
NT defect genetic
Highly
Folate defiency
Polymorphism in folate stuff
200
Anencephaly
Anterior NT prob
No brain and calvaria
Forebrain development disrupted 28 days of gestation
Only thing remaining is area cerebrovaculosa
201
What is area cerebrovaculoas
Flattened remnant of disorganized brain tissue with admired ependymal, choroid plexus, and meningothelial cells frog eye posterior fossa spared
202
What causes microencephaly
Decreased migration
FAS, HIV, chromosomal abnormalities
Simplified gyrus folding
203
Lissencephaly
Reduced gyri
204
Type 1 lissencephaly
Mutations that disrupt the signaling for migration and the cytoskeletal motor proteins that drive migration or neuroblasts
SMOOTH
205
Type 2 lissencephaly
Genetic alterations that disrupt stop signal for migrationcobblestone surfaced
Need glycosylated proteins and mutations in enzymes that place the sugars onto the proteins
206
Polymicroglia
Small unusually numerous cerebral convolutions 4 or less cortex layers
Entrap meningeal tissue
Tissue injury
Or symmetric and bilateral if genetic
207
Neural heteroropias
Neurons in inappropriate
Mutate filament a for assembly of complex meshworks of actin filaments X chromosome
Male fatal
Female-some normal some not
Or Double cortin DCX on X (microtubule associated protein)
Males-lissencephaly
Females-subcortical heterotopias (discrete nodules of neurons sitting in subcortical white matter or complete ribbons that parody overlying cortex)
208
Holoprosencephaly
Midline suture defect doesn’t separate
Cyclopes
Less severe absence of olfactory
DEFECT SHH
209
What is holoprosencephaly associated with
Trisomy thirteen
210
Agenesis of corpus callosum
Bat wing
Common
Fine or mentally retarded
211
Arnold chiari formation II
```
Vermis downward through foramen magnum
Tenting textual plate
Hydrocephalus
Myelomeningocele
Aqueductal stenosis
Heterotopias
Hydrolysis
```
212
Chiari type I malformation
Cerebellar tonsil down into vertebral canal
| Silent of symptomatic
213
Dandy walker
Rudimentary cerebellar vermis midline cyst
Lined by ependymal and is contiguous with letpmeninges
Represented roof of expanded fourth ventricle in absence of vermis
214
Joubert syndrome
Hypoplasia of vermis , elongation of superior cerebellar peduncle, altered brainstem shape
Molar tooth sign
Mutations of primary cilium
215
Syringomyelia
Fluid filled cavity in the inner portion of the cord
216
Syringobulbia
Syringomyelia extend into brainstem
217
What is syringomyelia associated with
Arnold chiariintraspinal tumor
| Traumatic injury
218
Histology syringomyelia
Destruction of adjacent grey and white mater surrounded by gliosis
219
When does syringomyelia occur
Second or third decade
220
Clinical presentation syringomyelia
Loss of pain and temperature in upper extremities from anterior spinal commissure
221
Hydromyelia
Expansion of ependymal lined central canal of the rod
222
Histology hydromyelia
Destruction of adjacent grey and white matter surrounded by a dense gliosis
223
When does hydromyelia occur
Second third decade
224
Cerebral palsy
Non progressice neurologic motor deficits -spasticity, dystonia, ataxia/athetosis, paresis attributable to insult that occur in the pre natal and perinatal periods from birth
225
IntraParenchymal hemorrhage
Terminal matrix hemorrhage
Intraventricular hemorrhage
Extend into the subarachnoid space (subarachnoid hemorrhage)
226
Sequelaea intraparenchymal hemorrhage
Larger hemorrhages can organize in aqueduct of Sylvia’s or 4th centriole foramina to obstruct CSF and lead to a non communicating hydrocephalus
227
Premature infants IntraParenchymal hemorrhage
Twenty two to twenty three weeks
| High cellularity and vascularity and vulnerable to insults even minor changes in cerebral blood
228
Where does IntraParenchymal hemorrhage occur
Junction of developing thalamus and caudate nucleus
229
Periventricular leukamalacia
Infarct in supratentorial periventricular white matter
Form of perinatal injury that is caused by hypoxic ischemic events or infections
Premature
In supratentorial periventricular white matter
Chalky yellow plaques consisting of discrete regions of white matter
230
Multicystic encephalopathy
Infarct more severe that periventricular leukamalaciagrey and white matter ischemia
Lead to large destructive system throughout hemisphere
231
Symptoms of multicystic encephalopathy
Thinned gliotic gyri (ulegyria)
Basal ganglia and thalamus suffer ischemic injury, with patchy neuronal loss and reactive gliosis
Lesions of caudate putamen and thalamus lead to choreoathetosis
232
Status marmoratus
| Periventricular leukomalacia
Abnormal myelinization that gives rise to a marble like appearance of the deep nuclei
233
Marbelized deep nuclei
Malignant peripheral nerve sheath tumors
Multicystic encephalopathy
234
Awake fracture
Front
235
Sleeping fracture
Back syncopal
236
Basal skull fracture
Bruise and CSF ears and eyes
237
Concussion
Altered consciousness
| No radiologic or pathological findings
238
Repeated concussion
Post consussion syndrome longer neurologic recovery
| Disabling neuropsychiatric manifestations
239
What part of Brian is most susceptible to direct parenchymal injury
Crest of gyri
240
Most commmon site of contusion
Frontal temporal
| Less frequent occipital brainstem cerebellum
241
Immobile head injury
Coup
242
Mobile head injury
Coup and counter coup
243
Hyperextension neck injury
Values pons from the medulla fromt he cord resulting in instant death
244
Morphology brain contusion
Wedge
1-pericapillary edema and hemorrhage
Hours-exravasation of blood through tissue of cerebral cortex, white matter, subarachnoid space
24 hours-pyknosis of the nucleus, eosinophilia, disintegration (EVIDENCE OF NEURONAL INJURY, axonal swelling_
245
Old traumatic lesion
Depressed, retracted yellow brown patches involving crest of gyri )plaque Jayne) most commonly of countercoup0inferior frontal cortec, temporal and occipital)
Can become foci of epileptic attacks
Larger cavitation more extensive hemorrhagic region
Gliosis and hemosiderin laden macrophages
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Diffuse axonal injury
Swelling and focal hemorrhagic lesions
| -50 percent of patients get coma after trauma without contusion FROM diffuse axonal injury
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Morphology diffuse axonal swelling
Hours of injury
Silver impregnating or immunoperoxidase stainsfor transported proteins
(APP, a synuclein_
Increased microglia
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Subdural
Slowing evolve
| Bleeding from low pressure vein s
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Subarachnoid
AVM berry aneurysm
Thunderclap headache
Underlying conditions
250
Trauma intraparenchymal hemorrhage
Trauma
Crests of gyri where contact skull
Frontotemporal tips or orbitofrontal sulcus
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IntraParenchymal hemorrhagic conversions of an ischemic infarction
Usually petechial hemorrhages in an area previously ischemic brain following cortical ribbon
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IntraParenchymal CAA
Local hemorrhage involving cerebral cortec, often with extension into subarachnoid space
253
IntraParenchymal hypertension
Centers in the deep white matter, thalamus, basal ganglia or brainstem may extend into the ventricular system
254
IntraParenchymal tumor hemorrhage (primary of metastatic
Associated with high grade gliomas ormetastases
255
Thrombosis intraparenchymal hemorrhage
Thrombosis of an intracranial artery may lead to infarction; infarction may be hemorrhagic hemorrhage typically does not extend into subarachnoid or subdural locations
256
Epidural hematoma
Lens shape
Kids who have deformable skill
Vessel tears cause extravasion
257
Lucid interval
Epidural hematoma lucid for several hours then bad as bp causes dura to separate and compress brain
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Subdural hematoma
Bridging veins tear veins where penetrate cure
More common in old people bc veins are already stretched or in infants since they have thin walled veins
Is chronis subdural hemorrhage slowly there may not be herniation
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Morphology acute subdural hematoma
Collection freshly clotted blood along the brain surface without extension into depths of sulci
Underlying brain flattened and subarachnoid space clear
Venous bleeding self limited and resulting hematoma is broken down and organized over time (lyse after a week, growth of fibroblasts from the dural surface into hematoma after 2 weeks, hyalinized CT in one to three month_
Lesion retracts to a thin layer of CT called subdural membranes
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Chronic subdural hematoma
Recurrent episodes of bleeding called chronic subdural hematoma that is due to the thin walled vessels of the granulation tissue
Risk is greatest for this int he first few months
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Clinical subdural hematoma
Symptomatic hematoma will typically present within forty eight hours
Along lateral aspects of the cerebral hemispheres and bilateral in ten percent
Headache, confusion, slowly progressive neurological deterioration, but sometimes there is acute decompensation
Treat by evacuating blood
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Post traumatic hydrocephalus
Obstruct csf resorption from hemorrhage into the subarachnoid space
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Chronis traumatic encephalopathy, dementia pugilistica
Cementing illness that develops after repeated head trauma
Repeated conclusion
Brains are strophic with enlarged ventricles, accumulation of tau tangles in pattern involving the superficial frontal and temporal lobe cortex
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Post traumatic epilepsy
Ok
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Post traumatic dementia
From repeated blows to the head often has pathological findings of neurofibrillary tangles and neuritis plaques
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Spinal cord injury-vulnerable to skeletal encasement
Most injuries that damag the cord injury are associated with transient or permanent displacement fo vertebral column
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Lesions below thoracic level
Paraplegia
268
Lesion above c4
Quadriplegia and diaphragm issue-respiratoy compromise
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Acute spinal cord injury
Hemorrhage, necrosis, axonal swelling in the surrounding white matter-taper above and below site of injury
270
Spinal cord injury later
Central areas become cystic and gliotic
Cord sections above and below injury show secondary ascending and descending wallerian degeneration, respectively, involving the long what matter tracts affected at the site of trauma
