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Neuroanatomie (Subject) / Alles (Lesson)

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• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Global aphasia _ MCA/Hemispheric branch (total)/Left
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Neglect syndromes _ MCA/Hemispheric branch/Left
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Visulospatial dysfunction _ MCA/Hemispheric branch/Right
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Variable lacunar syndromes _ MCA/Lateral lenticulostriate branches/Either
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Hemianopsia _ PCA/Hemispheric branch/Either
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Cortical blindness _ PCA/Hemispheric branch/Both
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Memory deficits _ PCA/Hemispheric branch/Both
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Somnolence _ PCA/Thalamoperforators/Either
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Sensory disturbances _ PCA/Thalamoperforators/Either
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Ataxia, vertigo, vomiting _ Cerebellar/PICA, AICA, or SCA/ Either
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• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Coma if mass effect _ Cerebellar/PICA, AICA, or SCA/ Either
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), ± brainstem deficits _ Cerebellar/PICA, AICA, or SCA/ Either
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Man-in-a-barrel syndrome _ Watershed/ACA,MCA,PCA/Either
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Severe memory problems _ Watershed/ACA,MCA,PCA/Bilateral
• Order of cerebellar branches going from top to bottom can be remembered using the acronym SAP_ Superior cerebellar artery. Anterior inferior cerebellar artery. Posterior inferior cerebellar artery.
• SCA territory Superior vermis. Middle and superior cerebellar peduncles. Superolateral aspects of cerebellar hemispheres.
• Anterior Inferior Cerebellar Arteries (AICA) arise from Proximal basilar artery.
• Posterior Inferior Cerebellar Arteries (PICA) arise from Distal vertebral artery, 1 to 2 cm below basilar origin.
• Involvement of the medulla in PICA infarction adds elements of Wallenberg syndrome, which include Ataxia. Facial numbness. Horner syndrome. Dysphagia. Dysarthria.
• Lacunes Small subcortical infarcts. May occur in any territory. Characteristic locations_ Lenticular nucleus (37%). Pons (16%). Thalamus (14%). Caudate (10%). Internal capsule/corona radiata (10%).
• Beginning at the genu and working back, the internal capsule carries somatotopically organized fibers Corticobulbar fibers. HAL_ Head fibers. Arm fibers. Leg fibers.
• Perivascular spaces Virchow-Robin spaces. May simulate lacunes. Follow CSF signal. No mass effect. Occur along path of a penetrating vessel.
• Small-Vessel Ischemic Changes Small foci of T2 hyperintensity scattered throughout brains of older patients. May or may not have clinical symptoms. Commonly associated with patchy or diffuse T2 hyperintensity in the centrum semiovale.
• Some cerebral vasculitides Autoimmune disorders. Drug exposure (heroin, amphetamines). Polyarteritis nodosa. Idiopathic processes (giant cell arteritis).
• Venous sinus thrombosis predisposing factors include Hypercoagulable states. Pregnancy. Infection (spread from contiguous scalp, face, middle ear, or sinus). Dehydration. Meningitis. Direct invasion by tumor.
• Empty delta sign Filling defect within sagittal sinus on postcontrast CT. Indicates venous sinus thrombosis.
• Superficial hemosiderosis (or superficial siderosis) Diffuse hemosiderin deposition on brain surface. Due to large or recurrent subarachnoid hemorrhages.
• MR oxyhemoglobin per time, RBC, and T1 and T2 signal Less than 1 day. RBC intact. T1 iso/dark. T2 bright.
• MR deoxyhemoglobin per time, RBC, and T1 and T2 signal 0-2 days. RBC intact. T1 iso/dark. T2 dark.
• MR methemoglobin (intracellular) per time, RBC, and T1 and T2 signal 2-14 days. RBC intact. T1 bright. T2 dark.
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• MR methemoglobin (extracellular) per time, RBC, and T1 and T2 signal 10-21 days. RBC lysed. T1 bright. T2 bright.
• MR hemosiderin/ferritin per time, RBC, and T1 and T2 signal > 21 days. RBC lysed. T1 dark. T2 dark.
• Most sensitive areas for detecting SAH Dependent parts of occipital horns. Interpeduncular fossa.
• Main finding in patients whose condition continues to deteriorate after the initial SAH Infarcts from post SAH increased intracranial pressure or arterial vasospasm.
• Congenital berry aneursym May be due to congenital absence of arterial media. Those larger than 3 to 5 mm are at increased risk for rupture. Often occur near branch points of circle of Willis.
• Distal branch cerebral aneurysms are seen in what conditions Prior trauma. Systemic infection (bacterial endocarditis with mycotic aneurysm).
• Besides berry aneursyms, list other causes of cerebral aneurysms Atherosclerosis. Fibromuscular disease. Polycystic kidney disease. Mycotic. Post-traumatic.
• Main differential considerations for cerebral parenchymal hemorrhage Hypertensive hemorrhage. Vascular malformations. Drug effects. Amyloid angiopathy. Bloody tumors.
• Common locations for intracranial hypertensive hemorrhages Putamen (35% to 50%). Subcortical white matter (30%). Cerebellum (15%). Thalamus (10% to 15%). Pons (5% to 10%).
• Intracranial hemorrhage cause in young patients, less common than hypertension Vascular malformations_ AVMs. Cavernous malformations. Telangiectasias. Venous malformations.
• Arteriovenous malformations Most common type of brain vascular malformation. Abnormal tangle of arteries directly connected to veins without intervening capillaries. Most present with hemorrhage or seizures. 2% to 3% annual risk of bleeding,
• Cavernous malformations Thin-walled sinusoidal vessels (neither arteries nor veins). May present with seizures or small parenchymal hemorrhages.
• Venous malformations Anomalous veins that drain normal brain. Occur in 1% to 2% of patients. Enlarged enhancing stellate venous complex that extends to ventricular or cortical surface.
• Amyloid angiopathy cerebral hemorrhage Can cause intracranial, frequently lobar, hemorrhage. Amyloid deposits within media and adventitia of medium size and small cortical arteries. Not associated with systemic vascular amyloidosis. Affects elderly.
• Hemorrhagic cerebral neoplasm Primary_ Glioblastomas. Metastatses_ Bronchogenic carcinoma. Thyroid. Melanoma. Choriocarcinoma. Renal cell carcinoma.
• Features of Benign Versus Malignant Intracranial Hemorrhage Benign_ Complete hemosiderin rim. Mild edema. Minimal acute enhancement (unless AVM). Blood products evolve from periphery to center. Malignant_ Delayed or incomplete hemosiderin ring. Moderate surrounding edema. Moderate to severe acute enhancement. Irregular or complex blood product evolution.
• Glial cell intracranial neoplasms (gliomas) Astrocytoma. Oligodendroglioma. Ependymoma. Choroid plexus tumor.
• Nerve sheath intracranial neoplasms Schwannoma, Neurofibroma.
• Extra-axial tumors Tumors occuring along brain meninges or within the ventricles. Most nonglial tumors.
• Hallmarks of uncal herniation? Effacement of ambient cistern. Contralateral hydrocephalus. May compromise ipsilateral oculomotor (III) nerve (pupillary dilation).

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