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Y2B4 - Central Nervous System πŸ“™ > Pathology 🩺 > Flashcards

Pathology 🩺 Flashcards

1
Q

what does CNS develop from?

A

neuroectoderm

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2
Q

steps of development of the CNS

A

The neural plate (thickening of the ectodermal layer) β†’ neural folds with a neural groove in between β†’ neural tube β†’ ventricular system, brain and spinal cord.

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3
Q

anatomy of the CNS

A

The central nervous system (CNS) includes:

  • The brain and the spinal cord with their meningeal coverings (meninges).
  • The rain is Protected by the cranium (Skull)
  • The spinal cord is protected by the vertebral column
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4
Q

what are the meninges?

A

3 membranous layers
1. Dura mater
2. arachinoid mater
3. Pia mater

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5
Q

histology and origin of Dura Mater

A

Thick connective tissue [C.T.], mesenchyme-derived

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6
Q

histology and origin of arachinoid matter

A

Delicate C.T., have arachnoid granulations, neural crest-derived

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7
Q

anatomy and origin of pia matter

A

Adherent to the brain surface, richly vascularized, neural crest-derived

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8
Q

histology of the CNS

A

Neurons

Glial cells (neuroglia): (4 types)
1. Ependymal cells
2. Microglia
3. Oligodendrocytes
4. Astrocytes

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9
Q

what are the main functions of CNS cells?

A
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10
Q

Etiology of congenital CNS malformations

A
  • Unknown
  • Genetic factors
  • Environmental factors: Teratogens (e.g., chemicals, infectious
  • Maternal conditions: Folic acid deficiency early in pregnancy, alcoholism.
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11
Q

categories of congenital CNS malformations

A

I. Neural tube defects
II. Forebrain malformations
III. Posterior fossa malformations
IV. Spinal cord malformation

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12
Q

what is a neural tube defect?

A
  • Failure of a part of the neural tube to close β†’malformations involving: neural tissue, meninges, and overlying bone or soft tissues.
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13
Q

types of neural tube defects

A

It may be Spinal (more common) or Cranial.

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14
Q

incidence of neural tube defects

A

Most frequent CNS malformation.

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15
Q

risk factors of neural tube defects

A

Maternal folic acid deficiency or defective enzymes involved in folic acid metabolism.

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16
Q

recurrence rate of neural tube defects

A

about 4% to 5% in subsequent pregnancies.

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17
Q

what is used to screen neural tube defects?

A

Maternal serum level of alpha-fetoprotein (MSAFP) is used to screen neural tube defects (elevated).

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18
Q

what region is Affected in spinal neural tube defects?

A

Affects the lumbo-sacral region (mostly S1 to S2).

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19
Q

what are the types of spinal neural tube defects?

A
  • Spina bifida occulta
  • Meningocele
  • Myelomeningocele
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20
Q

characters of spina bifida occulta

A
  • A bone gap of the vertebral spine
  • other layers are normal
  • no opening on the back.
  • Associated with moles, angioma, lipoma, and a hair patch over the affected area.
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21
Q

what is the least severe type of spinal neural tube defects?

A

Spina bifida occulta

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22
Q

symptoms of spina bifida occulta

A

Very few cases have symptoms as bowel or bladder dysfunction, back pain, leg weakness or scoliosis.

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23
Q

characters of meningocele

A
  • The meninges are protruded through the bone opening forming a CSF-filled sac.
  • In most cases, the spinal cord and the nerves are normal or not severely affected.
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24
Q

what is the most rare type of spinal neural tube defects?

A

Meningocele

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25
Q

characters of Myelo-meningocele

A
  • Protrusion of a segment of flattened spinal cord and nerves with an overlying meningeal outpouching through the back.
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26
Q

what is the most severe type of spinal Neural tube defects?

A

Myelomeningocele

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27
Q

what does Myelo-meningocele lead to?

A

β–ͺ Leads to: Bowel and bladder dysfunction, or total paralysis of the lower limbs & have risk of infections.

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28
Q

what are cranial neural tube defects?

A
  • Anencephaly
  • Encephalocele
  • Holoprosencephaly
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29
Q

what is anencephaly?

A
  • absence of most of the brain and calvarium. Usually incompatible with postnatal life.
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30
Q

what is encephalocele?

A

Cranial defect with a sac-like protrusion of malformed brain tissue and membranes. It most often occurs in the occipital region.

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31
Q

Characters of holoprosenceephaly

A

β–ͺUnpaired cerebral hemisphere and ventricles.

β–ͺ Fused thalami, single central incisor, cyclopia, arhinencephaly and absent olfactory nerves.

β–ͺ Aassociated with trisomy 13.

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32
Q

Etiology of forebrain malformations

A

Abnormal generation and migration of neurons.

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33
Q

what do forebrain malformations include?

A
  • Microencephaly (more common)
  • Megalencephaly
  • Lissencephaly
  • Polymicrogyria
  • Neuronal heterotopia
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34
Q

characters of microencephaly

A

Small brain volume, with a small head circumference.

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35
Q

what causes microencephaly?

A

Caused by: chromosomal abnormalities, fetal alcohol syndrome, intrauterine human immunodeficiency virus 1 (HIV-1) infection.

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36
Q

characters of megaloencephaly

A

Large brain volume (less common).

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37
Q

characters of lissencephaly

A

Reduction in the number of gyri, or no gyral pattern (agyria).

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38
Q

characters of polymicrogyria

A

Increased number of abnormal gyri with altered cortical structure

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39
Q

characters of neuronal heterotopia

A

A collection of neurons in inappropriate locations β†’epilepsy

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40
Q

what are posterior cranial fossa abnormalities?

A
  • Chiari malformations (Type I and Type II)
  • Dandy-Walker malformation
  • Aqueductal stenosis
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41
Q

what are the types of Arnold Chiari malformations?

A

Type I and Type II

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42
Q

characters of type I Arnold-Chiari malformation

A
  • Low-lying cerebellar tonsils into the vertebral canal β†’medullary compression.
  • Associated with syringomyelia
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43
Q

characters of type II Arnold-Chiari malformation

A
  • Extension of cerebellar vermis through the foramen magnumβ†’ hydrocephalus.
  • Associated with myelomeningocele.
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44
Q

Characters of Dandy-walker malformation

A
  • Enlarged posterior fossa, absent cerebellar vermis with a large midline cyst (expanded fourth ventricle).
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45
Q

what does aqueductal stenosis lead to?

A

hydrocephalus

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46
Q

what are spinal cord abnormalities?

A
  • Hydromyelia
  • Syringomyelia (syrinx)
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47
Q

characters of Hydromyelia

A
  • Expansion of the central canal of the cord.
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48
Q

characters of syringomyelia (Syrinx)

A
  • A central fluid-filled cleft-like cavity in the cord β†’loss of pain and temperature sensation in the upper extremities.
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49
Q

what are the categories of cerebrovascular diseases?

A
  • Hypoxia, Ischemia, and Infarction
  • Intracranial Hemorrhage
  • Hypertensive Cerebrovascular Diseases
  • Other Vascular Diseases
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50
Q

Types of (Hypoxia - Ischemia - Infarction)

A

A) Global cerebral ischemia
B) Focal cerebral ischemia & infarction

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51
Q

what are the types of intracanial henorrhage?

A
  • Intra-parenchymal, Subarachnoid, Subdural, Extradural
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52
Q

what are other vascular diseases?

A
  • Cerebral amyloid angiopathy
  • Aneurysms
  • Vascular malformations
  • Vasculitis.
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53
Q

Definition of global cerebral ischemia

A
  • Widespread ischemic-hypoxic brain injury.
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54
Q

Cause of Global cerebral ischemia

A
  • Severe systemic hypotension (systolic pressure below 50 mm Hg) as in cardiac arrest and shock.
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55
Q

Clinical outcome of Global cerebral ischemia

A

Varies with severity and duration.

  • Mild, transient β†’ complete recovery.
  • Moderateβ†’ damage to vulnerable areas.
  • Severe, long-standing β†’ widespread neuronal death.
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56
Q

what type of tissue is more liable to damage by ischemia?

A
  • Neurons are more liable to hypoxic injury than glial cells.
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57
Q
  • what are brain death manifestations?
A
  • Flat (Isoelectric) electroencephalogram (EEG)
  • loss of reflexes
  • loss of respiratory drive
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58
Q

N/E of global cerebral ischemia

A
  • Brain swelling, wide gyri & narrow sulci.
  • Poor gray/white matter demarcation
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59
Q

M/E of global cerebral ischemia

A

Early changes:
β–ͺ Red neurons (cytoplasmic eosinophilia, nuclear dissolution).
β–ͺ Similar changes occur later in astrocytes and oligodendroglia.

Subacute changes:
β–ͺ Necrosis, Influx of phagocytic cells to remove necrotic tissue.

Repair:
β–ͺ Loss of organized CNS structure
β–ͺ Gliosis.

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60
Q

Manifestations of focal cerebral ischemia

A
  • Manifests as infarction (cerebral stroke) in the distribution of the affected vessel.
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61
Q

what is Stroke?

A
  • Clinical term for acute onset of neurologic deficits resulting from hemorrhagic or obstructive vascular lesions
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62
Q

what does focal cerebral ischemia complicate?

A
  • complicates Embolic occlusion or thrombotic occlusion
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63
Q

what are the areas that are most affected in cases of focal cerebral ischemia?

A
  • Thalamus, basal ganglia and deep white matter are more affected due to deficient collaterals.
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64
Q

what are the aread that are least affected by focal cerebral ischemia?

A
  • Circle of Willis and cortical leptomeningeal surface are protected by collaterals.
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65
Q

what are the clinical manifestations of focal cerbral ischemia?

A
  • Neurologic deficit according to the area supplied by the affected vessel.
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66
Q

what are the types of brain infarctions?

A
  • Embolic infarctions (More common)
  • Thrombotic infarctions
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67
Q

Source of emboli in brain infarcation

A
  1. Cardiac mural thrombi and valvular vegetations.
  2. Atheromatous plaques within the carotid arteries or aortic arch.
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68
Q

what is the site of emboli in brain infarctions?

A

middle cerebral artery (most frequently affected).

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69
Q

what are the sources of thrombi in brain infarctions?

A
  1. Thrombosis on top of atherosclerosis of carotid bifurcation, the origin of the middle cerebral artery, and either end of the basilar artery.
  2. Thrombi of dural venous sinuses or deep cerebral veins (less common).
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70
Q

what are the types of infarctions? (In morphology)

A
  • Non-hemorrhagic Infarct
  • Hemorrhagic infarction
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71
Q

Morphology of non-hemmoragic infarct

A
  • Early: Pale, opaque.
  • Liquefactive necrosis β†’ creamy fluid-filled cavity.
  • Healing β†’ destruction of cortex + gliosis.
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72
Q

what causes hemorrhagic infarctions?

A
  • Reperfusion of ischemic tissue (collaterals or therapeutic/spontaneous dissolution of emboli).
  • Infarcts caused by venous occlusion.
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73
Q

Causes of intra-parenchymal hemorrhage

A
  1. Most common in hypertension (see sites affected by hypertensive lesions).
  2. Atherosclerosis.
  3. Tumors.
  4. Cerebral contusions (trauma).
  5. Clotting disorders.
  6. Cerebral amyloid angiopathy.
  7. Vascular malformations.
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74
Q

Causes of subarachinoid hemorrhage

A
  • due to ruptured aneurysms and vascular malformations or brain trauma.
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75
Q

Clinical manifestations of subarachinoid hemorrhage

A
  • meningeal irritation with a rapid increase in the intracranial pressure
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76
Q

Causes of subdural hemorrhage (Hematoma)

A
  • rupture of venous sinuses or bridging cerebral veins crossing the subdural space.
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77
Q

where is subdural hemorrhage (Hematoma) more common?

A
  • old patients with brain atrophy, alcoholics.
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78
Q

what are the clinical manifestaions of subdural hemorrhage (Hematoma)?

A

Acute: a rapid increase in intracranial pressure (ICP).

Chronic: e.g., personality changes, memory loss and confusion.

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79
Q

causes of epidural (Extradural) hemorrhage (Hematoma)

A
  • Caused by traumatic skull fracture, especially temporal or parietal bones (tear of middle meningeal artery).
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80
Q

what are the manifestations of epidural (Extradural) hemorrhage (Hematoma)?

A
  • Expands rapidly (arterial bleeding) with rapid increase of ICP
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81
Q

what is the case of epidural (Extradural) hemorrhage (Hematoma) considered as?

A
  • It is a neurosurgical emergency (drainage and repair to prevent death).
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82
Q

Sites of hypertensive cerebrovascular diseases

A
  • Thalamus, basal ganglia, deep white mater, internal Capsule and pons.
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83
Q

Lesions of hypertensive cerebrovascular diseases

A
  1. Hyaline arterio-sclerosis of cerebral arterioles,
  2. Charcot-Bouchard microaneurysms,
  3. Lacunar infarcts: few millimeters in size,
  4. Slit hemorrhages: Rupture of the small penetrating vessels,
  5. Massive intra-parenchymal hemorrhage: arterial rupture
  6. Cerebral edema
  7. Acute hypertensive encephalopathy
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84
Q

Explain acute hypertensive encephalopathy

A

if diastolic blood pressure exceeds 130 mm Hg. β†’ cerebral dysfunction, headaches, confusion, vomiting, convulsions, and sometimes coma.

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85
Q

Explain cerebral amyloid angiopathy (CAA)

A
  • Amyloid beta peptide (AΞ²) (as Alzheimer disease) deposit in the walls of medium and small meningeal and cortical vessels.
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86
Q

Staining of cerebral amyloid angiopathy

A

stains positive with Congo red (polarized light examination→ apple-green color).

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87
Q

what does CAA lead to overtime?

A

Weak vessels β†’hemorrhages in the lobes of the cerebral cortex (lobar hemorrhages).

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88
Q

what are the types of cerebral aneurysms?

A
  • Congenital berry (saccular) aneurysms
  • Microaneurysms of essential hypertension (Charcot-Bouchard).
  • Atheromatous aneurysms.
  • Traumatic aneurysms.
89
Q

Site of congenital (Berry) aneurysms

A

circle of Willis (small, multiple).

90
Q

Pathology of congenital (Berry) aneurysms

A

internal elastic lamina & medial weakness at bifurcation of arteries.

91
Q

what is the most frequent cause of spontaneous subarachinoid hge. ?

A

Congenital berry (saccular) aneurysms

92
Q

what does the rupture of cerebral aneurysms associate?

A

Rupture associates straining (increase intracranial pressure. e.g., constipation).

93
Q

what are the clinical effects of cerebral aneurysms?

A
  • Pressure on the surrounding, rupture and subarachnoid or intraparenchymal hemorrhages.
94
Q

Give example of vascular malformations of the brain

A
  • Arteriovenous malformations (AVMs)
  • Other types: Cavernous malformations, capillary telangiectasias, venous angiomas.
95
Q

what is the most dangerous vascular malformations of the brain?

A

Arteriovenous malformations (AVMs)

96
Q

appearence of AVMs

A
  • appears as a tangled network of worm-like vascular channels
97
Q

what does AVM lead to?

A

mixed intra-parenchymal or subarachnoid hemorrhages.

98
Q

CSF Circulation

A
  • CSF is produced by choroid plexus in the lateral ventricles β†’ 3rd ventricle β†’ Aqueduct of Sylvius β†’ 4th ventricle β†’ Foramina of Luschka and Magendieβ†’ Resorbed by arachnoid granulations in subarachnoid space β†’ The dural venous sinuses β†’Blood stream.
  • The balance between CSF production and resorption regulates its volume.
99
Q

What is Hydrocephalus?

A
  • Accumulation of excess cerebrospinal fluid (CSF) within the ventricular system of the brain.
100
Q

Pathogenesis of Hydrocephalus

A

3 mechanisms:

  1. Increased CSF production
  2. Decreased CSF absorption.
  3. CSF flow obstruction
101
Q

Causes of Increased CSF production

A
  • Choroid plexus neoplasm (papilloma, carcinoma).
  • Choroiditis.
102
Q

Causes of Decreased CSF absorbtion

A
103
Q

Causes of CSF flow obstruction

A
104
Q

what are the types of hydrocephalus?

A
  • Communicating
  • Non-Communicating
  • Compensatory
105
Q

Definition of Communicating hydrocephelus

A
  • The ventricles communicate with the subarachnoid space (mainly increased production).
106
Q

Def. of non-Communicating hydrocephelus

A
  • The ventricles are not communicating with the subarachnoid space (mainly obstruction to CSF flow).
107
Q

Definition of Compensatory hydrocephalus

A
  • increased amount of CSF to compensate loss of brain tissue (atrophy, infarcts, surgery).
108
Q

Pathological effects of hydrocephalus

A
  1. Dilated ventricular system.
  2. In infancy: Enlarged skull, thin skull bones, large fontanelles, separated sutures and affected neurologic and mental status.
  3. After closure of skull sutures:
    - Increased intracranial pressure (ICP) and brain herniation
    - Pressure atrophy of the brain
    - Prominent convolutional markings of the skull (copper-beaten appearance of the skull).
109
Q

Routes of CNS Infections

A
  1. Hematogenous: most common; by arterial circulation, or retrograde venous spread from face veins.
  2. Direct implantation: traumatic, iatrogenic (lumbar puncture) or with congenital malformations (e.g., meningomyelocele).
  3. Local spread: from adjacent structures, such as air sinuses, teeth, skull, or vertebrae.
  4. Nerve spread: Viruses transported along the peripheral nerves (rabies and herpes zoster viruses).
110
Q

Classification & Organisms of CNS infections

A
111
Q

Definition of Acute Pyogenic (Bacterial) Meningitis

A
  • Acute suppurative inflammation of leptomeninges involving the subarachnoid space.
112
Q

Organisms causing Acute Pyogenic (Bacterial) Meningitis

A
  • In neonates: Escherichia coli and group B streptococci.
  • Young children: Haemophilus influenzae.
  • In adolescents and young adults: Neisseria meningitidis.
  • In older adults: Streptococcus pneumoniae and Listeria monocytogenes.
113
Q

Clinical features of Acute Pyogenic (Bacterial) Meningitis

A
  • Signs of systemic infection (e.g., fever)
  • Signs of meningeal irritation (headache, irritability, neck stiffness, confusion)
114
Q

CSF changes in Acute Pyogenic (Bacterial) Meningitis

A
  • Turbid, increased pressure, increased neutrophils, markedly increased protein, markedly low glucose, bacteria detected in smear or by culture.
115
Q

N/E of Acute Pyogenic (Bacterial) Meningitis

A
  • Exudate (pus) within the subarachnoid space and on brain surface specially at the base.
  • Edema, congested leptomeningeal vessels.
  • Turbid CSF.
116
Q

M/E of Acute Pyogenic (Bacterial) Meningitis

A
  • Neutrophils and pus cells fill the subarachnoid space and infiltrate leptomeninges.
  • Edema around the congested blood vessels.
117
Q

Complications & Fate of Acute Pyogenic (Bacterial) Meningitis

A
  • Increased intracranial pressure (ICP).
  • Pressure on cranial nerves and nerve paresis (3,4,6)
  • Cerebritis, ventriculitis, thrombophlebitis with venous occlusion and hemorrhagic infarction, subdural or brain abscess.
  • Meningococcal septicaemia (suprarenal gland hemorrhage and failure= Waterhouse-Friderichsen syndrome).
  • Post-meningitis adhesions and hydrocephalus.
  • Death (untreated cases).
118
Q

what are types of Chronic Bacterial Meningoencephalitis?

A
  • Tuberculosis
  • Neurosyphilis
119
Q

Pathological lesions of TB

A

TB meningitis:
- Subarachnoid space contains gelatinous or fibrinous exudate mainly at the base of the brain, and coating the cranial nerves.

Tuberculomas of the brain:
- effects of space-occupying lesion.

120
Q

what is Neurosyphilis?

A

A manifestation of the tertiary stage of syphilis.

121
Q

Patterns of CNS involvment in neurosyphilis

A
  1. Meningovascular neurosyphilis.
  2. Paretic neurosyphilis
  3. Tabes dorsalis
122
Q

Paretic neurosyphilis

A

Involves mainly frontal cortex, ends in severe dementia.

123
Q

Tabes dorsalis

A
  • Destroys sensory dorsal roots of spinal cord (loss of pain sense, locomotor ataxia and other sensory disturbances).
124
Q

What is Viral (Aseptic) Meningitis?

A
  • Acute inflammation of leptomeninges in absence of organisms by bacterial culture.
125
Q

Causative viruses of Viral (Aseptic) Meningitis

A
  • Most commonly enteroviruses (polio-, echo-, coxackie-).
126
Q

Clinical features of Viral (Aseptic) Meningitis

A
  • Signs of meningeal irritation, fever, and alterations of consciousness of relatively acute onset.
  • Usually self-limited.
127
Q

CSF changes in Viral (Aseptic) Meningitis

A
  • Lymphocytosis, mild to moderate increase in protein, normal glucose.
128
Q

General features of Viral Encephalitis and Meningoencephalitis

A
  1. Focal necrosis of grey and white mater.
  2. Cerebral mononuclear infiltrates (perivascular).
  3. Microglial nodules.
  4. Neuronophagia.
  5. Intracellular viral inclusion bodies.
129
Q

CSF changes in Viral Encephalitis and Meningoencephalitis

A
  • Initial neutrophilic pleocytosis, followed by lymphocytosis, moderately increased protein, normal glucose.
130
Q

Causative viruses of Viral Encephalitis and Meningoencephalitis

A
  1. Arboviruses
  2. Herpes Simplex Virus (HSV):
  3. Varicella-Zoster Virus
  4. Cytomegalovirus (CMV)
  5. JC polyomavirus
  6. Human Immunodeficiency Virus (HIV, AIDS)
131
Q

Arboviruses

A
  • Arthropod born endemic encephalitis.
132
Q

Herpes Simplex Virus (HSV) and CNS affection

A
133
Q

who does Varicella-Zoster Virus (Herpes Zoster; chickenpox) Affect?

A
  • Affects immunocompromised patients.
134
Q

Patterns of infection by Cytomegalovirus (CMV)

A

2 patterns: Adult infection and intrauterine infection:

135
Q

Characters of viral encephalitis by Cytomegalovirus (CMV)

A
  • Involves the periventricular regions.
  • Large cells with intranuclear cytomegalic inclusions.
  • Microcephaly & periventricular calcification in newborn.
136
Q

Characters of viral encephalitis by HIV

A
  • Acute aseptic meningitis.
  • Subacute HIV encephalitis.
  • Opportunistic infections (Fungal, parasitic, viral).
  • Leukoencephalopathy (myelinopahty).
  • Tumors as cerebral lymphoma.
  • Congenital HIV encephalitis is more severe than the adult and may result in microcephaly.
137
Q

what does JC polyomavirus cause?

A
  • progressive multifocal leukoencephalopathy (PML).
138
Q

what does JC polyomavirus infect?

A

Infects oligodendrocytes→ demyelination and white mater destruction.

139
Q

what is Polio virus?

A
  • Is an enterovirus transmitted by ingestion causing mild gastroenteritis in young children.
140
Q

What is Paralytic poliomyelitis?

A
  • is a disease that has been eradicated by vaccination in most parts of the world.
141
Q

Pathological features of polio virus

A
  • Acute cases
  • Some acute cases
  • Polio aseptic meningitis
  • Ascending infection
  • Permanent flaccid paralysis (about 1% of cases)
  • Post-polio syndrome
142
Q

Acute cases of polio virus

A
  • mononuclear cell infiltrate and neuronophagia of the anterior horn motor neurons of spinal cord.
143
Q

Some acute cases of polio virus

A
  • suffer acute myocarditis or die from paralysis of respiratory muscles.
144
Q

Polio aseptic meningitis

A
  • meningeal irritation and a CSF picture of aseptic meningitis.
145
Q

Ascending infection of polio virus

A
  • Bulbar polio (brainstem), polio-encephalitis.
146
Q

Permanent flaccid paralysis (about 1% of cases) by polio

A
  • muscle wasting and hyporeflexia in the corresponding region of the body, mostly lower limbs.
147
Q

Post-polio syndrome

A
  • progressive weakness, decreased muscle mass and pain (affects polio survivors many years after recovery from an initial acute attack of the poliomyelitis virus).
148
Q

How is Rabies virus transmitted?

A
  • transmitted by bites of rabid animals (e.g., dogs, bats, wild mammals).
149
Q

Route of Rabies virus

A
  • Reaches the CNS along peripheral nerves from the wound site.
150
Q

IP of Rabies virus

A
  • 1-3 months, depends on the distance between the wound and the brain.
151
Q

Clinical features of rabies

A
  • Non-specific symptoms (malaise, headache, and fever).
  • Local paresthesia around the wound.
  • CNS excitability (painful touch, violent motor responses, convulsions).
  • Hydrophobia (Pharyngeal spasm).
  • Coma and death from respiratory failure.
152
Q

Pathological lesions in rabies

A
  • Severe encephalitis with edema and congestion.
153
Q

M/E of rabies

A
  • Diffuse neuronal degeneration.
  • Inflammation is most severe in the brainstem.
  • The basal ganglia, spinal cord, and dorsal root ganglia may also be involved.
  • Negri bodies (pathognomonic microscopic finding): cytoplasmic eosinophilic inclusions found in pyramidal neurons of the hippocampus, Purkinje cells of the cerebellum and brainstem nuclei.
154
Q

Def. of Brain Abscess

A
  • Localized focus of liquefactive necrosis of brain tissue with inflammation, mostly caused by a bacterial infection (e.g. staphylococcus aureus).
155
Q

Routes of Brain Abscess

A
  • Direct implantation of organisms, or local extension from adjacent foci (mastoiditis, paranasal sinusitis),
  • Hematogenous spread (infective endocarditis, lung suppuration, or osteomyelitis of bones of the extremities, or after tooth extraction).
156
Q

Clinical features of Brain Abscess

A

Focal neurologic deficits; increased ICP.

157
Q

Pathological features of Brain Abscess

A

Acute:

  • Central liquefactive necrosis (pus) surrounded by edema and hyperaemia.
  • Granulation tissue around the necrosis.

Chronic:

  • Thick wall of fibro-gliosis.
158
Q

CSF in cases of Brain Abscess

A

High pressure, high white cell count, increased protein, but the glucose is normal.

159
Q

Complications of Brain Abscess

A
  • Spread: encephalitis, subdural or extradural abscess.
  • Rupture: ventriculitis or meningitis.
  • Brain herniation (high ICP).
  • Venous sinus thrombosis.
160
Q

what is Prion Disease?

A

Very rare diseases (sporadic, familial, iatrogenic, and Creutzfeldt-Jakob disease [CJD]).

161
Q

Infective agent of Prion Disease

A

Abnormal misfolded cellular protein.

162
Q

what does Prion Disease cause?

A

causes fatal and transmissible neurodegenerative diseases in humans and many other animals.

163
Q

Primary method of infection by Prion Disease

A
  • by ingestion (ususally by infected meat products), less likely by inoculation.
164
Q

what are Nervous System Tumors?

A
  • Tumors of neuroepithelial tissues
  • Tumors of Meninges
  • Tumors of peripheral nerves
  • Other tumors
165
Q

what are Tumors of neuroepithelial tissues?

A
  • Gliomas
  • Embryonal tumors (Medulloblastoma)
166
Q

what are the commonest primary C.N.S tumors?

A

Gliomas

167
Q

what are Gliomas?

A
  • Astrocytoma
  • Oligodendroglioma
  • Ependymoma
168
Q

what is the commonest glioma?

A
  • Astrocytoma
169
Q

Site of Astrocytoma

A
  • Cerebellum of children.
  • Cerebrum of adults.
170
Q

N/E of Astrocytoma

A
  • Soft grey mass with ill-defined outline. The cut surface shows areas of cystic degeneration.
  • In high grade forms it shows necrosis and haemorrhages.
171
Q

M/E of Astrocytoma (In general)

A
  • Neoplastic Astrocytes, branched cells with fibrillary background it may be of variable grades of differentiation.
172
Q

what are microscopic types of Astrocytoma?

A
  • Localized astrocytomas (Pilocytic astrocytoma - grade I)
  • Diffuse astrocytomas:
    1. Diffuse fibrillary astrocytoma - grade (II)
    2. Anaplastic astrocytoma - grade (III)
    3. Glioblastoma Multiforme - grade (IV)
173
Q

Localized astrocytomas(Pilocytic astrocytoma - grade I)

A
  • Mildly cellular, formed of mature astrocytes within excess fibrillary back ground
  • Cells are bipalor with stroma of eosinophilic elongated and coma shaped fibers (Rosenthal fibers).
174
Q

what are Diffuse astrocytomas?

A
  1. Diffuse fibrillary astrocytoma - grade (II)
  2. Anaplastic astrocytoma - grade (III)
  3. Glioblastoma Multiforme - grade (IV)
175
Q

Diffusefibrillaryastrocytoma - grade (II)

A
  • Hypercellular, formed of pleomorphic astrocytes within excess fibrillary background.
  • A subtype of Grade II diffuse astrocytoma show Large astrocytes with excess esinophilic cytoplasm and eccentric nuclei, called gemistocytic astrocytoma.
176
Q

Anaplastic astrocytoma - grade (III)

A
  • Formed of pleomorphic astrocytes with excess mitosis without necrosis
177
Q

Glioblastoma Multiforme - grade (IV)

A
  • Formed of primitive astrocytes with marked Pleomorphism, Giant cells, mitosis, nerosis and vascular endothelial proliferation in glomeruloid manner.
178
Q

where does Oligodendroglioma arise from?

A
  • From oligodendroglia cells of cerebrum.
179
Q

Incidence of Oligodendroglioma

A

Middle age.

180
Q

N/E of Oligodendroglioma

A
  • Localized, pink, gelatinous with cyst formations and calcification.
181
Q

M/E of Oligodendroglioma

A
  • Rounded cells, with uniform swollen nuclei and clear cytoplasm with focal of calcification.
182
Q

Incidence of Ependymoma

A
  • Children and young adults
183
Q

Origin of Ependymoma

A
  • From ependymal cells lining the ventricles, commonly the fourth ventricle and Lower part of the spinal cord
184
Q

M/E of Ependymoma

A
  • Fleshy vascular mass.
185
Q

M/E of Ependymoma

A

(a) Elongated cells arranged perivascular in pseudorosettes, commonest

(b) Papillary type.

186
Q

Incidence of Embryonal tumors (Medulloblastoma)

A

Common childhood brain tumor

187
Q

Site of Embryonal tumors (Medulloblastoma)

A

At the roof of fourth ventricle

188
Q

N/E of Embryonal tumors (Medulloblastoma)

A
  • Fleshy soft grey mass projections in the 4th ventricle may penetrate the brain to reach the subarachnoid space (trans-coelomic spread)
189
Q

M/E of Embryonal tumors (Medulloblastoma)

A
  • Small dark stained cells arranged in rosettes.
190
Q

what are similar nerve tumors to Embryonal tumors (Medulloblastoma)?

A

Similar nerve cell tumors are:

  • Retinoblastoma from retina
  • Neuroblastoma of from sympathetic nervous system
191
Q

what are Tumors of Meninges?

A
  • Meningothelial tumors (Meningioma)
  • Mesenchynal (non meningothelial tumors)
192
Q

Incidence of Meningothelial tumors (Meningioma)

A

In adults

193
Q

Origin of Meningothelial tumors (Meningioma)

A
  • Originates from the endothelial cells of the arachnoid villi commonly in relation to superior sagittal sinus.
194
Q

N/E of Meningothelial tumors (Meningioma)

A
  • Rounded firm capsulated tumor attached externally to the dura and imbedded in the brain tissue internally.
  • Cut surface: greyish white and often show whorly appearance.
  • Older tumors slow secondary changes as bone, cartilage and fat (metaplastic changes)
195
Q

M/E of Meningothelial tumors (Meningioma)

A
  • Formed of spindle shaped cells arranged in concentric layers with calcifications in the center (Psammoma bodies).
196
Q

where is Meningothelial tumors (Meningioma) more common, males or females?

A
  • It is more common female and some tumors have estrogen receptors so it grows rapidly during pregnancy.
  • It may turn malignant.
197
Q

what are Mesenchynal (non meningothelial tumors)?

A
  • Lipoma.
  • Angiolipoma
  • Vascular tumors
  • Haemangioblastoma: Benign tumor arises in cerebellum.
198
Q

what are Tumors of peripheral nerves?

A
199
Q

Origin of Neurilemmoma or schwannoma

A
200
Q

Incidence of Neurilemmoma or schwannoma

A
201
Q

N/E of Neurilemmoma or schwannoma

A
202
Q

M/E of Neurilemmoma or schwannoma

A
203
Q

N/E of Neurofibroma

A
204
Q

M/E of Neurofibroma

A
205
Q

Nature od Multiple neurofibromatosis. (Von-Reckling-Hausen disease of nerves)

A
206
Q

N/E of Multiple neurofibromatosis. (Von-Reckling-Hausen disease of nerves)

A
207
Q

Qhat causes Maligmant peripheral nerve sheath tumors?

A
208
Q

N/E of Maligmant peripheral nerve sheath tumors

A
209
Q

what are Other tumors related to the nervous system?

A
210
Q

what are the most common malignant tumor in the brain?

A
211
Q

what is the nature of most of Metastatic tumors of the brain?

A
212
Q

Incidence of Metastatic tumors of the brain

A
213
Q

How do Metastatic tumors of the brain reach it?

A
214
Q

Common sources of Metastatic tumors of the brain

A
215
Q

N/E of Metastatic tumors of the brain

A
216
Q

M/E of Metastatic tumors of the brain

A
217
Q

Effects of intracranial tumors

A
218
Q

Manifestations of of intracranial tumors

A

Y2B4 - Central Nervous System πŸ“™ (8 decks)

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