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Neuroanatomie (Subject) / Alles (Lesson)

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• Most common CNS AIDS tumor Primary CNS lymphoma.
• HIV Encephalopathy Diffuse atrophy is most common manifestation. White matter lesions are seen with AIDS dementia complex. Diffuse pattern of increased T2 signal in deep white matter or multiple small punctate white matter lesions.
• Most common opportunistic CNS infection in AIDS Toxoplasmosis.
• Toxoplasmosis Multiple high T2 signal and enhancing mass lesions (1-4 cm) with surrounding vasogenic edema. Larger lesions usually exhibit ring enhancement. Unlike bacterial abscesses, toxoplasmosis lesions are not high in signal on DWI. Preferred sites: Basal ganglia. White matter. Cortex. Main differential consideration is primary CNS lymphoma.
• Most common AIDS CNS fungal infection Cryptococcosis.
• Progressive multifocal leukoencephalopathy Infection of immunosuppressed patients (AIDS, transplants, leukemics) caused by reactivation of JC virus. Progressive course to death within months. In non-AIDS patients, has a predilection for occipital lobes. In AIDS patients, any part of brain may be involved. High T2 and low T1 lesions within subcortical and deep white matter. Mass effect and contrast enhancement are almost always absent.
• Primary CNS lymphoma Most common intracranial tumor in AIDS. Solitary or multiple enhancing mass lesions, centrally located within deep white matter or basal ganglia. Lesions usually are T2 isointense to white matter with homogeneous enhancement. Toxoplasmosis lesions usually are T2 hypointense.
• Dysmyelination Inherited disorder (leukodystrophy), affecting formation or maintenance of myelin. Generally encountered within pediatric population.
• Demyelination Acquired disorder that affects normal myelin. Generally encountered within adult population.
• Multiple sclerosis (MS, Primary Demyelination) Multiple CNS lesions separated in time and space. Typical lesions are high T2 signal and round or ovoid in a periventricular (perpendicular to ventricle) or subcortical location. Enhancement reflects new lesions. Dark T1 lesions are due to acutal neuronal tissue loss. Other sites affected: Cerebellar and cerebral peduncles. Corpus callosum. Medulla. Spinal cord. Conglomerate large lesions may be mistake for a neoplasm (tumefactive).
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• Involvement of callosal-septal interface is quite specific for MS.
• Nonspecific punctuate white matter lesions (small bright lesions on T2WIs) are more prominent in any patient with Vasculopathy or hypercoagulable state.
• A classic case presentation is that of a young adult female with prior miscarriages presenting with headaches/migraines and ischemic white matter changes. Antiphospholipid syndrome (phospholipid antibody syndrome). Hypercoagulable state with white matter and ischemic changes.
• Ependymitis granularis Normal anatomic finding. May mimic pathology. High T2 signal at tips of frontal horns. Due to porous ependyma allowing transependymal flow of CSF.
• Senescent periventricular hyperintensity Age-related high T2 signal along entire length of lateral ventricles.
• Prominent perivascular spaces CSF-filled perivascular clefts. Also called Virchow-Robin spaces. Punctate foci of high T2 signal. Typically within centrum semiovale and lower basal ganglia at the level of the anterior commissure, where lenticulostriate arteries enter the brain.
• MR sequences that help distinguish perivascular spaces from parenchymal lesions Proton-density and FLAIR sequences. PD: CSF has similar signal intensity as white matter. Perivascular space is isointense to brain. Ischemic lesions are bright due to gliosis. FLAIR: Parenchymal lesions with gliosis have abnormal signal.
• Central pontine myelinolysis (CPM) Demyelination of central pons. Due to electrolyte abnormalities, particularly hyponatremia, that are rapidly corrected. Oligodendroglial cells are most susceptible: Central pons. Thalamus. Globus pallidus. Putamen. Lateral geniculate body.
• Posterior reversible encephalopathy syndrome (PRE) Symmetric subcortical and cortical vasogenic edema within parietooccipital lobes. Temporary failure of autoregulation of cerebral arteries. Associations: Cyclosporin A or tacrolimus (FK506). Acute renal failure/uremia. Hemolytic uremic syndrome. Eclampsia. Thrombotic thrombocytopenia purpura. Chemotherapy (interferon).
• Marchiafava-Bignami disease Rare demyelination seen frequently in alcoholics. Involves central fibers (medial zone) of corpus callosum. Anterior and posterior commissures. Centrum semiovale. Mddle cerebral peduncles. Felt to reflect a form of osmotic demyelination
• Wernicke encephalopathy and Korsakoff syndrome Metabolic disorders caused by thiamine (B1 vitamin) deficiency: alcoholics, hematologic malignancies, hyperemesis gravidarum. Wernicke encephalopathy clinical triad of acute ocular movement abnormalities, ataxia, and confusion. If longterm memory and learning problems result then Korsakoff syndrome. Early stage may reveal T2 hyperintensity or contrast enhancement of mamillary bodies, basal ganglia, thalamus, brainstem, and periaqueductal involvement. Chronic stage may show mamillary body and tegmentum atrophy and dilation of third ventricle.
• Radiation Leukoencephalitis Occurs 6 to 9 months after treatment in excess of 40 Gy. Confluent high T2 signal within white matter extending to subcortical U fibers.
• Radiation Necrosis Commonly occurs 6 to 24 months postradiation. Enhancing lesion with mass effect and ring enhancement. Or multiple foci of enhancement, Mimicks recurrent neoplasm. MR spectroscopy (MRS): Elevated lactate and lipids (0.9 to 1.3 ppm). Reduced other major metabolites (choline, creatine, and N-acetylaspartate).
• Metachromatic leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement Normal head size. Infantile form 1-2 yo. Juvenile form 5-7 yo. Diffuse white matter involvement. No gray matter invovlement. Most common Leukodystrophy. Deficiency of the enzyme arylsulfatase A.
• Adrenoleukodystrophy leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement Normal head size. 5-10 yo. Symmetric occiptal and splenium of corpus callossom white matter invovlement. No gray matter involvement. Sex-linked recessive condition (peroxisomal enzyme deficiency) occurring only in boys.
• Leigh disease: head size, age of onset, white matter involvement, gray matter involvement Normal head size. Less than 5 yo. Focal areas of subcortical white matter. Basal ganglia and periaquaductal gray matter involvement. Also called subacute necrotizing encephalomyelopathy. Mitochondrial enzyme defect.
• Alexander disease: head size, age of onset, white matter involvement, gray matter involvement Normal to large head size. Less than 1 yo. Frontal white matter involvement. No gray matter involvement.
• Canavan disease: head size, age of onset, white matter involvement, gray matter involvement Normal to large head size. less than 1 yo. Diffuse white matter involvement. Vacuolization of cortical gray matter. deficiency of aspartoacylase, leads to the buildup of NAA (MRS).
• Transependymal flow of CSF Occurs in acute hydrocephalus. May mimic periventricular white matter disease. Important means of CSF reabsorption during ventricular obstruction.
• CSF circulation route Produced mainly by choroid plexus of lateral, third, and fourth ventricles. Flows from lateral ventricles through foramina of Monro to third ventricle through cerebral aqueduct to fourth ventricle through lateral and medial fourth foramina (Luschka and Magendie) to basilar cisterns and over hemisphere surfaces. Principal site of absorption is into venous circulation through arachnoid villi.
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• Will commonly demonstrate supratentorial ventriculomegaly, with a fourth ventricle that appears normal. Communicating hydrocephalus. Dilated 4th ventricle can be seen in communicating and non-communicating hydrocephalus.
• Ex Vacuo Ventriculomegaly Enlarged ventricles due to cerebral atrophy. Prominence of both sulci and ventricles.
• Normal pressure hydrocephalus Chronic, low-level form of hydrocephalus. Clinical triad: Dementia, gait disturbance, and urinary incontinence. CSF pressure is within normal limits. Slight gradient exists between ventricular system and subarachnoid space due to incomplete subarachnoid CSF block. Commonly results from prior subarachnoid hemorrhage or meningitis. Diffuse ventriculomegaly out of proportion to sulcal prominence. Early entry of radiotracer into lateral ventricles, with persistence at 24 and 48 hours. Delay ascent to parasagittal region.
• Alzheimer disease (AD) Most common cause of dementia. Prefential atrophy of: Hippocampal formation. Temporal lobes. Parietotemporal cortices. Enlargement of temporal horns, suprasellar cisterns, and sylvian fissures may distinguish from age-related atrophy.
• Parkinson disease Most common basal ganglia disorder. Deficiency of dopamine specifically within pars compacta of the substantia nigra. MR imaging is relatively insensitive but is useful in excluded other causes of movement disorders (stroke).
• Huntington disease Progressive hereditary disorder occuring in fourth and fifth decades. Findings: Diffuse cortical atrophy. Caudate nucleus atrophy. Putamen atrophy. Enlargement of frontal horns (heart-shaped).
• Wilson disease Hepatolenticular degeneration. Inborn error of copper metabolism. Hepatic cirrhosis and degenerative changes of basal ganglia. Diffuse atrophy with signal abnormalities involving deep gray matter nuclei and deep white matter.
• Bilateral lesions of basal ganglia can be seen in a variety of insults Carbon monoxide exposure (globus pallidus). Methanol toxicity (putaminal). Metabolic conditions (Wilson disease). Hallervorden-Spatz disease (iron deposition within globus pallidus). Mitochondrial disorders (Leigh disease and Kearns-Sayre syndrome).
• Myelination Landmarks by Age 0 days High T1 signal: Dorsal brainstem. Ventrolateral thalamus. Lentiform nucleus. Central corticospinal tracts. Low T2 signal: Posterior limb internal capsule posterior portion.
• Myelination Landmarks by Age 3 months High T1 signal: Anterior limb internal capsule. Cerebellar white matter.
• Myelination Landmarks by Age 6 months High T1 signal: Genu of corpus callosum. Low T2 signal: Splenium of corpus callosum.
• Myelination Landmarks by Age 11 months Low T2 signal: Anterior limb internal capsule.
• Myelination Landmarks by Age 18 months Adult appearance except for terminal myelination zones (periatrial and adjacent to frontal horns)
• Myelination Landmarks by Age 24 months Dark white matter on T2 (some minimal high-signal areas may persist peripherally)
• Pelizaeus-Merzbacher Disease Rare X-linked leukodystrophy. Arrest of myelin development, usually in neonatal period. Shows lack only of myelin formation, rather than myelin formation followed by destruction.
• HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE) Damage to brain from hypoxia/ischemia occurring in utero or around time of delivery.
• Hydranencephaly Ischemic infarction of both cerebral hemispheres. Early compromise of both carotid arteries with preservation of posterior circulation. Mimics severe hydrocephalus (thin rind of cortical gray matter). Complete infarction of supratentorial cerebral tissues with preservation of thalami and cerebellum.
• Hypoxic ischemic encephalopathy occuring within 1st trimester Cortical irregularity and/or hydranencephaly.
• Hypoxic ischemic encephalopathy occuring at less than 26 weeks of gestation Periatrial injury. No gliosis. Ex vacuo enlargement.
• Hypoxic ischemic encephalopathy occuring at greather than 28 weeks Periatrial gliosis: high T2 signal.

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