A non-progressive neurologic motor deficit characterized by combinations of spasticity, dystonia, ataxia/atheosis, and paresis.
No, mature neurons are incapable of cell division.
The formation of an arteriovenous fistula.
Folate deficiency during the first several weeks of gestation.
Binswanger disease.
60 years old.
An infarct occurring in the supratentorial periventricular white matter, especially in premature infants, characterized by chalky, yellow plaques with regions of white matter necrosis and calcifications.
Reactive glial changes.
Lymphocytic pleocytosis, moderate protein elevation, and nearly always normal glucose content.
Inflammation of the ventricles in fulminant meningitis.
A diverticulum of malformed brain tissue.
Hypertensive Encephalopathy.
Because they share one or more properties.
Shrinkage of cell body, pyknosis of nucleus, disappearance of nucleolus, loss of Nissl substance with intense eosinophilia.
Intracytoplasmic inclusions seen in myoclonic epilepsy (Lafora body myoclonus with epilepsy).
A reduction in the number of gyri, with extreme cases showing no gyral patterns (agyria).
Radial migration (becomes excitatory neurons) and tangential migration (becomes inhibitory neurons).
Microencephaly is an abnormally small brain volume, associated with fetal alcohol syndrome, HIV infection in utero, and chromosomal abnormalities.
Trauma.
Hypertension.
Extravasation of blood with compression of adjacent parenchyma.
The ability to receive and transmit information.
A coup injury occurs at the point of impact, while a contrecoup injury occurs on the surface diametrically opposite to the point of impact.
A condition in pneumococcal meningitis where the capsular polysaccharide of the organism produces a gelatinous exudate that promotes arachnoid fibrosis.
In the posterior fossa.
A manifestation of the tertiary stage of syphilis, occurring in 10% of cases, with major patterns including meningovascular neurosyphilis, paretic neurosyphilis, and tabes dorsalis.
Transient neurologic dysfunction, loss of consciousness, temporary respiratory arrest, and loss of reflexes.
Klebsiella and anaerobes.
Hypertrophy and hyperplasia of astrocytes, with nuclei becoming enlarged and vesicular, and cytoplasm becoming bright pink.
Underlying cerebrovascular disease.
Developmental disorders.
Mendelian disorders, Fibromuscular Dysplasia, Coarctation of the Aorta, smoking, and hypertension.
An inflammatory disorder involving multiple small- to medium-sized parenchymal and subarachnoid vessels, characterized by chronic inflammation, multinucleated giant cells, and destruction of the vessel wall.
The level of cord injury.
Within the germinal matrix, often near the junction between the caudate nucleus and thalamus.
In perinatal ischemia, the depths of sulci bear the brunt of injury, resulting in thinned-out, gliotic gyri.
Thick, elongated, brightly eosinophilic structures found in regions with long-standing gliosis and characteristic of pilocytic astrocytoma.
Aggregates of microglia in foci of necrosis.
Motor and sensory deficits of lower extremities, disturbances in bowel and bladder control, and infection of the overlying skin.
Small, numerous, irregularly formed cerebral convolutions with gray matter composed of four layers or fewer.
Minute aneurysms associated with chronic hypertension, most common in the basal ganglia.
Tangled network of worm-like vascular channels with prominent, pulsatile, AV shunting and high blood flow, greatly enlarged vessels separated by gliotic tissue.
Small hemorrhages caused by the rupture of small-caliber penetrating vessels due to hypertension, which resorb over time leaving a slitlike cavity.
Perinatal brain injury.
Meningitis-associated septicemia with hemorrhagic infarction of adrenal glands and cutaneous petechiae, mostly in pneumococcal and meningococcal infections.
Streptococcus and Staphylococcus.
Headache, malaise, confusion, vomiting, with CSF showing mononuclear pleocytosis, elevated proteins, and moderately reduced or normal glucose.
Cerebral atherosclerosis, thrombosis or embolization from carotid vessels or heart, and cerebral arteriolar sclerosis from chronic hypertension.
An enlarged posterior fossa with an absent or rudimentary cerebellar vermis and a large midline cyst.
The brain becomes edematous and swollen, producing widening of the gyri and narrowing of the sulci.
Increased risk of additional ischemic injury, meningeal fibrosis, and scarring which may lead to obstruction of CSF flow.
Non-hemorrhagic infarcts begin with loss of blood supply, while hemorrhagic infarcts can occur from ischemia-reperfusion injury.
Bleeding between the two layers of the dura.
Astrocytes and oligodendrocytes, which make up the glia.
A condition where both gray and white matter are involved, leading to large destructive cystic lesions throughout the hemispheres.
Dispersion of Nissl substance from the center to the periphery of the cell during axonal reaction.
The absence of an organism by bacterial culture in a patient with manifestations of meningitis, generally of viral etiology.
An aseptic meningitis-like picture due to the rupture of an epidermoid cyst introducing chemical irritants, with sterile CSF, pleocytosis with neutrophils, increased proteins, and normal glucose content.
In the lumbosacral region.
A bacterial or fungal infection of skull bones or air sinuses that can spread to the subdural space, producing mass effect or thrombophlebitis.
By day 28.
A small posterior fossa with a misshapen midline cerebellum extending downward through the foramen magnum, often associated with hydrocephalus and lumbar myelomeningocele.
Blood extravasates into the arachnoid space, the parenchyma of the brain, or both.
Cloudy, purulent CSF, approximately 90,000 neutrophils per mm³, increased protein concentration, and reduced glucose content.
Generalized brain edema, increased CSF volume, and focally expanding mass lesions.
The neuron.
A condition characterized by widespread, asymmetric axonal swelling due to mechanical forces, best demonstrated with silver impregnation techniques or immunoperoxidase stains for axonally transported proteins.
Invasion of the brain by T. pallidum, leading to cognitive impairment and mood alterations that may terminate in severe dementia.
An edematous brain with or without transtentorial or tonsillar herniation, petechiae, and fibrinoid necrosis of arterioles.
Incomplete separation of the cerebral hemispheres, often associated with midline facial anomalies and Trisomy 13.
Formation of a fluid-filled cleft-like cavity in the inner portion of the spinal cord, which may extend to the brainstem.
Microvacuolization, eosinophilia of neuronal cytoplasm, and later nuclear pyknosis and karyorrhexis.
Tissue necrosis, macrophage influx, vascular proliferation, and gliosis.
Removal of necrotic tissue, loss of normal CNS architecture, and gliosis.
A pattern of injury in the cerebral neocortex characterized by uneven neuronal loss and gliosis, with preservation of some layers and destruction of others.
Reduction or cessation of blood flow to a localized area of the brain due to arterial occlusion or hypoperfusion.
Most common subtype, affects males twice as often as females, presents between ages 10-30 as a seizure disorder, intracerebral hemorrhage, and subarachnoid hemorrhage.
Acute Pyogenic (usually bacterial), Aseptic (acute or subacute viral), and Chronic (tuberculous, spirochetal, cryptococcal).
Smooth inner contour that compresses the brain surface.
Acute processes (e.g., depletion of oxygen or glucose, trauma) and slow processes (e.g., accumulation of abnormal protein aggregates).
Neurologic diseases resulting from the injurious effects of accumulated misfolded proteins.
A marble-like appearance of deep nuclei due to aberrant and irregular myelinization following perinatal ischemia.
Proliferating, developing elongated nuclei (Rod cells), forming microglial nodules, and congregating around dying neurons (neuronophagia).
High white count, increased protein, and normal glucose.
A malformation of the anterior end of the neural tube, with absence of most of the brain and calvarium.
Vascular (multi-infarct) dementia.
Saccular (berry) aneurysm.
Recurrent strokes and dementia.
The circle of Willis, supplemented by the external carotid-ophthalmic pathway.
Arteriovenous Malformations, Cavernous Malformations, Capillary Telangiectasias, and Venous Angiomas.
In neonates: E. coli, group B S. pneumoniae; in children and older: S. pneumoniae, L. monocytogenes; in adolescents and young adults: N. meningitidis.
Thoracic level below – paraplegia; cervical lesions – quadriplegia; above C4 – respiratory compromise.
Neurons in the pyramidal cell layer of the hippocampus (CA1, 'Sommer sector'), cerebellar Purkinje cells, and pyramidal neurons in the cerebral cortex.
Embolization from a distant source, in situ thrombosis, or various forms of vasculitides.
Mutations in the NOTCH3 gene.
A thin-walled outpouching usually at an arterial branch point along the circle of Willis, ranging from a few mm to 2-3 cm with a bright red, shiny, thin, translucent wall.
Presence of ε2 or ε4 allele increases the risk of repeat bleeding.
Cardiac mural thrombi are blood clots that form on the walls of the heart and are common culprits of embolism to the brain.
External collagenous layer and inner layer with scant fibroblasts.
Lysis of the clot (about 1 week), growth of fibroblasts from dural space to hematoma (2 weeks), development of hyalinized connective tissue (1-3 months).
Posttraumatic hydrocephalus, chronic traumatic encephalopathy (CTE), epilepsy, infection, psychiatric disorders.
Neural tube defects are caused by the failure of a portion of the neural tube to close or the reopening of a region of the tube after successful closure.
Most frequent in the 5th decade of life, more common in women, aneurysms greater than 10mm have a 50% risk of bleeding per year, rupture may occur anytime but often with acute increases in ICP, sudden excruciating headache, and rapid loss of consciousness.
An inflammatory process of the leptomeninges and CSF within the subarachnoid space, usually caused by infection.
Systemic signs of infection superimposed on clinical evidence of meningeal irritation and neurologic impairments such as headache, photophobia, irritability, clouding, and stiff neck.
A collection of freshly clotted blood along the brain surface without extension into the depths of sulci.
Interstitial edema occurs around the lateral ventricles when increased intravascular pressure causes abnormal flow of fluid from CSF to the white matter.
Ischemic and hemorrhagic.
Hydrocephalus ex vacuo is a compensatory increase in ventricular volume secondary to the loss of brain parenchyma.
Spinal dysraphism, or spina bifida, can be an asymptomatic bony defect (spina bifida occulta) or a severe malformation with a flattened, disorganized segment of the spinal cord with meningeal outpouching.
Middle meningeal artery.
Localized gray matter damage at the level of impact.
Hematogenous, direct implantation, local extension, and peripheral nervous system.
They can tear at the point where they penetrate the dura due to brain displacement.
Cerebral edema, more precisely brain parenchymal edema, is the result of increased fluid leakage from blood vessels to various cells of the CNS.
Hypertension and vascular anomalies (aneurysm and malformations).
Subfalcine herniation occurs when unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the falx, compressing the anterior cerebral artery and its branches.
A condition where the brain gradually undergoes autolytic process with gradual liquefaction due to severe global cerebral ischemia maintained on mechanical ventilation.
Small, cavitary infarcts less than 15 mm wide, occurring in the lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, and pons.
Extravasation of blood.
Multiple recurrent episodes of bleeding from thin-walled vessels of granulation tissues.
Transtentorial herniation involves the medial aspect of the temporal lobe being compressed against the free margin of the tentorium, potentially compressing the 3rd cranial nerve, posterior cerebral artery, and causing Kernohan Notch and Duret Hemorrhage.
Vasogenic edema is an increase in extracellular fluid caused by BBB disruption and increased vascular permeability, allowing fluid to shift from the intravascular compartment to the intercellular spaces of the brain.
Gyri are flattened, sulci are narrowed, and ventricular cavities are compressed.
Hydrocephalus is the accumulation of excessive CSF within the ventricular system, most commonly due to impaired flow and resorption, with overproduction being a rare cause.
Non-communicating hydrocephalus occurs when the ventricular system is obstructed and does not communicate with the subarachnoid space, possibly due to a mass in the third ventricle.
Myelomeningocele is the extension of CNS tissue through a defect in the vertebra, while meningocele involves only meningeal extrusion.
Cytotoxic edema is an increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury, often encountered in generalized ischemia or metabolic derangements.
Embolism.
An area of 'at risk' tissue between necrotic and normal brain tissue.
Tonsillar herniation is the displacement of cerebellar tonsils through the foramen magnum, leading to brainstem compression that compromises vital respiratory and cardiac centers in the medulla.
There is an enlargement of the head, resulting in increased head circumference.
Communicating hydrocephalus occurs when there is communication within the ventricular system but with enlargement of the whole ventricular system.
Herniation is the displacement of brain tissue past rigid dural folds (falx and tentorium) or through openings of the skull due to increased intracranial pressure.
Infarcts that occur in regions of the brain or spinal cord that lay at the most distal reach of the arterial blood, often seen after hypotensive episodes.
