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pathology Flashcards

1
Q

what are the types of glial cells ?

A

Astrocyte: are the principal cells responsible for
repair and scar formation in the brain, a process
termed gliosis.

Oligodendrocyte: produce myelin

Ependymal cells: line the ventricular system and
the central canal of the spinal cord.

Microglia: are bone-marrow–derived cells that function as the resident phagocytes of the CNS

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2
Q

what are the reactions of NEURONS to injury?

A

A- Acute Neuronal injury : RED NEURONS
B - Chronic or subacute injury: Degeneration
C -Axonal reaction:central chromatolysis
D- Inclusions

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3
Q

acute neuronal injury ;
cell death in(time)?
histologic pic. 5

A
  • 12-24hrs Ischemia/ hypoxia
  • shrinkage in cell body ,pyknosis of the nucleus,disappearance of the nucleolus, and loss of Nissl substance, with intense eosinophilia of the cytoplasm (“red neurons”)
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4
Q

Chronic or subacute injury;

A

Neuronal loss & replacement by gliosis in progressive diseases, usually selective

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5
Q

-Axonal reaction(central chromatolysis);

histologic pic.? 4

A

(Enlargement of cell body, peripheral displacement of nuc.,
enlargement of nucleolus, dispersion of Nissl substance from
center to periphery)

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6
Q

Inclusions in neurons;

A

Nuclear or cytoplasmic:
Aging (lipofuscin,protien or carbohydrate)
-Viral infections

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7
Q

what are the reactions of ASTROCYTES to injury?

A

1-undergo both
hypertrophy and hyperplasia (Gliosis or Astrogliosis)

2-Rosenthal fibers: are thick, elongated,
brightly eosinophilic protein aggregates found in astrocytic processes in chronic gliosis and in some low-grade gliomas

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8
Q

what are the reactions of OLIGODENDROCYTES to injury?

A
  • Synthesis & maintenance of myelin
  • Injury or apoptosis in demyelinating disorders and leukodystrophies
  • Inclusions in specific viral infection
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9
Q

what are the reactions of EPYNDEMAL CELLS to injury?

A

Inclusions in CMV infection

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10
Q

what are the reactions of MICROGLIA to injury?

A

1-Proliferation
2-Elongated nuclei in syphilis :( Rod cells)
3-(Microglial nodules):Forming aggregates around small foci of tissue
necrosis
4-(Neuronophagia):Aggregate around dead neurons:

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11
Q 
ICP ;
normal level?
compensation?
fail of coompensation?
what are the manifestations if ICP increased more than 15mmhg ?
causes?
A

Normally 7–15 mmHg.

  • Expansion in any component is first
    compensated by ↓ in the rest
    i.e. ↓ CSF, ↓ blood , ↓ ventricular size
  • When volume of brain increases beyond limit →
    compensation fails → Displacements &
    Herniations
  • Papilledema & visual disturbances
  • Nausea & vomiting
  • Headache
  • Neck stiffness
  • Mental status

causes;
1- Cerebral Edema
2- Infarction &Hemorrhage
3- Infections - Abscesses & meningitis
4- Tumors - Primary & Secondary
5- Trauma - specially in diffuse brain damage
6- Hydrocephalus

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12
Q

Cerebral Edema;
define it?
types?due to? localized or generalized ?

A

-is the accumulation of excess fluid within the brain parenchyma.

1-VASOGENIC: due disruption of blood brain barrier
allowing fluid to shift from the vascular
compartment into the extracellular spaces of the brain.
-Localized (adjacent to inflammation or neoplasms)
-Generalized

2- CYTOTOXIC: due to neuronal, glial, or endothelial cell membrane injury
-Generalized hypoxic/ischemic insult or metabolic damage

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13
Q

HYDROCEPHALUS;
define it?
causes?
types?

A

-Accumulation of excessive CSF within the ventricular system with enlarged ventricles

1- Impaired flow or resorption of CSF
2- Overproduction of CSF in some tumors of choroid plexus

-Noncommunicating,Communicating,Hydrocephalus ex vacuo

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14
Q

Noncommunicating hydrocephalus;
due to?
localized or generalized?

A

-Due to obstruction of CSF flow from
ventricles to the subarachnoid space.

-Localized to site of obstruction.

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15
Q

Communicating hudrocephalus;
due to?
L/G?

A
  • Impaired resorption.

- Generalized to all ventricles.

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16
Q

Hydrocephalus ex vacuo:

due to?

A
  • Compensatory dilatation of ventricles due to loss of brain parenchyma
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17
Q

types of herniations?

A

1- Subfalcine(Cingulate) herniation
2- Transtentorial (Uncinate, mesial
temporal) hernation
3- Tonsillar herniation

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18
Q

Subfalcine (Cingulate) herniation;
define it?
compression on?

A 
Herniation of Cingulate gyrus under falx cerebri
into the subfalcine
space
-on branches of Anterior
Cerebral Artery →
Cerebral infarction
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19
Q 
Transtentorial (Uncinate, mesial
temporal) hernation;
define it?
compression on?
progression is accompanied by?cause?
A

-Herniation of medial
temporal lobe through
tentorium.

1-3rd Cranial Nerve
compression →
Ipsilateral dilated pupil & impaired eye movement
2- Pressure on Post.cerebral artery→
Occipital infarction,
including visual cortex
3- Cerebral peduncle
compression → ipsilateral hemiparesis

-by DURET’S Hemorrhage
(Secondary Brain stem hemorrhage
-Linear hemorrhagic lesions in midbrain and pons)

*cause;Tearing of penetrating veins
and arteries supplying upper brain stem

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20
Q

Tonsillar herniation;
define it?
why is it life threatening ?

A

-Herniation of cerebellar tonsils through foramen
magnum
-

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21
Q

What are the three main pathogenic mechanisms of cerebrovascular diseases ?

A

Thrombotic occlusion
Embolic occlusion
Vascular rupture

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22
Q

Superficial vessels are most commonly occluded by…..
Deep penetrating vessels are most commonly affected by…..
What is the watershed zones? And they vunerable to …..

A

Emboli
Hypertension
The border zones at junction btwn two main arterial territories , vunerable to hypotention

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23
Q

Define ;
Stroke (cerebrovascular accident)
TIA ( transient ischemic attack)

A
  • acute neurological dysfunction occurring as a result of a vascular process causing irreversible damage or death
  • transient episode of neurologic dysfunction lasting only a few min and causing no permanent damage
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24
Q

What are the types of cerebrovascular disease ?

A

A- impairment of blood supply &oxygenation :
1-global hypoxic/ischemic encephalopathy due to generalized BF
2- infarction : localized vascular obstruction due to thrombosis or embolism

B- rupture of CNS blood vessels

  • intracerebral hemorrhage
  • subarachnoid h
  • subdural
  • epidural
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25
Q 
Global ischemia /hypoxia
(Hypotension, hypoperfusion and low flow states (diffuse hypoxic ischemic encephalopathy ));
 Defenition?
Causes?
Features?
A
  • generalized reduction of cerebral perfusion ,symptoms(mild- irreversible damage)
  • cardiac arrest , shock, sever hypotension

-Cells: neurons affected > glia, but all if severe and prolonged
-Selective Vulnerability of neurons in certain
locations :
1-Pyramidal cells in CA1 of hippocampus
(Sommer sector)
2-Purkinje cells of the cerebellum
3-Cortical pyramidal neurons

  • Watershed(Borderzone ) infarcts include :
  • Boundary between anterior & middle cerebral arteries (Cerebral Convexities)
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26
Q

MORPHOLOGY of Global ischemia?

Microscopical changes?acute/subacute/repair

A

-Brain swelling
-Wide gyri and narrow sulci
-Poor demarcation between grey & white
matter

#Acute : after 12 hrs
- RED NEURONS
- Infiltration by neutrophils
# Subacute changes: 24 hrs – 2 weeks
- tissue necrosis, macrophages & gliosis
#  Repair: after 2 weeks
- Removal of necrotic tissue
- Loss of normally organized CNS structure
- Gliosis
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27
Q

Outcome of Global ischemia;

Depends on:?

A

1-Presence of collateral circulation
2-Duration of ischemia
3-Magnitude and rapidity of reduction of flow

  • Result varies from persistent neurological deficit to brain death → Deep coma & flat EEG
  • Patients maintained by mechanical ventilation →Brain autolysis
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28
Q 
Local Infarction (Focal Cerebral Ischemia);
Definition ?
Mechanisms?
A

Embolic occlusion : “hemorrhagic/ red”

-necrosis due to complete and prolonged ischemia

#Thrombotic occlusion, mainly due to Atherosclerosis
\: "Ischemic/ pale"
1.Carotid bifurcation
2.Origin of middle cerebral artery
3.Basilar artery at either end

1- Source: heart or atherosclerosis in carotid
2- Middle Cerebral artery most affected

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29
Q

Types of infarction?

Outcome depends on?

A

1-Acute white infarct in the distribution of the
right middle cerebral artery.
2-Acute red infarct in the distribution of the
right anterior cerebral artery.

  • Size of the infarct
  • Site of the infarct
  • State of collateral circulation
  • Rapidity of onset
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30
Q

MAcroscopic appearance
Of infarction?
Microscopic appearance ?
Clinical picture?

A

-No gross change before 48 hrs
- Soft swollen pale or hemorrhagic WEDGE SHAPED
infarct involving grey & white matter.
-Blurred demarcation
-Red infarcts: surrounding hemorrhage due to
reperfusion of damaged vessels and tissue
-After 10 days-3 weeks : liquefaction
- Cavity within 1- 6 months

-Very similar to global ischemia but more
regional.

  • *linked to site of infarction:
  • Contralateral hemiparesis
  • Loss of sensation
  • Visual field abnormalities
  • Aphasia
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31
Q

INTRACRANIAL HEMORRHAGE ;

According to location, divided into ?

A
  • Intracerebral (intraparenchymal)
  • Subarachnoid
  • Epidural
  • subdural
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32
Q

Primary intracerebral hemorrhage ;

Causes?

A 
1-Commonest is HYPERTENSION 50%
2- CEREBRAL AMYLOID ANGIOPATHY
-vasculitis 
- coagulation disorders
- neoplasms
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33
Q

Hypertensive cerebrovascular disease;

Vascular lesions include?

A
  • atherosclerosis ;in larger arteries
  • hyaline arteriolosclerosis ;in smaller vessels—>hemorrhage
  • arteriolosclerosis ;in vessels <=150micro.m—> lacunar infarcts
  • charcot bouchard microaneurysms ;in vessels <=300micrometer in basal ganglia —>rupture
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34
Q

CNS lesions in hypertention?

A 
Lacunar infarcts 
Slit hemorrhages
htpertensive encephalopathy 
Intracerebral hemorrhage 
Cerebral amyloid angiopathy
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35
Q

What is lacunar infarcts?
Shape?
Clinically ?

A

Tiny cystic infarcts in hemispheric WM ,basal ganglia &brain stem due to hypertensive arteriolosclerosis of deep penetrating arteries and arterioles

  • multiple small cavitary infarcts (lake like spaces ,less than 15mm wide)
  • asymptomatic or sever neurologic impairment
36
Q

What is Slit hemorrhages?

A
  • Rupture of smaller penetrating vessels

- Resorb,leaving behind a slit like cavity

37
Q

Hypertensive encephalopathy ;

Acute/chronic?

A

Acute : malignant hypertension
-diffuse cerebral dysfunction :headaches , confusion,vomiting,convulsions,coma

#chronic: over for many months and yrs ,multi bilateral gray and wm infarcts :
Dementia, gait disturbances , pseudobulbar signs
38
Q

Intracerebral hemorrhages;
Sites?
Acute/old?

A
  • putaman 60%,thalamus , pons, cerebellar hemi and others
  • acute: extravasation of blood wt compression of adjacent parenchyma
  • old: cavitary destruction of brain wt a rim of brown discoloration
39
Q

Cerebral amyloid angiopathy?

A

Deposition of amyloid in wall of medium &small meningeal &cortical vessels —>weak wall—>hemorrhage

40
Q

Subarachnoid hemorrhage ;

Causes?

A

1-rupture saccular (berry) aneurysm *commonest cause
2-vascular malformation
3-hematological disturbances
4- tumors

41
Q 
Saccular berry aneurysm;
Age ? Gender? 
Causes?
-if congenital will not be present at birth ,why?
Rate of bleeding?
More in(site)?
A
  • 5th decade,female
  • mostly sporadic ,but may be genetic
  • because it develop over time due to underlying defect in media of vessels
  • 1.3%/yr
  • 90% near anterior circulation ,20-30% multi
42
Q

What are the conditions associated wt saccular aneurysms?

Genetic/non genetic/predisposing conditions

A 
Genetic:
– Polycystic kidney disease (autosomal dominant) 
– Defects in extracellular matrix proteins
e.g. Marfan’s syndrome, Others
• Non-genetic:
– Coarctation(constriction) of aorta
• Predisposing conditions: 
– Hypertension
– Cigarette smoking
43
Q 
Morphology of saccular aneurysm;
Size? 
What is absent beyond the neck of the aneurysm?
Lining of the sac?
Where the rupture occur?
A
  • Size: from few mm to 2-3 cm.
  • Muscular wall and internal elastic lamina are absent
  • Aneurysm sac is lined only by thickened hyalinized intima. The adventitia covering the sac is continuous with that of the parent artery.
  • occurs at the apex of the sac, releasing blood into the subarachnoid space or the substance of the brain, or both
44
Q

Clinical feature of berry aneurysm?

Sequelae?acute/chronic

A

Acute: in the first few days

”Worst headache of my entire life”, sudden, excruciating with loss of consciousness
- 25-50% die at time of first

– Vasospasm :
• Increased risk of additional ischemic injury

#Repeat bleeding
•Associated with ↑mortality 
#Chronic (healing phase):
Meningeal fibrosis and scarring —>obstruction of CSF flow, interruption of normal pathways of CSF resorption
45
Q

What are the types of vascular malformations?

A

1) Arteriovenous malformations (AVM)
2) Cavernous malformation
3) Venous angioma
4) Capillary telangiectasis

**1+2 are the types associated with risk of hemorrhage and development of neurological symptoms.

46
Q 
1.Arteriovenous malformation ;
More common in? 
Age?
Clinical problems?
Site?
Grossly ?
Microscopic?
A
  • males
  • 10-30yrs
  • seizures ,intracerebral or subarachnoid hemorrhage
  • vessels in subarachnoid &cerebrum
  • prominent pulsatile wormlike vascular channels
  • enlarged BV separated by gliotic tissue
47
Q

2.Cavernous hemangioma ;
Definition?
Site?

A
  • dilated thin walled vascular channels devoid of intervening brain tissue
  • cerebellum ,pons and subcortical region
48
Q

3.Capillary telengectasis ;
Defintion?

4.Venous angioma (varices)
Definition?
Occur in?

A

Microscopic foci of dilated thin walled vascular channels separated by normal brain parenchyma

-aggregates of ectatic venous channels
-in brain ,SC &meninges
Progressive neurological symptoms

49
Q

Epidural and subdural hemorrhage is usually ….

A

Traumatic

50
Q

CNS TRAUMA ;

Result and morphology depend on? 5

A

•Penetrating or Blunt trauma→ Open or Closed
• Mobile or immobile head at time of trauma
• Lesions at bony prominences e.g
- Frontal, orbital, temporal & occipital poles - Spinal cord
• Edema may occur & worsen the condition
• Skull fracture

51
Q

Types of CNS TRAUMAS?

A

1-parenchymal injury
2-diffuse axonal injury
3- traumatic vascular injuries

53
Q 
A-parenchymal injury ;
Types?
Definition of each?
Neuronal injury?
Types of contusion?site,and mobile or immobile head?
A

Direct Parenchymal injury: Contusions & lacerations:

#Concussion (Traumatic brain injury) :
– Instantaneous onset of transient neurologic dysfunction, including loss of consciousness, and loss of reflexes
– Due to change in the momentum of the head. 
– Complete neurologic recovery

– More on crests of gyri
•Contusions :wedge shape broad vase along the surface deep to the point of impact
Early: edema and hemorrhage
Neuronal injury :take about 24 hr

Types:
1-Coup lesions:
- Contusions at point of contact
 - Immobile or mobile head
2-Contrecoup lesions :
- Contusions opposite to the point of trauma
- Mobile head
54
Q

Diffuse axonal injury ;
Seen in pts wt?
Affect?
Microscopically?

A
  • 50%wt post traumatic coma even wtout cerebral contusions
  • affect deep WM (CC, paraventricles ,hippo.)&cerebral peduncles

-axonal swelling ,micro hemorrhages ,microglia ,later gliosis

55
Q

B-traumatic vascular injuries ;

Types?

A

1-epidural hematoma

2-subdural hematoma

56
Q 
Epidural hematoma ;
Acute or chronic?
Rupture of which artery?
Does it have mass effect?
Clinically?
A

-Usually acute & accompanied by skull fracture
• Rupture of middle meningeal artery
• Mass effect → Dura & Brain compression”more mass effect”
• Clinically :
- When blood accumulates slowly: Patient has short LUCID interval followed by rapid loss of consciousness
- May expand rapidly → Neurologic emergency

57
Q 
Subdural hematoma ;
Rupture of which vein?
Grossly?
Does it have mass effect?
Clinically ?
ttt?
A

Tearing of Bridging Veins
• Gross: Collection of fresh blood
• Mass effect → Brain compression
• Clinically: - Headache and confusion
- Slow progressive neurologic deterioration
• Treatment: remove blood and associated organizing tissue.

58
Q

What are the secondary complication s of CNS trauma?5

A

1- Post traumatic hydrocephalus 2- Post traumatic dementia
3- Epilepsy
4- Infection
5- Psychiatric disorders

59
Q 
Acute bacterial meningitis;
What is the Most predominant pathogen related to age?
Clinical pic.?
CSF findings ?
Morphology?
A

Fever, headache, vomiting, neck stiffness

  • Neonates: group B Streptococci & E.coli
  • > 6M : S.Pneumoniae, H.influenza,
  • Adolescents & young adults :N. meningitidis
  • Elderly :S.pneumonia& L.monocytogenes

#Waterhouse Friderichsen Syndrome:1.- Results from meningitis associated
septicemia with hemorrhagic infarction of the adrenal glands and cutaneous petechiae.
2.- Occurs with meningococcal and pneumococcal meningitis

*CSF:Cloudy or frankly purulant
↑P, ↑Protein, ↓glucose, numerous neutrophils
Bacteria may be seen or cultured

Morphology:Exudate within the leptomeninges
Meningeal vessels: Severely congested
May cause cerebritis & ventriculitis
May show phlebitis → venous occlusion &
hemorrhagic infarction of underlying brain.
Fibrosis → Hydrocephalus

60
Q

Acute aseptic meningitis(viral);
Clinical pic.?
CSF?

A

Clinical: Less fulminant, self-limiting often seasonal

CSF: moderate↑ protein, normal glucose , ↑↑
lymphocytes

61
Q 
Chronic bacterial meningioencephlaitis :
1-tuberculous meningitis ;
Spread from?
Morphology?2
Microscopic pic?
CSF?
A
  • Hematogenous spread from lung → brain
  • Direct spread from Tuberculous vertebra

1#Diffuse meningoencephalitis: Gelatinous or fibrinous exudate, mostly at the base, obliterating the cisterns, and encasing cranial nerves.
2# Tuberculoma: Single or multiple intraparenchymal
mass.

*Microscopy:
-Mixtures of lymphocytes, plasma cells and
macrophages
- Caseating granulomas
-Obliterative endartritis: inflammation in the
wall, marked intimal thickening → arterial
occlusion → infarction
-Dense fibrous adhesive archnoiditis → Hydrocephalus

*CSF : Marked ↑Protein, , glucose normal or
↓, ↑ lymphocytes and neutrophils.

62
Q

2- neurosyphilis ;
Caused by?
Types ?

A

-caused by spirochete
(T.pallidum) ,Tertiary stage

1-meningovascular syphilis
2-paretic neurosyphilis
3- tabes dorsalis
4- acute syphilitic meningitis

63
Q

Features of Meningovascular syphilis?

A
  • Chronic Meningitis
  • Obliterative endarteritis (Heubner arteritis):
    Perivascular plasma cells and lymphocytes
  • Cerebral gummas: Plasma cell-rich mass lesion
64
Q

Features of paretic neurosyphilis;
Invasion of?
Clinically?
Microscopic?

A

-Invasion of the brain, mainly frontal lobe by T.pallidum

#-Insidious, but progressive mental deficits with mood
alteration → General paresis of the insane

gliosis
-Granular ependymitis: ependymal cells damage with proliferation of subependymal glia → Hydrocephalus
-Spirochetes may be seen in tissue section

65
Q

Tabes dorsalis;
Damage to?
Clinically?

Acute syphilitic meningitis;
Caused by?

A 
#- Damage to the sensory nerves in the dorsal root
- Loss of axons &amp; myelin → pallor and atrophy of dorsal
columns
#-clinically: Impaired joint position sense and ataxia (locomotor
ataxia), loss of pain sensation → skin and joint damage → Charcot joints
- Others: lightning pains, absence of deep tendon
reflexes
#Acute syphilitic meningitis :
- HIV infected patients
66
Q

What are the complications of bacterial meningitis ?5

prognosis depend on?

A 
1- Hydrocephalus
2- Cerebral infarction
3- Cerebral abscess
4- Epilepsy
5- Cranial nerve palsy
#Prognosis depends on rapidity of proper
antibiotic therapy
67
Q 
Parenchymal infection;
-localized/ diffuse?
•Brain abscess;
Caused by? 
Route of infection?
Grossly? 
Microscopic pic?
CSF?
Clinical?
Complications?
A

Grossly: Discrete lesion with central liquefactive necrosis surrounded by fibroblasts.

  • Localized : abscess, tuberculoma,toxoplasmosis, parasites
  • Diffuse : encephalitis, usually viral
#-Usually bacterial
#-Direct infection from paranasal sinuses,mastoiditis &amp; middle ear Hematogenous route from heart, lungs or after
tooth extraction.
  • Localized suppuration surrounded by granulation
    tissue , reactive astrocytes & severe edema
    leading to ↑ ICP .
  • Fibrous capsule, outer zone of reactive gliosis
#Clinical presentation: Progressive focal deficit, and
signs of ↑ ICP

3Complications :
If rupture → ventriculitis, meningitis, venous sinus
thrombosis

68
Q 
Viral encephalitis and myelitis;
Type of infection wt related pathogen:
Sporadic infection
Latent infection?
Neurotropic?
Antenatal?
Immunodeficiency?
A

-Sporadic infection : HSV
-Latent infections : Herpes Zoster, PML
-Neurotropic : Polio, Rabies
-Antenatal : CMV, Rubella
-Immune deficiency :
HIV, CMV, PML, Herpes Zoster

69
Q 
Some viruses have selective sites;
HSV? 
CMV?
Polio?
Herpes zoster ?
A

-HSV :Temporal lobe & orbital frontal area
-CMV : Subependymal region
-Polio : Anterior horn cells of spinal cord
-Herpes Zoster: Sensory neurons of dorsal root
ganglia

70
Q

What are the common features of viral infections?4

A

1- Perivascular mononuclear infiltrate
2- Neuronophagia
3- Microglial nodules
4- Nuclear or cytoplasmic inclusions

71
Q 
HSV1 and 2 ;
Age?
Feature? 
clinically?
Seen wt?
A

Alteration in mood, memory and behavior

#Children or young adults
#Hemorrhagic necrotizing inflammation in
temporal lobe &amp; orbital gyri of frontal lobe
#All common features of viral encephalitis seen
with Cowdry type A intranuclear viral inclusions in
neurons &amp; glial cells

**HSV-2 in adults may cause meningitis

72
Q 
Varicella-zoster virus (herpes zoster);
Cause?
 infection in?
Reactivation?
What does it show in immunocompromised pt?
Features ?
A 
#Chicken pox in children
-latent infection in dorsal root ganglia in adults
#Reactivation (Shingles): Self limited painful
vesicular skin eruption along a dorsal nerve in a
single or limited dermatomal distribution.
#In immunosuppressed patients, may show acute
encephalitis.
#Lesion is typical of viral infection
± granulomatous arteritis &amp; infarction
73
Q

Rabies;
Cause? 2
The first is transmitted by? IP?
diagnose it by presence of?

A

1.Severe encephalitis
- Transmitted to humans by bite of a rabid animal such as
dog
- Ascends along peripheral nerve from bite
- Incubation period (1-3 months) depends on the distance between the wound and the brain

2-Neuronal degeneration and inflammatory reaction ,
most severe in brain stem
- also can be in basal ganglia, S.C, dorsal root
ganglia

##Presence of Negri bodies : cytoplasmic, eosinophilic
inclusions in pyramidal neurons of the hippocampus
&amp; Purkinje cells of cerebellum, in sites usually devoid of inflammation
74
Q

Poliovirus;
Cause?
Acute /chronic manifestations?
Clinically?

A

- Acute :

#Enterovirus causing mild gastroenteritis
-Involvement of CNS in the non- immunized

mononuclear cell perivascular cuffs and neuronophagia of
the anterior horn motor neurons of the spinal cord

Loss of neurons and atrophy of the anterior (motor)
spinal roots,and neurogenic atrophy of denervated
muscle.

  • Meningitis
  • Flaccid paralysis with muscle wasting
  • Death can occur from paralysis of the respiratory muscles
75
Q 
JC virus ,PML(progressive multifocal leuko-encephalopathy );
Caused by?
Infect mainly?
Result?
grossly?
Microscopic?
A

Grossly:

-Caused by JC polyomavirus exposure during childhood

-mainly AIDS patients & other immunosuppressed
patients
-Infect oligodendrocytes

#RESULT : Progressive demyelination of white
matter

Patches of irregular, ill-defined destruction of white
matter from mm to extensive involvement of the
entire lobe

Patch of demyelination , with scattered lipid laden
macrophages at the center, and reduced number of
axons
-Enlarged oligodendrocyte nuclei with viral inclusions
-Large astrocytes are also seen.

76
Q 
Prion diseases (transmissible SPONGIFORM encephalopathy )
Pathogenesis?
Include a variety of conditions?
A

-Disease occurs when the PrP undergoes

conformational changes from its normal shape
(PrPc) to an abnormal conformation called
PrPsc (sc for scrapie)

#-Creutzfeldt- Jacob Disease
-Fatal Familial Insomnia
-Kuru
-Scrapie in sheep
-bovine spongiform encephalopathy in cattle
(“mad cow disease”)
77
Q 
CJD (creutzfeldt -jakob) 
Sporadic /familial cases?
Form of transmission?
Clinically?
Microscopic?
A

Iatrogenic Transmitted ! Contaminated material

-Sporadic cases 85%,Familial cases (15%), younger

-Onset of subtle changes in memory and behavior
to death is only 7 months
-FATAL, no treatment known, like ALL prion diseases

  • Multifocal spongiform transformation
    (Intracellular vacuoles in neurons and glia) of
    cortex & deep gray matter→ multiple small empty microscopic vacuoles , most in caudate &putamen.
    **- No inflammatory response
  • Advanced cases:Neuronal loss ,Gliosis
78
Q 
Fungal encephalitis ;
Infect mainly?
Way of invasion?
Features?
AIDS pt are prone to?
pathogens? 4
A
  • Mainly in Immunocompromised patient
  • Hematogenous or direct invasion
  • Parenchymal granulomas or abscesses, often associated with meningitis

-AIDS patients are prone to cryptococcal
meningoencephalitis

-Candida, Cryptoccocus , Aspergillus, & Mucor

79
Q

mucormycosis;

#Candida albicans;
Features?

Present primarily as?
May spread to?

#aspergillus fumigatus ;
Feature?

Cryptoccocus neoformans ;
Cause?
Features?

A

Mucormycosis :

#Candida albicans : Multiple microabscesses,
with or without granuloma formation.

-Presents as an infection of the nasal cavity or
sinuses of a diabetic patient with ketoacidosis.
-May spread to the brain through vascular
invasion or by direct extension through the
cribriform plate.

-Meningitis or meningoencephalitis
-Immunosuppressed patients
- Extension into the brain follows vessels in the
Virchow-Robin spaces.
- As organisms proliferate, these spaces expand,
giving rise to a “soap bubble”–like appearance

80
Q

What is neural tube defects?
Caused by? What can reduce the risk by70%?
The most common defects involve?
Other defects?

A

Partial failure or reversal of neural tube closure

#-Genetic factor.
-Folate deficiency during the initial weeks of gestation
#- Prenatal Folate vitamins can reduce the risk
up to 70%.
#The most common defects involve the
posterior end of the neural tube ,
-Spina bifida occulta: Asymptomatic bony defects
81
Q

What is the difference btwn meningocele and meningomyelocele ?

A

Myelomeningocele:Extension of CNS tissue through a defect in the vertebral column that

occurs most commonly in the LS region.
**- Motor and sensory deficits in the lower extremities and
problems with bowel and bladder control.

82
Q

What is anencephaly?

What is encephalocele? Involve mostly which part?

A

Encephalocele: diverticulum of malformed

**both are Malformation of the anterior end of the
neural tube:

#Anencephaly: absence of the brain and the
top of skull.

CNS tissue extending through a defect in the
cranium.
- It most often involves the occipital region or the
posterior fossa.

83
Q

Forebrain malformations ;
What is Megalencephaly and microencephaly?

Associated wt what?

A

- associated with chromosome abnormalities, fetal alcohol syndrome, and (HIV-1) infection acquired in utero.

-Megalencephaly : abnormally large brain

Microencephaly: Small, associated with a
small head (microcephaly).
84
Q

What could lead to abnormalities of gyration?

What is lissencephaly / polymicrogyria / holoprosencephaly?

A

(agyria) : absent gyration

-Disruption of neuronal migration and differentiation
during development

leading to a smooth-surfaced brain.
#Polymicrogyria: increased number of irregularly formed gyri.
#Holoprosencephaly : disruption of the normal
midline patterning.

85
Q

Posterior fossa malformation ;
What is Chiari type 2 malformation
And type 1?

A

The Arnold-Chiari malformation (Chiari type II

malformation) :
- Small posterior fossa
- Misshapen midline cerebellum
- Downward extension of the vermis through the foramen magnum
- hydrocephalus and a lumbar
myelomeningocele are also present.

  • low-lying cerebellar tonsils that extend through the
    foramen magnum.
86
Q

Spinal cord abnormalities ;

What is hydromyelia / syringomyelia?

A

Neural tube defects

#Hydromyelia : Expansions of the ependyma-lined
central canal of the cord
87
Q

Types of Meningitis ?

A

1-acute bacterial

2- acute aseptic(viral)

3-chronic bacterial meningo-encephalitis :
•TB
•neurosyphilis
•neuroborreiosis

CNS (4 decks)

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