Neuro I (b) Flashcards
HTN in the brain leads to?
1) Hyaline arterioscelrosis
2) Charcot-Bouchard Micro-Aneurysm
3) Lacunar Infarcts
4) Rupture of the small-caliber penetrating vessels
5) Acute Hypertensive Encephalopathy
loc of Hyaline Arteriosclerosis
basal ganglia and brain stem
———-: Small cavitary infarcts in basal ganglia, thalamus, internal capsule, pons, etc which is a result in Occlusion of a penetrating artery
Lacunar infarcts
CF of Acute Hypertensive Encephalopathy
Sudden, sustained increase in diastolic blood pressure (>130mm Hg) –> Increased intracranial pressure –> Headaches, confusion, vomiting, convulsions
DD of Acute Hypertensive Encephalopathy
Stroke
Rupture of the small-caliber penetrating vessels suplying deep structures if the brain will result in?
Slit haemorrhage (slit-like cavity)
———: Infectious arteritis of small and large vessels
Vasculitis
cause of Vasculitis
Opportunistic infections in immunocompromised individuals
Vasculitis
In systemic forms of Vasculitis there is Involvement of ———— (e.g. polyarteritis nodosa) –> ————
In systemic forms of Vasculitis there is Involvement of cerebral vessles (e.g. polyarteritis nodosa) –> -Multiple infarcts
————: Form of vasculitis, affecting small- to medium-sized parenchymal and subarachnoid vessels
Primary Angiitis of the CNS
Microscopic Findings:
* Chronic inflammatory cell infiltrates
* Multinucleate giant cells (+/- granuloma formation)
* Destruction of vessel walls
* Amyloid-β deposits
* Lumen Oblitertion
features of?
Primary Angiitis of the CNS
* Form fo Vasculitis
———: Rapid tissue displacement –>Damage of vessels -> Haemorrhage, tissue injury and oedema
Contusion
Contusion Will cause?
haemorrhage, tissue damage and oedema in the brain
Loc of a Contusion
1) Orbito-frontal regions
2) Temporal lobe tips
the 2 types of Contusion
Coup and Contre-Coup injuries
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?
Contusion
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 —————-
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
cause/ patho of Diffuse Axonal injury
Angular acceleration –> Axonal injury and haemorrhage
location of Diffuse Axonal injury (DAI)
- Near the angles of the lateral ventricles
- Corpus callosum
- Brain-Stem
Microscopic Findings:
* Axonal swellings (“bulbs”), within hours of the injury
* Axonal Spheroids
* Immuno-histochemistry : β-APP
features of?
Diffuse Axonal injury
Diffuse Axonal injury
Microscopic Findings:
* Axonal swellings (“——-”), within hours of the injury
* Axonal ——-
* Immuno-histochemistry : ——-
Microscopic Findings:
* Axonal swellings (“bulbs”), within hours of the injury
* Axonal Spheroids
* Immuno-histochemistry : β-APP
Histochemical stain for diffuse Axonal Injury ?
Silver stain
(detects axonal swelling)
Immuno-Histochemistry findings in Diffuse Axonal Injury
Amyloid Precussor ProteinAPP
————– :Penetration of the brain by a projectile (e.g. bullet, bone fragment of the skull –> Tissue tearing, vascular disruption and haemorrhage
Laceration
——–: Reversible altered consciousness from head injury in the absence of contusion
Concussion
CM of Concussions
- Loss of consciousness
- Temporary respiratory arrest (Due to sever perssure ont the brain stem)
- Loss of reflexes
CNS trauma –> Disruption of the vessel wall -> ———–
Haemorrhage
The 4 types of Haemorrahge
1) Epidural
2) Subdural
3) Subarachnoid
4) Intra-parenchymal
Cause of Epidural Haematoma
Traumatic injury of the middle meningeal artery, after a skull fracture
CM of Epidural Haematoma
Neurosurgical emergency; If left untreated –> Death
causes of Subdural Haematoma
Tear of the bridging veins, after trauma
Cause of Subdural Haematoma in Elderly?
Elderly individuals with brain atrophy, due to stretching of the bridging veins
patho of Subdural Haematoma
Vein disruption (tear of bridging veins) –> Bleeding into the subdural space
location of Subdural Haematoma
lateral aspects of the cerebral hemispheres
CM of Subdural Haematoma
Within 48 hrs after injury:
* Headache
* Confusion
* Slowly progressive neurologic deterioration
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
?? not sure if we need to know this
stain for Siderophages
Prussian-blue reaction
?? not sure if we need know this
Stain used for Erythrophagocytosis
Azan
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)
Most frequent type of CNS malformation?
Neural tube malformations
Risk factors of Neural tube defects
Folate deficiency during the initial weeks of gestation
Defects in the posterior end of the Neural Tube will result in
1) Spina Bifida Occulta
2) Meningocele and
3) Myelo-Meningocele
Defects in the anterior end of the Neural Tube
1) Anencephaly: Absence of the brain and the top of skull
2) Encephalocele
————: Abnormally large brain volume
Megaloencephaly
———: Abnormally small brain volume, which occurs together with a small head
Micro(en)cephaly
Risk factors of Microencephaly
Fetal alcohol syndrome, HIV infection
(acquired in utero), Zika virus
patho of Microencephaly
Decreased generation of neurons that will populate the cerebral cortex
Which condition is known as “Smooth brain” ?
Lissencephaly
patho of Lissencephaly
Total absence of gyration or pachygyria (patchy involvement) –> “Smooth brain”
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
Patho of Polymicrogyria
Numerous irregularly formed gyri –> Cobblestone-like surface
Macroscopic features:
* Numerous irregulary formed gyri –> Cobbelstone - like surface
* Many gyri
Microscopic features:
* A festooned cortex w/ fusion of Gyri
features of?
Polymicrogyria
pathophysio of Holoprosencephaly
Absence of the olfactory bulbs
(Arrhinencephaly)
Absence of the olfactory bulb is known as ?
Arrhinencephaly
* Mild form of Holoprosencephaly
Mild form of Holoprosencephaly?
Arrhinencephaly - Absence of The Olfactory bulbs
sever forms of Holoprosecncephaly are associated w?
facial midline defects (e.g. cyclopia)
Macroscopic features:
* Fused cerebral hemispheres and thalamus
* Absent sulci
* Absence of Olfactory nerve
features of?
Alobar Holoprosencephaly
Posterior Fossa Anomalies
1) Chiari Type I malformation
2) Arnold-Chiari (Chiari Type II) Malformation
3) Dandy-Walker Malformation
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
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
Arnold-Chiari (Type II) Malformation Coexists w?
hydrocephalus and lumbar myelo-meningocele
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
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
Spinal cord Abnormalities examples
1) Hydromyelia
2) Syringomyelia
Hydromyelia are associated w?
hydrocephalus or Chiary malformation
type II and Dandy-Walker syndrome
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
Syingomyelia commonly coexists w?
Chiari malformation type I or have
experienced spinal cord trauma
Cerebral palsy is a non-progressive neurological motor deficit, characterized by?
1) Ataxia or Athetosis
2) Spasticity
3) Dystonia
4) Paresis (muscle weakness)
Types of Brain Injuries in the Perinatal Period
1) Haemorrhages (Eventually causes Hydrocephalus)
2) Infarcts
