Neuro I (b) Flashcards

1
Q

HTN in the brain leads to?

A

1) Hyaline arterioscelrosis
2) Charcot-Bouchard Micro-Aneurysm
3) Lacunar Infarcts
4) Rupture of the small-caliber penetrating vessels
5) Acute Hypertensive Encephalopathy

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2
Q

loc of Hyaline Arteriosclerosis

A

basal ganglia and brain stem

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3
Q

———-: Small cavitary infarcts in basal ganglia, thalamus, internal capsule, pons, etc which is a result in Occlusion of a penetrating artery

A

Lacunar infarcts

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4
Q

CF of Acute Hypertensive Encephalopathy

A

Sudden, sustained increase in diastolic blood pressure (>130mm Hg) –> Increased intracranial pressure –> Headaches, confusion, vomiting, convulsions

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5
Q

DD of Acute Hypertensive Encephalopathy

A

Stroke

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6
Q

Rupture of the small-caliber penetrating vessels suplying deep structures if the brain will result in?

A

Slit haemorrhage (slit-like cavity)

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7
Q

———: Infectious arteritis of small and large vessels

A

Vasculitis

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8
Q

cause of Vasculitis

A

Opportunistic infections in immunocompromised individuals

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9
Q

Vasculitis

In systemic forms of Vasculitis there is Involvement of ———— (e.g. polyarteritis nodosa) –> ————

A

In systemic forms of Vasculitis there is Involvement of cerebral vessles (e.g. polyarteritis nodosa) –> -Multiple infarcts

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10
Q

————: Form of vasculitis, affecting small- to medium-sized parenchymal and subarachnoid vessels

A

Primary Angiitis of the CNS

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11
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

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12
Q

———: Rapid tissue displacement –>Damage of vessels -> Haemorrhage, tissue injury and oedema

A

Contusion

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13
Q

Contusion Will cause?

A

haemorrhage, tissue damage and oedema in the brain

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14
Q

Loc of a Contusion

A

1) Orbito-frontal regions
2) Temporal lobe tips

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15
Q

the 2 types of Contusion

A

Coup and Contre-Coup injuries

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16
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

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17
Q

Contusion

Macroscopic Features:
* Cross-section: ———– -shaped
* Old lesions: Depressed, ————– patches (Crests of gyri)

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

A

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

* pyknosis: nuclear shrinking

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18
Q

cause/ patho of Diffuse Axonal injury

A

Angular acceleration –> Axonal injury and haemorrhage

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19
Q

location of Diffuse Axonal injury (DAI)

A
  • Near the angles of the lateral ventricles
  • Corpus callosum
  • Brain-Stem
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20
Q

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

features of?

A

Diffuse Axonal injury

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21
Q

Diffuse Axonal injury

Microscopic Findings:
* Axonal swellings (“——-”), within hours of the injury
* Axonal ——-
* Immuno-histochemistry : ——-

A

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

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22
Q

Histochemical stain for diffuse Axonal Injury ?

A

Silver stain
(detects axonal swelling)

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23
Q

Immuno-Histochemistry findings in Diffuse Axonal Injury

A

Amyloid Precussor ProteinAPP

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24
Q

————– :Penetration of the brain by a projectile (e.g. bullet, bone fragment of the skull –> Tissue tearing, vascular disruption and haemorrhage

A

Laceration

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25
**--------**: Reversible altered consciousness from head injury in the absence of contusion
Concussion
26
CM of Concussions
* **Loss of consciousness** * **Temporary respiratory arrest** (Due to sever perssure ont the brain stem) * **Loss of reflexes**
27
CNS trauma --> Disruption of the vessel wall -> **-----------**
**Haemorrhage**
28
The 4 types of Haemorrahge
1) Epidural 2) Subdural 3) Subarachnoid 4) Intra-parenchymal
29
Cause of Epidural Haematoma
Traumatic injury of the **middle meningeal artery,** after a skull fracture
30
CM of Epidural Haematoma
Neurosurgical emergency; If left untreated --> Death
31
causes of Subdural Haematoma
**Tear of the bridging veins**, after trauma
32
Cause of Subdural Haematoma in Elderly?
Elderly individuals with brain atrophy, due to **stretching of the bridging veins**
33
patho of Subdural Haematoma
Vein disruption (tear of bridging veins) --> Bleeding into the subdural space
34
location of Subdural Haematoma
lateral aspects of the cerebral hemispheres
35
CM of Subdural Haematoma
Within **48 hrs** after injury: * Headache * Confusion * Slowly progressive neurologic deterioration
36
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 ?
Subdural Haematoma
37
# ?? not sure if we need to know this stain for Siderophages
Prussian-blue reaction
38
# ?? not sure if we need know this Stain used for Erythrophagocytosis
Azan
39
# 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)
* **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)
40
Most frequent type of CNS malformation?
Neural tube malformations
41
Risk factors of Neural tube defects
Folate deficiency during the initial weeks of gestation
42
Defects in the posterior end of the Neural Tube will result in
1) Spina Bifida Occulta 2) Meningocele and 3) Myelo-Meningocele
43
Defects in the anterior end of the Neural Tube
1) **Anencephaly:** Absence of the brain and the top of skull 2) **Encephalocele**
44
**------------**: Abnormally large brain volume
Megaloencephaly
45
**---------**: Abnormally small brain volume, which occurs together with a small head
Micro(en)cephaly
46
Risk factors of Microencephaly
Fetal alcohol syndrome, HIV infection (acquired in utero), **Zika virus**
47
patho of Microencephaly
**Decreased generation of neurons** that will populate the cerebral cortex
48
Which condition is known as **"Smooth brain"** ?
Lissencephaly
49
patho of Lissencephaly
**Total absence of gyration** or pachygyria (patchy involvement) --> **“Smooth brain”**
50
Macroscopic features: * Complete absence of Gyration --> **"Smooth brain"** * Abnormally thickened cortex * **Four cortical layers** Microscopic features: * Mylein sheath * reactive astrocytes around vessles * reticullar pattern of the deep cortical layer features of?
Lissencephaly
51
Patho of Polymicrogyria
Numerous **irregularly formed gyri** --> **Cobblestone-like surface**
52
Macroscopic features: * Numerous irregulary formed gyri --> **Cobbelstone - like surface** * Many gyri Microscopic features: * **A festooned cortex w/ fusion of Gyri** features of?
Polymicrogyria
53
pathophysio of Holoprosencephaly
Absence of the olfactory bulbs **(Arrhinencephaly)**
54
Absence of the olfactory bulb is known as ?
Arrhinencephaly | * Mild form of Holoprosencephaly
55
Mild form of Holoprosencephaly?
**Arrhinencephaly** - Absence of The Olfactory bulbs
56
sever forms of Holoprosecncephaly are associated w?
facial midline defects (e.g. **cyclopia**)
57
Macroscopic features: * Fused cerebral hemispheres and thalamus * Absent sulci * **Absence of Olfactory nerve** features of?
**Alobar** Holoprosencephaly
58
Posterior Fossa Anomalies
1) Chiari Type I malformation 2) Arnold-Chiari (Chiari Type II) Malformation 3) Dandy-Walker Malformation
59
CM of Chiari Type I Malformation
partial Obstruction of the CSF flow and compression of the medulla --> **Sever headaches** or **Cranial nerver deficits** | * manifested in adulthood
60
Macroscopic features: * Low-lying cerebellar tonsils, extending through the foramen magnum * **Protrusion of the tonsils** into the foramen magnum features of?
Chiari Type I malformation
61
Arnold-Chiari (Type II) Malformation Coexists w?
**hydrocephalus** and lumbar myelo-meningocele
62
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?
Arnold-Chiari Malformation
63
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?
Dandy-Walker Malformation
64
Spinal cord Abnormalities examples
1) Hydromyelia 2) Syringomyelia
65
Hydromyelia are associated w?
hydrocephalus or Chiary malformation type II and Dandy-Walker syndrome
66
Pathophysio of Hydromyelia Abnormal **---------------** of the central canal of the **--------** --> Cavity connected to the 4th ventricle, with possible build up of **----------**--> pressure on the spinal cord--> **-------------** of nerve cells and their connections
Abnormal **widening** of the central canal of the **spinal cord** --> Cavity connected to the 4th ventricle, with possible build up of **CSF**--> pressure on the spinal cord--> **Damage** of nerve cells and their connections
67
Syingomyelia commonly coexists w?
Chiari malformation type I or have experienced spinal cord trauma
68
Cerebral palsy is a non-progressive neurological motor deficit, characterized by?
1) Ataxia or Athetosis 2) Spasticity 3) Dystonia 4) Paresis (muscle weakness)
69
Types of Brain Injuries in the Perinatal Period
1) Haemorrhages (Eventually causes Hydrocephalus) 2) Infarcts
70