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patho II > Neuro > Flashcards

Neuro Flashcards

1
Q

Epi/ Grading of pilocytic astrocytoma

A

Benign tumours; Grade I (WHO)
* Children and young adults

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2
Q

Location of Pilocytic astrocytoma

A

* Cerebellum (most common)
* Third ventricle
* Optic pathways
* Spinal cord
* Cerebral hemispheres

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3
Q

Macroscopic Features: ‘
* Cystic lesion with a mural nodule in the wall of the cyst or
* Solid, well circumscribed mass
Microscopic Findings:
* Bipolar cells with long, thin hair-like processes
* Rosenthal fibers
* Eosinophilic granular bodies
* Microcystic changes

features of ?

A

Pilocytic astrocytoma (WHO GRADE 1)

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4
Q

Epi of Diffuse Astrocytomas

A

80% of adult gliomas

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5
Q

loc of Diffuse astrocytomas

A

Cerebral hemispheres

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6
Q

Classification of Diffuse astrocytomas

A

1) Well-differentiated astrocytoma (WHO Grade II)
2) Anaplastic astrocytoma (WHO Grade III)
3) Glioblastoma (WHO Grade IV)

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7
Q

Gentic predisposition of Diffuse Astrocytomas

A

1) Loss of function mutations in p53 and Rb genes (Glioblastomas)
2) Mutations in the IDH1and IDH2 genes (Low grade astrocytomas) –> Important diagnostic utility

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8
Q

Macro features:
* Gray, poorly defined, infiltrative tumours

Microscopic features:
* Mild to moderate hypercellularity
* Variable nuclear pleomorphism
* Fibrillary appearance  Fine (GFAP [+]) astrocytic cell processes
* Irregular and Hyper-chromatic “Naked nuclei”

features of?

A

Well-differentiated astrocytoma -WHO Grade II

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9
Q

Macro features:
* Firm and white
* Soft and yellow
* Cystic degeneration and haemorrhage

Micro features:
* “Glomeruloid” bodies: Larger tufts of microvascular hyperplasia with multiple lumens
* Marked cellularity
* Pseudo-palisading necrosis

features of?

A

Glioblastoma (WHO Grade IV)

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10
Q

Macroscopic Features:
* Gelatinous, gray masses, possible with cysts, focal haemorrhage and calcification

Microscopic features:
* Sheets of sphaerical cells with spherical nuclei
* Finely granular chromatin
* Perinuclear halo (“fried egg appearance”)
* Delicate network of anastomosing capillaries (“chicken-wire appearance”)
* Focal or diffuse deposits of calcification

features of?

A

Well- Differentiated Oligodendroglioma

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11
Q

Loc of Epyndymoma

A
  • Children and adolescents –> Near 4th ventricle
  • Adults –> Spinal cord
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12
Q

Macroscopic Features:
* Solid or papillary masses (originating from the ventricular floor)

Microscopic Findings:
* Cells with regular round to oval nuclei
* Abundant granular chromatin
* Dense fibrillary background
* True rosettes (around a lumen)
* Perivascular pseudo-rosettes

featues of?

A

Conventional Ependymoma (WHO GRADE II)

  • Increased cell density, nuclear pleomorphism, high mitotic index, necrosis (Anaplastic Ependymomas)
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13
Q

3 Examples of neuronal Tumours

A

1) Central Neurocytoma (low-grade)
2) Gangliogliomas (low-grade astrocytoma)
3) Dysembryoplastic Neuroepithelial Tumour (low-grade childhood tumour)

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14
Q

loc of Central Neurocytoma

A

lateral or 3rd ventricles

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15
Q

Microscopic Findings:
* Evenly spaced, round, uniform nuclei
* Often islands of neuropil
* Densely packed small- to medium- sized, round bland tumour cells

features of ?

A

Central neurocytoma

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16
Q

CM of Gangliogliomas

A

Seizures

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17
Q

loc of Dysembryoplastic neuroepithelial tumour (DNT)

A

Superficial temporal lobe

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18
Q

Microscopic Findings:
* Small round neuronal cells arranged in columns and around central cores of processes
* Intra-cortical nodules with myxoid background
* “Floating neurons” within a myxoid fluid (Mucin-filled cyst)

features of?

A

Dysembryoplastic Neuroepithelial Tumour (DNT)

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19
Q

CM of Dysembryoplastic Nuro-Epithelial tumour (DNT)

A

Seizures

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20
Q

Embryonal (Primitive) Neoplasms are known to have what distinctive appearance ?

A

Primitive “small round cell” appearance –> Resemblance to normal progenitor cells of CNS

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21
Q

Macroscopic Features:
* Well circumscribed, gray and friable
* Extension to the leptomeninges

Microscopic Findings:
* Extremely cellular tumours
* Sheets of anaplastic (“small blue”) cells
* Hyperchromatic nuclei
* Mitoses
* Focal neuronal differentiation with Homer-Wright rosettes

featurs of?

A

Medulloblastoma

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22
Q

Loc of Medulloblastoma

A
  • Midline of the cerebellum (children);
  • Lateral cerebellar tumours (adults)
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23
Q

who is as high risk of developing primary CNS Lymphomas

A

immune-compromised individuals <> EBV [+]

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24
Q

Macroscopic Features:
* Multiple nodules within the brain parenchyma
* Well defined tumours
* Necroses (EBV[+] tumours)
* Localisation: Deep gray structures, white matter and cortex

Microscopic Findings:
* Diffuse Large B-Cell Lymphomas (DLBCL)
* Perivascular accumulation of neoplastic cells
* Infiltration of the adjacent brain parenchyma

features of?

A

Primary CNS lymphoma

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25
Q

Most common CNS germ cell neoplasm ?

A

Germinoma (resemblance to testicular Seminoma)

* seminoma -> lymphocytic infiltrates

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26
Q

Loc of Germ Cell tumours

A

i. Pineal, ii. Supra-sellar regions

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27
Q

Loc of Meningioma

A
  • Anywhere on the external surfaces of the brain (meninges)
  • Within the ventricular system
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28
Q

Micro findings:
* Sheets or clusters of cells without visible cell membranes
* Large nests of epithelioid cells
* Numerous nuclear clear holes

Features of what type of Grade I Meningioma?

A

Meningotheliomatous (Synctial)

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29
Q

Micro features:
* Elongated cells with abundant collagen deposits between them
* Intersecting fascicles of spindled cells

features of what type of Grade I Meningioma?

A

Fibroblastic Meningioma

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30
Q

Micro features:
* Combined features of syncytial and fibroblastic tumours
* Psamoma bodies
* characteristic “Whorls”

fetaures of what type of Grade I Meningioma?

A

Transitional Meningioma

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31
Q

micro features:
* Presence of numerous psammoma bodies

features of what type of Grade I Meningioma?

A

Psammomatous Meningioma

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32
Q

Micro features:
* Presence of pseudo-psammoma bodies (PAS [+] eosinophilic secretions)
* Tan Appearance on cut surface

features of what type of Grade I Menongioma?

A

Secretory Meningioma

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33
Q

What stain is used for the identification eosinophilic pseudo-psammoma bodies in Secretory Meningioma ?

A

PAS ([+])

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34
Q

Macroscopic features:
* soft fleshy appearance with papillary (cauliflower-like) configuration

Microscopic features:
* Prominant nucleoli
* Focus of “spontaneous necrosis”
* MIB-1 (Ki-67 > 4%)

features of?

A

Atypical Meningioma (WHO GRADE II)

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35
Q

Macroscopic features:
* Tumour with irregular contour and inhomogeneous signal characteristics
* Central hypodensity (suggestive of necrosis)
* Tumour with soft, almost gelatinous cut surface (suggestive of high cellularity)

Microscopic featuers:
* Fibrosarcoma-like spindled region
* Carcinoma-like region ; Multiple necrosis
* patchy postitivity to EMA (stain)
* MIB-1 (Ki-67) > 20%

features of?

A

Anaplastic Meningioma (WHO Grarde III)

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36
Q

Microscopic features:
* Tongue-like protrusions
* Entrapped brain parenchyma [GFAP]

features of?

A

Brain invasive meningioma (WHO GRADE II)

* GFAB stains the glial cells in the brain parenchyma

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37
Q

Macroscopic Features:
* Sharply demarcated masses with peri-tumoural oedema

Microscopic features:
* Tall columnar cells
* Cribriform glands
* “Dirty necrosis”

features of?

A

Metastaic barin tumour from the GI tract (Colon Carcinoma)

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38
Q

A mononeuropathy Syndrom

* peripheral nerve injury (single nerve)

A

Carpal Tunnel Syndrom
(compression of the median nerve)

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39
Q

cause of Gullain-Barre Syndrome

* Rapidly progressive acute demyelinating disorder

A

1) Infection (e.g. CMV, EBV, HIV, etc.) or vaccine –> Break down of self-tolerance –> Autoimmune response
2) Involvement of both humoral and cellular immune responses

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40
Q

Epi of Schwannomas (Neurilemmomas)

A
  • bening
  • Sporadic (most common); 10% associated with familial NF2
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41
Q

loc of Schwannomas

A
  • Soft tissues
  • Internal organs
  • Spinal nerve roots
  • Cranial nerves (Vestibular portion of the 8th nerve
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42
Q

Macroscopic Features:
* Circumscribed masses next to a nerve
* Globualr enlargment of a fascicle
* Yellow colouration of the cut surface, due to lipid accumulation

Microscopic Findings:
* Alternating areas of dense (“Antoni A”) and loose (“Antoni B”) texture
* **“Antoni A” **areas: Bland spindle cells arranged into intersecting fascicles
* “Verocay bodies”: Structures composed of alternating bands of nuclear palisading and anuclear strands between them
* Thick-walled hyalinised vessels
* Possible, presence of haemorrhage or cystic changes

features of?

A

Shwannomas (Neurilemmomas)

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43
Q

caues of Neurofibromatois Type 2

A

Loss of function mutation of the NF2 gene affecting Merlin (Schwannomin) protein

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44
Q

CF of NF2

A

Bilateral vestibular Schwannomas -> Hallmark of Neurofibromatosis Type 2

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45
Q

Hallmark of Neurofibromatosis Type 2?

A

Bilateral vestibular Schwannomas

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46
Q

Microscopic Findings:
* Non-encapsulated tumours
* Haphazard cellular growth pattern
* Admixture of Schwann cells w wavy nuclei, mast cells, fibroblast-like cells and perineurial-like cells
* Background stroma: Loose wavy or dense collagen bundles or even myxoid consistency

features of?

A

Neurofibromatosis Type 2

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47
Q

localized Cutaneous Neurofibromas can exist as?

A
  • solitary lesions or multiple in the context of NF1
  • Superficial nodular or polypoid masses
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48
Q

Pathogonomic (symptom/sign) of NF1

A

Plexiform Neurofibromas

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49
Q

Microscopic Findings:
* Presence of residual axons found among the neoplastic cells
* Proliferation of schwann cells and fibroblasts
* Enlargement of the nerve
* Intact perineurium
* Classic “bag of worms appearance”

features of?

A

Plexifrom Neurofibromas

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50
Q

Diffuse Neurofibromas are ass w/?

A

NF1

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51
Q

Microscopic findings:
* Extensive infiltration of the dermis and subcutis
* Subcuataneous masses
* Marked expansion of dermal tissue

features of?

A

Diffuse Neurofibromas

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52
Q

Neurofibromatosis Type 1 is AKA?

A

Von Recklinghausen disease

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53
Q

who is likely to develop Malignant Peripheral Nerve Sheath tumours?

A

NF1 px

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54
Q

Cause of Conjuctivitis

A

Adenovirus (most common), bacteria

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55
Q

CM of Retinitis Pigmentosa

A

1) Retinal pigmentation
2) Peripheral vision loss (“Tunnel vision”) and progressive loss of Central Vision

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56
Q

patho of Senile Macular Degenration

A

Loss of central vision and pigmentary changes or haemorrhage in the macula

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57
Q

patho/CM of Angle-Closure Galucoma

A

Angle-Closure Glaucoma:
* Narrow anterior chamber angle
* Increase in intraocular pressure on dilatation of pupil

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58
Q

symptoms of open angle Glaucoma

A

1) Gradual loss of peripheral (side to side & up/down) visions, usually in both eyes
2) Tunnel vission

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59
Q

Explain the “two hit” hypothesis of tumour development in Retinoblastoma

A

1) First “hit”: Inherited deletion in germ cells (familial cases) or somatic mutation (sporadic cases)
2) Second “hit”: Somatic mutation (both familial and sporadic cases)

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60
Q

Signs of Retinoblastoma

A

1) swollen eyes
2) shrunken eyes
3) A red, sore or swollen eye w/o infection
4) A white refelction in the pupil

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61
Q

Microscopic features:
- Multiple foci of necrosis
- Numerous apoptotic cells
- True rosette
- scant cytoplasm
- Flexner-Wintersteiner rosette
- Round to oval nuceli and finely granualr chromattin

features of?

A

Retinoblastoma

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62
Q

what are the 2 types of cerebral odema

A

1) Vasogenic oedema
2) Cytotoxic oedema

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63
Q

Macroscopic Features:

  • Flattening of the gyri and narrowing of the intervening sulci
  • Compression of the ventricular cavities

features of?

A

Cerebral Oedema

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64
Q

What are the 3 types of Herniation syndromes

A

1) Subfalcine (Cingulate) herniation under Falx cerebri
2) Uncal Transtentorial herniation <>Tentorium cerebelli
3) Cerbellar tonsillar herniation into the Foramen magnum

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65
Q

What are the 3 sites of brain herniation?

A

1) Falx cerebri –> (Subfalcine (Cingulate) herniation)
2) tentorium cerebelli -> (transtentorial [Uncinate] hernia)
3) Foramen magnum –> Tonsillar hernia)

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66
Q

Compression of which artery is caused by Subfalcine (Cingulate) Herniation ?

A

anterior cerebral artery

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67
Q

microscopic features:
- Cortical spongious alteration
- Peri-neuronal/ Peri-vascualar swelling of astrocytic processes

features of?

A

Cytotoxic Cerebal Oedema

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68
Q

Compression ————- nerve in a Transitional (Ucinate) Hernitation –> Pupilary dilatation

A

Third cranial nerve

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69
Q

In a Transtenotorial (Uncinate) Herniation , the compression of ———– –> Kernohan’s notch

A

Contralateral cerebral peduncle against the tentorium

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70
Q

In a Transtentorial (Uncinate) Herniation, the compression of ———– -> Ischaemic injury of the primary visual cortex

A

Posterior cerebral artery

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71
Q

The 2 mechanisms that deprive O2 from the brain

A

1) Functional Hypoxia
2) Ischaemia due to tissue Hypoperfusion

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72
Q

cause of Global Cerebral Ischaemia

A

Severe systemic hypotension (as in cardiac arrest or shock)

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73
Q

Macroscopic Features of Global Cerebral Ischaemia:
* ————-, with ————— and narrowed sulci
* Poor demarcation between gray and white matter

A

Swollen brain, with widened gyri and narrowed sulci

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74
Q

What neuronal cells are affected by Global cerebral Ischaemia

A
  • Pyramidal cells of hippocampus and neocortex
  • Purkinje cells of the cerebellum
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75
Q

Immunohistochemistry used to stain Astrocytes

A

GFAP

76
Q

Marker used for microglia staining

* microglia –> macrophages of the brain

A

CD68

* stains macropahges

77
Q

cause of “Watershed infarcts”

A

Hypotensive episodes
(Anaphylactic shock, sudden blood loss, sever infections)

78
Q

location of “Watershed infarcts”

A

The border-zone between the anterior and middle cerebral artery distributions

79
Q

CF of “watershed” infarcts

A

1) Transient post-ischaemic confusional state –> Complete recovery (mild insult)
2) Sever global cerebral ischaemia–> Widespread neuronal death; Severely neurologically impaired and in a persistent vegetetative state

80
Q

Most common site of embolic infarction

A

Middle Cerebral Artery (MCA)

81
Q

locations of thrombotic occlusions

A

Carotid bifurcation (,origin of middle cerebral artery)

*carotid bifurcation is the point where the common carotid artery divides into internal and external carotid arteries

82
Q

The 2 types of infarcts

A

1) Non-haemorrhagic (Result of acute vascular occlusions)
2) Haemorrhagic (Result of reperfusion of ischaemic tissue, either through collaterals or dissolution of emboli)

*reperfusion->restortion of blood flow to a tissue that has been blocked

83
Q

Macroscopic Features:
Blood extravasation -> Compression of the neighbouring brain parenchyma –> Cavity formation with brown discoloured rim

Microscopic Findings -Early findings:
* Extra-vasated, clotted blood
* Anoxic neural changes of the adjacent neuropil
* Oedema of the brain parenchyma, around the haemorrhagic focus

features of?

* Anoxic: complete loss of O2 supply

A

Primary brain Parenchymal Haemorrhage (Early findings)

84
Q

Late Microscopic findings of Primary brain parenchymal haemorrhage:
* Pigment and ——————–
* ——————— at the periphery of the lesion

A
  • Pigment and lipid-laden macrophages
  • Reactive astrogliosis at the periphery of the lesion
85
Q

Histochemical stain for Beta Amyloid (in Cerebral Amyloid Angiopathy)

A

Apple-green birefringence on Congo-red

86
Q

stain used for Haemosiderin (in Cerebral Amyloid Angiopathy)

A

Pearl’s/Prassin blue iron staining

87
Q

Pathologocial identifcation of cerebral Amyloid Angiopathy

A

1) Aβ immuno stain/ Congo red stain for Beta Amyloid
2) Pearl’s blue iron stain for Haemosiderin

88
Q

causes of Subarrachnoid haemorrahge & Saccular aneurysms

A
  • Rupture of a berry aneurysm (most common)
  • Vascular malformation
  • Trauma
  • Rupture of an intra-cerebral haemorrhage into the ventricular system
  • Tumours
89
Q

loactions of Subarachnoid haemorrhage & Saccular Aneurysms

A

~90% of Berry aneurysms in the anterior circulation

90
Q

Microscopic Findings:
* Absent muscle wall and intimal elastic lamina (thinning of vessels)
* Presence of a thickened hyalinised intima, and the adventitia

features of?

A

Subarachnoid haemorrhage & saccular aneurysms

91
Q

CF of Subarachnoid haemorrhage & saccular aneurysms

A
  • Sudden, severe headache
  • Rapid loss of consciousness
  • Death (from the first bleed in 25-50% of cases)
  • blood in CSF
  • Postive Kernig & Burdzinski sign
92
Q

the 4 types of Vascular Malformations

A

1) Arterio-Venous Malformations (AVMs)
2) Cavernous Malformations
3) Capillary Telangiectasias
4) Venous Angiomas

93
Q

Epi of AVMs (Anter-venous mal.)

A

Most common vascular malformation
* M:F = 2:1; Age: 10-30 years

94
Q

Macroscopic Features:
* Tangled network of worm-like vascular channels
Microscopic Findings:
* Enlarged blood vessels, separated by gliotic tissue (shown w/ GFAP)
* Presence of haemo-siderophages

features of?

A

AVMs (Arterio-venous malformations)

95
Q

loc of Cavernous Malformations

A

Cerebellum, Pons

96
Q

Microscopic Findings:
* Distended, loosely organised vascular channels (Back to back dilated vesseles- Trichome stain)
* Collagenised walls
* No intervening nervous tissue
* Foci of old haemorrhage, infarction and calcification

features of?

A

Cavernous (Vascular) Malformation

97
Q

Micro:
* Dilated thin-walled vascular channels
* Intervening normal brain parenchyma
* several large, thin-walled vascualr spaces
* “Pencil fibers” = white matter tracts of the basal ganglia

features of?

A

Capillary Telangicetasias

98
Q

Micro:
* Aggregates of ectatic venous channels
* Capillary Hindus resembles the head of medusa

features of?

A

Venous Angiomas (Varcies)

99
Q

Microscopic Findings:
* Chronic inflammatory cell infiltrates
* Multinucleate giant cells (+/- granuloma formation)
* Destruction of vessel walls
* Amyloid-β deposits
* Lumen Oblitertion

features of?

A

Primary Angiitis of the CNS

* Form fo Vasculitis

100
Q

Contusion Will cause?

A

haemorrhage, tissue damage and oedema in the brain

101
Q

Loc of a Contusion

A

1) Orbito-frontal regions
2) Temporal lobe tips

102
Q

the 2 types of Contusion

A

Coup and Contre-Coup injuries

103
Q

Macroscopic Features:
* Cross-section: Wedge-shaped
* Old lesions: Depressed, yellowish-brown patches (Crests of gyri)

Microscopic Findings:
* Involvement of superficial layer
* Neuronal cell body injury (nuclear pyknosis and cytoplasmic eosinophilia) within 24 hours
* Inflammatory response: Initially neutrophils and later also macrophages
* Old lesions: Gliosis and haemo-siderophages

features of?

A

Contusion

104
Q

location of Diffuse Axonal injury (DAI)

A
  • Near the angles of the lateral ventricles
  • Corpus callosum
  • Brain-Stem
105
Q

Microscopic Findings:
* Axonal swellings (“bulbs”), within hours of the injury
* Axonal Spheroids
* Immuno-histochemistry : β-APP

features of?

A

Diffuse Axonal injury

106
Q

Histochemical stain for diffuse Axonal Injury ?

A

Silver stain
(detects axonal swelling)

107
Q

Immuno-Histochemistry findings in Diffuse Axonal Injury

A

Amyloid Precussor ProteinAPP

108
Q

Cause of Epidural Haematoma

A

Traumatic injury of the middle meningeal artery, after a skull fracture

109
Q

causes of Subdural Haematoma

A

Tear of the bridging veins, after trauma

110
Q

location of Subdural Haematoma

A

lateral aspects of the cerebral hemispheres

111
Q

Macroscopic Features:
* Collection of freshly clotted blood, over the brain convexity
* Flattening of the underlying brain
* Ruprture of Bridging veins
* star-like invasion of Collagen fibers
* Immuno-histo: Combined leukocyes-macrophage rxn, Siderophages

features of ?

A

Subdural Haematoma

112
Q

?? not sure if we need to know this

stain for Siderophages

A

Prussian-blue reaction

113
Q

?? not sure if we need know this

Stain used for Erythrophagocytosis

A

Azan

114
Q

Progression of Subdural Haematoma

  • ——— of the clot (~1 week)
  • Development of ————– from dura (2 weeks)
  • ——– (1-3 months)
  • ———- of the fibrosing lesion -> Thin layer of connective tissue (————”)
  • Commonly, ————– (chronic subdural haematoma)
A
  • Lysis of the clot (~1 week)
  • Development of Granulation tissue from dura (2 weeks)
  • Fibrosis (1-3 months)
  • Retraction of the fibrosing lesion -> Thin layer of connective tissue (“Subdural membrane”)
  • Commonly, re-bleeding (chronic subdural haematoma)
115
Q

Which condition is known as “Smooth brain” ?

A

Lissencephaly

116
Q

patho of Lissencephaly

A

Total absence of gyration or pachygyria (patchy involvement) –> “Smooth brain”

117
Q

Macroscopic features:
* Numerous irregulary formed gyri –> Cobbelstone - like surface
* Many gyri

Microscopic features:
* A festooned cortex w/ fusion of Gyri

features of?

A

Polymicrogyria

118
Q

Absence of the olfactory bulb is known as ?

A

Arrhinencephaly

* Mild form of Holoprosencephaly

119
Q

Posterior Fossa Anomalies

A

1) Chiari Type I malformation
2) Arnold-Chiari (Chiari Type II) Malformation
3) Dandy-Walker Malformation

120
Q

Macroscopic features:
* Low-lying cerebellar tonsils, extending through the
foramen magnum
* Protrusion of the tonsils into the foramen magnum

features of?

A

Chiari Type I malformation

121
Q

Arnold-Chiari (Type II) Malformation Coexists w?

A

hydrocephalus and lumbar myelo-meningocele

122
Q

Macroscopic features:
* Small posterior fossa
* Misshaped midline cerebellum
* Protrusion of tonsil and vermis below the foramen magnum
* Hydrocephalus
* Narrowing of the 4th Ventricle
* Elongation of the brain stem and Vermis

features of?

A

Arnold-Chiari Malformation

123
Q

Macroscopic features:
* Enlarged posterior fossa
* Absence of the cerebellar vermis
* Large midline cyst
* Cystic dilatation of the 4th Ventricle

Microscopic features:
* Agenesis of the cerebellar Vermis
* Microgyri in the cerebral cortex

features of?

A

Dandy-Walker Malformation

124
Q

Patho of Multiple Sclerosis:
* ————– -> Increased risk for MS
* Polymorphisms in the genes encoding receptors for ———-
* Increased Th17 and Th1 CD4+ cells
* Contribution from CD8+ T cells and B cells

A
  • HLA-DR2 Variants–> Increased risk for MS
  • Polymorphisms in the genes encoding receptors for IL-1 & IL-7
  • Increased Th17 and Th1 CD4+ cells
  • Contribution from CD8+ T cells and B cells
125
Q

Macroscopic Features:
Characteristic lesions (“plaques”): Multiple, well circumscribed, slightly depressed, glassy-appearing, gray-tan, irregular shaped

features of?

A

Multiple Sclerosis

126
Q

location of “Plaques” in Multiple sclerosis

A
  • Paraventricular regions (most common)
  • Optic nerves and chiasm
  • Brain stem
  • Cerebellum
  • Spinal cord
127
Q

Macroscopic Features:
* Diffuse gray and translucent colour of the white matter
* Decrease in the volume of the white matter –> Brain atrophy, Ventricular enlargement, Secondary changes in the gray matter

Microscopic Findings:
* Myelin loss
* Lipid stuffed macrophages

features of?

A

Leukodystrophies

128
Q

Clinical presentation of Leukodystrophies

A
  • Affected children –> Normal at birth, but developmental abnormalities manifested during infancy and childhood
  • Deterioration in motor skills
  • Spasticity
  • Hypotonia
  • Ataxia
129
Q

Macroscopic features:
* Swollen and softened Pons and Medulla

Microscopic features:
* perivascular cellular infiltrate, composed of Macropahges and mononuclear cells
* Myelin loss associated w/ a perivascular macrophage infiltrate (Heidenhain stain)

features of?

A

Acute Disseminated Encephalo-Myelitis

130
Q

Macroscopic features:
* Multiple scatterd petechial haemorrhages

Microscopic features:
* Multiple foci of inflammatory demyelination,
with diffuse oedema in the adjacent white matter
* Perivascular neutrophil infiltrates in cerebral white matter

features of?

A

Acute Haemorrhagic Leukoencephalitis

131
Q

Microscopic features:
* Spinal Cord lesion with extensive destruction of the parenchyma
* Perivascular infiltrates of eosinophils and neutrophils

features of?

A

Neuro-Myelitis Optica (NMO)

132
Q

CM of Central Pontine Myelinolysis

A

Rapidly evolving quadriplegia
(paralysis of the 4 limbs)

133
Q

Central Pontine Myelinolysis is characterised by the development of ———-, induced by changes in osmotic pressure –> loss of ——- in the ——- of the ——–

A

Central Pontine Myelinolysis is characterised by the development of Oedema, induced by changes in osmotic pressure –> loss of Mylein in the center of the pons

134
Q

Thiamine Deficiency –> ———

A

Wernicke Encephalopathy

135
Q

Macroscopic Features:
* Foci of haemorrhage and necrosis, in the mamillary bodies and para-ventricular (3rd & 4th ventricles)

Microscopic Findings:
* Early lesions: Dilated capillaries with prominent endothelial cells Haemorrhages
* Late lesions: Cystic spaces with haemosiderin-laden macrophages
* Lesions in the medial dorsal nucleus of thalamus –> Association with Korsakoff syndrome

features of?

A

Wernick Encephalopathy Thaimine Deficiency

136
Q

Microscopic features of Acute/Chronic Wernike’s Encephalopathy

A
137
Q

Microscopic Findings:
* Astrocytes (Alzheimer type II cells) with swollen, pale nuclei in the cortex and basal ganglia

featurse of?

A

Hepatic Encephalopathy

138
Q

Toxic Disorder caused by Lead?

A

Diffuse Encephalopathy

139
Q

Toxicity from Aresnic causes?

A

Encephalopathy and peripheral Neuropathy (SensoryMotor Axonopathy)

140
Q

Mercury Toxicity –> ——

A

Tremors, emotional changes, insomnia, muscle
atrophy, disturbances in sensations, changes in nerve responses, cognitive dysfunction

141
Q

Methanol Toxicity –> ——-

A

Blindness

142
Q

**

Carbon Monoxide Toxicity –> ——-

A

Hypoxic injury to the Globus pallidus

143
Q

Ethanol Toxicity –> ——

A

Chronic alcoholism –> Atrophy in the anterior
cerebellar vermis –> Truncal ataxia, unsteady gait
and nystagmu

144
Q

Ionising radiation toxicity –> ——

A

Headaches, nausea,
vomiting and papilloedema

145
Q

Microscopic features:
* Large areas of coagulative necrosis,
* oedema and
* thick-walled vessels with intramural fibrin-like material
* Haemosiderin accumulation
* Extensive vascular hyalinisation
* Neurofibrillary tangles

features of?

A

Toxicity due Ionising radiation

146
Q

Pathogenesis of Alzheimer Disease:
* Progressive accumulation of ———— in the brain
* —– leads to hyper-phosphorylation of —– –> Redistribution of tau from axons into dendrites and cell bodies –> Formation of ———–

A
  • Progressive accumulation of beta Amyloid (Αβ) in the brain
  • Αβ leads to hyper-phosphorylation of Tau –> Redistribution of tau from axons into dendrites and
    cell bodies –> Formation of tangles
147
Q

Macroscopic Features:
* Variable degree of cortical atrophy –> Widening of the cerebral sulci and thinning of the gyri
* Hydrocephalus ex vacuo
* Neuritic and Diffuse Plaques (extra-cellular lesion)
* Neurofibrillary tangles (intra-cellular lesion)

features of?

A

Alzheimer Disease

148
Q

Alzeheimer Disease

Microscopic Findings:
——————-:
* Paired helical filaments –> Basophilic fibrillary
structures in the cytoplasm of the neurons
* Abnormally hyper-phosphorylated tau protein –> Major component of paired helical filaments
* Localisation: Entorhinal cortex, hippocampus, amygdala, basal forebrain

A

Neuro-Fibrillary Tangles (NFTs)

149
Q

Subtype of Fronto-Temporal Degeneration-tau ?

A

Pick disease
(characteristic smooth, globular, pale basophilic inclusions, [Pick bodies])

150
Q

Macroscopic features:
* “Knife-like” thinning of the gyri

Microscopic features:
* Pick bodies

features of?

A

Pick disease

151
Q

Macroscopic Features:
* Pallor of the substantia nigra and locus coeruleus

Microscopic Findings:
* Loss of the pigmented Neurons and gliosis in the above regions
* Presence of Lewy Bodies in the remaining neurons
* Lewy Bodies:
- Intra-cytoplasmic, eosinophilic, round inclusions with a dense core and a peripheral pale halo
- Composed of α-Synuclein, Neurofilaments and Ubiquitin

  • Lewy Neurites: Dystrophic neurites containing abnormally aggregated α-Synuclein

features of?

A

Parkinson Disease

152
Q

CF of Parkinson Disease

A
  • Tremor
  • Rigidity
  • Bradykinesia
  • Instability
153
Q

Tx for Parkinson Disease

A

L-DOPA

154
Q

Macroscopic Features:
* Small brain
* Prominent atrophy of the Caudate Nucleus, and less severe the Putamen
* Atrophy of the Globus Pallidus, secondarily
* Dilatation of the lateral and third ventricles

Microscopic Findings:
* Severe loss of neurons from Striatum
* Fibrillary gliosis
* Intra-nuclear inclusions (aggregates of ubiquition)

features of?

A

Huntington Disease

155
Q

CM of Friedreich Ataxia

A
156
Q

Amyotrophic Lateral Sclerosis is caused by mutations in the genes —– and FUS

A

TDP-43

157
Q

CM of Amyotrophic Lateral Sclerosis based on loss of lower motor neurons

A
  • Denervation of muscles
  • Muscular atrophy
  • Weakness
  • Fasciculations
158
Q

CM of Amyotrophic Lateral Sclerosis based on Loss of Upper motor Neurons

A
  • Paresis
  • Hyper-reflexia
  • Spasticity
159
Q

Macroscopic Features:
* Thin and gray anterior roots of the spinal cord
* Mildly atrophic pre-central gyrus (severe cases)

Microscopic Findings:
* Lwey body-like inclusions
* Degeneration of the lateral cortico-spinal tracts
* Reactive gliosis
* Loss of anterior root myelinated fibers
* Cytoplasmic inclusions (TDP-43 [+]), with exception the SOD-1 cases
* Hyaline inclusions
* Bunina bodies

features of?

A

Amyotrophic Lateral Sclerosis

160
Q

Epidural Absces –> ————

A

Subdural Empyema

161
Q

The 3 forms of Infectious Meningitis

A

1) Acute pyogenic (bacterial)
2) Aseptic (viral)
3) Chronic (Tbc)

162
Q

cause of Acute Pyogenic Meningitis in neonants

A

E. coli, group B Streptococci

163
Q

Cause of Acute Meningitis in adolescents and young adults

A

Neisseria meningitidis

164
Q

Cause of Acute Meningitis in older individuals

A

Streptococcus pneumoniae and Listeria monocytogenes

165
Q

CF of Acute Pyogenic Meningitis

A

1) Positive Kernig’s and Brudzinki signs
2) Neck stiffness
3) Vomiting
4) headache
5) Photophobia
6) Clouding of Consciousness
7) Irritablity

166
Q

Macroscopic Features:
* Leptomeningeal exudate, over the surface
of the brain
* Engorged and prominent meningeal vessels

Microscopic Findings:
* Neutrophil cell infiltrates within subarachnoid
space
* Phlebitis and a thrombus
* Gram stain –> Pneumococcus meningitis- purulent exudate

featurse of?

A

Acute Pyogenic Meningitis

167
Q

Macroscopic Features:
* Brain swelling
* subtle Hyperaemia

Microscopic Findings:
* Mild to moderate leptomeningeal lymphocytic infiltrate

features of?

A

Aseptic Meningitis

168
Q

lab findings of Brain Abscess

A
  • Increased numbers of white blood cells
  • high protein levels
  • Normal glucose content
169
Q

Macroscopic Features:
* Discrete lesion
* Central liquefactive necrosis
* Surrounding fibrous capsule

Microscopic Findings:
* Granulation tissue and oedema around the necrotic core
* Zone of reactive gliosis, outside the fibrous capsule

features of?

A

Brain Abscess

170
Q

Characteristic Histologic Features:
* Perivascular and parenchymal mononuclear cell infiltrates
* Microglial nodules
* Neuronophagia
* Presence of inclusion bodies

features of?

A

Viral Encephalitis

171
Q

Important cause of Epidemic Encephalitis?

A

ARBO (ARthropod-BOrne) virus

172
Q

CM of ARBO (Arthropod-borne) disease

A
  • Seizures
  • Confusion
  • Delirium
  • Stupor or Coma
  • Reflex asymmetry
  • Ocular Palsies
  • yellow fever
173
Q

Lab findings of ARBO (Arthropod-borne) viruses

A

CSF:
* Colourless
* Early neutrophilic pleocytosis –>Conversion
to lymphocytosis
* Elevated protein level
* Normal glucose

174
Q

Microscopic Findings:
* Perivascular lymphocytic Meningoencephalitis
* Micro-Abscess in the white matter
* Multifocal gray and white matter necrosis
* Neuronophagia
* Microglial nodules
* Necrotising Vasculitis with focal haemorrhages
(severe cases)

features of?

A

Eastern Eqine Encephalitis
(ARBO Viruses)

175
Q

**

Macroscopic Features:
* Inferior and medial regions of the temporal lobes
and the orbital gyri of the frontal lobes
* Heamorrhagic Necrosis in the Temporal and frontal lobe

Microscopic Findings:
* Necrotising and haemorrhagic infection
* Perivascular inflammatory infiltrates
* Large eosinophilic intranuclear viral inclusions
(Cowdry type A bodies)

features of?

A

HSV Encephalitis (caused by HSV-1)

176
Q

Pathogensis and CM of Polio virus
* Subclinical or ————-
* Invasion of the CNS and destruction of the motor
neurons in spinal cord and brain stem (————–)
* Loss of motor neurons –> ———— and
————–, in the affected body region
* Paralysis of the respiratory muscles, in acute disease –> ———-

A
  • Subclinical or mild Gastroenteritis
  • Invasion of the CNS and destruction of the motor
    neurons in spinal cord and brain stem (Paralytic Poliomyelitis)
  • Loss of motor neurons –> Muscle wasting and
    hyporefelxia, in the affected body region
  • Paralysis of the respiratory muscles, in acute disease –> death
177
Q

Microscopic Findings:
* Discrete, intra-cytoplasmic, deeply eosinophilic
inclusions within neurons (Negri bodies)

features of?

A

Rabies virus

178
Q

Microscopic Findings:
* Predominantly, in subcortical white matter, diencephalon and brain stem
* Presence of microglial nodules, with multinucleate giant cells
* Abnormally prominent endothelial cells
* Perivascular foamy or pigment-laden macrophages
* Foci of tissue necrosis and reactive gliosis
* Multifocal or diffuse areas of myelin pallor, with axonal swellings and gliosis
* Identification of virus in CD4+ lymphocytes and multinucleate macrophages and microglia

features of?

A

HIV

179
Q

Myelin in the White matter can be identified using which histochemical stain ?

A

LFB- Luxol Fast Blue

180
Q

cause of Polymoa-Virus & Progressive multifocal leukoencenphalopathy

A

JC virus

181
Q

Macroscopic Features:
* Patchy, irregular, ill-defined areas of white matter destruction

Microscopic Findings:
* Centrally localised lipid-laden macrophages and reduced number of axons
* In the periphery of the lesion, enlarged oligodendrocyte nuclei (Plum-coloured) with glassy-appearing amphophilic viral inclusions
* Bizarre giant forms of astrocytes (irregular, hyperchromatic, sometimes multiple nuclei)

features of?

A

Polymoa-Virus & Progressive multifocal leukoencenphalopathy

182
Q

Morphology:
Proliferation of the organisms in the Virchow-Robin spaces –> Characteristic “soap bubble” like appearance

Features of?

A

Fungal Encepahlitis caused by Cyrptococcus Neofromans

183
Q

Macroscopic Features:
* Multiple Abscesses in the gray-white junction and the deep gray nuclei (immunosuppressed individuals)
* Oedema

Microscopic Findings:
* Central foci of necrosis with small haemorrhages
and mixed inflammatory cell infiltrates and vascular
proliferation
* Free Tachyzoites and encysted Bradyzoites at the periphery of the necrotic foci

features of?

A

Cerebral Toxoplasmosis

184
Q

cause of Cysticercosis

A

Taenia solium

185
Q

Macroscopic Features:
* Cysts with a smooth lining, within the brain and subarachnoid space

Microscopic Findings:
* Body wall and hooklets from mouth parts
* Intense inflammatory infiltrate (with eosinophils) - incase of dead encysted organism
* Marked gliosis

features of?

A

Cysticercosis

186
Q

Macroscopic Features:
* Little or no brain atrophy

Microscopic Findings:
* Spongiform changes in the cerebral cortex and deep gray matter structures (e.g. Nucleus caudatus, Putamen)
* Neurons w/ Microscopic vacuoles of variable size within the neuropil and neuronal perikaryon
* Severe cases:
* Severe neuronal loss
* Reactive (astro)gliosis
* Development of “status spongiosus”

features of?

A

Sporadic and Familial Creutzfeldt-Jakob disease

187
Q

Vareint Cretzfeldet-Jakob disease specific microscopic diffrence from other CJD forms

A

Amyloid plaques

patho II (29 decks)

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