Neurology Flashcards
Seen in acute hypoxia/ischemia
Evident by 12-24 hours
Shrinkage of cell body, pyknosis of nucleus, nucleolar disappearance, eosinophilia
Acute neuronal injury
Red neurons
Hallmark of acute neuronal injury
12-24 hours
Loss of Nissl substance
Seen in chronic and progressive neurodegenerative disease
Cell loss, reactive gliosis
Subacute and chronic neuronal injury
Degeneration
Seen during regeneration
Increased protein synthesis with axonal sprouting
Axonal reaction
Seen in aging, viral infections and degenerative diseases
Intracytoplasmic accumulation
Neuronal inclusions
Site of protein synthesis of neurons
Granular bodies of RER
Nissl susbtance
HSV body
Cowdry type A in temporal lobe
Rabies body
Negri body in pyramida cells of hippocampus and purkinje cells of cerebellum
Alzheimer’s body
Neurofibrillary tangles of hyperphosphorylated tau proteins
Parkinson’s disease body
Lewy Body of alpha synuclein protein
Hypertrophy and hyperplasia of astrocytes
Gliosis
Astrocyte functions
Metabolic buffers/detoxifiers
Control flow of substances between BBB and CSF
Recycle glutamate
Eosinophilic structures that occur within ASTROCYTIC processes that are found in regions of long-standing gliosis and pilocytic astrocytoma
Rosenthal fibers
Basophilic and lamellated structures found in advancing age, representing a degenerative change in astrocytes
Corpora amylacea
Sites where corpora amylacea are found
Brain
Lung
Prostate
Sum of the components of the intracranial cavity is constant
Brain, Blood, CSF
Monroe Kelly Doctrine
Sequence of compensation
CSF -> Venous blood -> Arterial blood (ischemia) -> Brain (herniation)
Due to BBB disruption and increased vascular permeability
Increased fluid leakage
Seen in inflammation or neoplasms
Vasogenic edema
Due to CNS injury that prevents maintenance of membrane ionic gradient
Increased CSF secretion
Seen in hypoxic/ischemic injury
Cytotoxic edema
Only type of cerebral edema responsive to steroids
Vasogenic edema
Increase in ventricular CSF volume due to loss of brain parenchyma
Hydrocephalus ex vacuo
Alzheimer’s
Dementia
Most common cause of congenital hydrocephalus
Congenital Aqueductal Stenosis
Cushing’s triad
Widened pulse pressure
Hypertension
Irregular breathing
Bradycardia
due to pressure on vagus nerve
Asymptomatic bony defect or a severe malformation with a flattened, disorganized segment of spinal cord
Spina bifida
Extension of CNS tissue through a defect in the vertebral column
Myelomeningocoele
Diverticulum and malformed brain tissue extending through a defect in cranium
Encephalocoele
Malformation of the anterior end of the neural tube
Anencephaly
Completely open brain and spinal cord
Craniorachischisis
Occipital skull and spine defect with extreme retroflexion of the head
Iniencephaly
Deficiency of at least two vertebral arches
Covered with lipoma
Closed spinal dysraphism
Prescribed period of intake of folic acid in women desirious of pregnancy
1 month before and first 3 months of pregnancy
400 mcg
0.4 mg
Reduced number of gyri
Lissencephaly
Small and irregular formed convolutions
Polymicrogyria
Incomplete separation of cerebral hemispheres across the midline
Holoprosencephaly
Associated with mental retardation
Agenesis of corpus callosum
Tonsillar extension into vertebral canal
Arnold Chiari Type I
Small posterior fossa
Vermis extension into foramen magnum
Hydrocephalus
Myelomeningocoele
Arnold Chiari Type II
Enlarged posterior fossa
+/- vermis
Large midline cyst
Dandy Walker
Fluid filled cavity in central canal from tumors or trauma
Pain centers of ventral white commisure damaged loss of pain and temp sensation in UE
Syringomyelia
Placque jaune are most commonly found at sites of
Can cause epileptic foci
contrecoup injury
Occurs in deep white matter region, cerebral peduncles, superior colliculi, deep reticular formation and brachium conjunctivum
Characterized by widespread and asymmetric axonal swellings
Coma shortly after trauma
Diffuse Axonal Injury
Pterion is the union of the
Frontal
Parietal
Sphenoid
Temporal
Chronic traumatic encephalopathy due to repeated head trauma causing accumulation of tangles in frontal and temporal lobes
Dementia pugilistica
Single most common cause of CVD
Cardioembolic stroke
Most sensitive neurons to hypoxia
Pyramidal cell layer of hippocampus (area CA1)
Cerebellar purkinje cells
Pyramidal neurons in cerebral cortex
Areas of the brain with little collateral flow
Thalamus
Basal ganglia
Deep white matter
Most common site of cardiam thromboemboli lodging
MCA
Most commonly associated with atherosclerosis and plaque rupture
Especially at Carotid bifurcation, MCA, Basilar artery
Thrombotic
Cytotoxic and vasogenic edema
Loss of gray and white matter differentiation
First 12 hours CVD infarct
Neutrophils (weeks)
Macrophages (months to years)
12-48 h CVD infarct
Reactive astrocytes
May be cause of seizure
48h-1 week CVD infarct
Angiogenesis and gliosis
1 month onwards CVD infarct
Golden hour for rTPA therapy in CVD
3-4.5 hours
Infarcts <15 mm Most common in lenticular nucleus Putamen Thalamus Internal capsule Deep white matter Caudate Pons
Lacunar infarct
Slit-like cavities secondary to resporption of hemorrhage
Slit hemorrhage
Cortical > subcortical
Dementia
Gait
Pseudobulbar signs +/- focal neurologic deficits
Vascular dementia