Anatomy of the Brain

The image on the left is a side view of the outside of the brain, showing the major lobes (frontal, parietal, temporal and occipital) and the brain stem structures (pons, medulla oblongata and cerebellum). The image on the right is a side view showing the location of the limbic system inside the brain. The limbic system consists of a number of structures, including the fornix, hippocampus, cingulate gyrus, amygdala, the parahippocampal gyrus and parts of the thalamus. The hippocampus is one of the first areas affected by Alzheimer's disease. As the disease progresses, damage extends throughout the lobes.

Glossary of Terms for an Anatomy of the Brain Amygdala limbic structure involved in many brain functions, including emotion, learning and memory. It is part of a system that processes "reflexive" emotions like fear and anxiety. Cerebellum governs movement. Cingulate gyrus plays a role in processing conscious emotional experience. Fornix an arch-like structure that connects the hippocampus to other parts of the limbic system. Frontal lobe helps control skilled muscle movements, mood, planning for the future, setting goals and judging priorities. Hippocampus plays a significant role in the formation of long-term memories. Medulla oblongata contains centers for the control of vital processes such as heart rate, respiration, blood pressure, and swallowing. Limbic system a group of interconnected structures that mediate emotions, learning and memory. Occipital lobe helps process visual information. Parahippocampal gyrus an important connecting pathway of the limbic system. Parietal lobe receives and processes information about temperature, taste, touch, and movement coming from the rest of the body. Reading and arithmetic are also processed in this region. Pons contains centers for the control of vital processes, including respiration and cardiovascular functions. It also is involved in the coordination of eye movements and balance. Temporal lobe processes hearing, memory and language functions. Thalamus a major relay station between the senses and the cortex (the outer layer of the brain consisting of the parietal, occipital, frontal and temporal lobes).

The parietal lobes can be divided into two functional regions. One involves sensation and perception and the other is concerned with integrating sensory input, primarily with the visual system. The first function integrates sensory information to form a single perception (cognition). The second function constructs a spatial coordinate system to represent the world around us. Individuals with damage to the parietal lobes often show striking deficits, such as abnormalities in body image and spatial relations (Kandel, Schwartz & Jessel, 1991). Damage to the left parietal lobe can result in what is called "Gerstmann's Syndrome." It includes right-left confusion, difficulty with writing (agraphia) and difficulty with mathematics (acalculia). It can also produce disorders of language (aphasia) and the inability to perceive objects normally (agnosia).

PERIVENTRICULAR LEUKOMALACIA Periventricular leukomalacia (PVL) is a form of ischemic white matter damage, which affects premature infants especially ones with cardiorespiratory abnormalities and sepsis. It develops usually in the neonatal period but may also occur in utero and is frequent in mature infants with congenital heart disease. Bilateral, roughly symmetric foci of white matter necrosis develop around the lateral ventricles, especially in the frontal and occipital lobes. The evolution of these lesions is similar to infarcts, i.e. liquefaction, phagocytosis, cavitation, and gliosis. Axonal damage is evident by the presence of axonal swellings, which may be obvious on H&E stains or detected with immunostains to Beta Amyloid Precursor Protein. An added feature of PVL and other necrotic brain lesions in fetuses and neonates is calcification, which makes lesions appear as whitish spots in the periventricular white matter. Large necrotic lesions cavitate in 2-4 weeks and remain cystic (cystic PVL). Small necrotic lesions do not cavitate at all or form small cysts that collapse into glial scars (non-cystic PVL). The cysts and scars are they epicenter of the pathology. They are surrounded by wide zone of gliosis. Cystic PVL is now infrequent, thanks to improved neonatal intensive care. A more common pattern is focal noncystic white matter injury (WMI) or diffuse white matter gliosis. At the end stage, myelin is diminished, white matter mass is decreased, the lateral ventricles enlarge, and the corpus callosum becomes atrophic. Cortical ischemic lesions and diffuse loss of cortical and thalamic neurons are present in some cases. The method of choice for the diagnosis of PVL is cranial ultrasound (US) but it is not suitable for imaging of WMI. The recommendation for infants less than 30 weeks gestation is a screening ultrasound at 7-14 days and a repeat ultrasound at 30-40 weeks. Echodensities correlate with the acute phase of necrosis. They transition into coalescent echolucencies (cavities) that give the affected white matter a Swiss cheese appearance. Ultrasound is best for the detection of cystic PVL. The MRI is more accurate than US for the detection of cystic and non-cystic PVL but is not practical for the diagnosis of acute PVL. More often, it is used for follow-up of acute lesions detected earlier by US. The burned out stage of PVL as detected by the MRI consists of: 1) loss of white matter with atrophy of the corpus callosum; 2) enlargement of the ventricles with an irregular angular (scalloped) appearance of their contours; and 3) abnormal or delayed myelination. Today, based on US and MRI, approximately 3% of neonates weighing less than 1,500 gm have cystic PVL and 20-50% have non-cystic PVL. WMI is also very common in mature infants with congenital heart disease, especially transposition of great vessels and hypoplastic left heart syndrome. In the setting of congenital heart disease, WMI occurs prenatally, presumably due to chronic hypoxia, or post-operatively, especially following cardiopulmonary bypass. The most important cause of of PVL is ischemia. The lesions are located at the termination of major cerebral vessels in the border zones between the ACA, MCA, and PCA and involve the deeper parts of the white matter, where the developing vascular tree has not yet advanced. Hypoxia causes activation of microglia, the tissue histiocyte in the CNS, leading to secretion of toxic oxygen and nitrogen radicals and the release of glutamate. Free radicals and glutamate are the key agents of cellular injury in PVL and other forms of HIE (see also Asphyxia and HIE in Mature Infants). Inflammatory cytokines and activated monocytes that are generated during maternal, placental, and fetal infection enter the brain by crossing the immature blood-brain barrier and activate microglial cells setting in motion the same toxic cascade that damages the white matter in ischemia. Clinical studies show a high association of PVL and CP with chorioamnionitis, funisitis and premature rupture of membranes. The principal target of oxygen and nitrogen radicals and of glutamate is the immature premyelinating oligodendrocyte (pre-OL). In the premature brain, there is no myelin. The white matter is populated by pre-OLs which are vulnerable to hypoxia because they are deficient in Superoxide Dismutase, the key antioxidant enzyme. Additionally, the premature white matter is rich in iron, the most important source of free radicals. So, the key event in PVL is loss of pre-OLs and the main outcome is deficient myelination. Advanced imaging methods and pathology show also loss and disarray of axons, which is especially obvious in cystic PVL.

White matter damage, especially during the second trimester, may also affect the subplate (an ephemeral neuronal layer under the permanent cortex) and late migrating neurons that traverse the white matter on their way to the deep cortical layers. The subplate is important for the development of connections between the thalamus and cortex. Its premature loss disconnects the cortex from the thalamus. Damage of migrating neurons results in decreased cortical volume. Neuronal loss in PVL adds to the devastating effects of myelin and axonal damage. The clinical manifestations of PVL are spastic diplegia or tetraplegia due to damage of corticospinal tract axons, visual impairment due to damage of the optic radiations, cognitive deficits, and seizures. The clinical deficits of PVL are not apparent initially. They are only fully appreciated months or years after the injury occurs. PVL is the substrate of cerebral palsy (CP). The leading risk factor in 75% of CP is prematurity and the underlying pathology in most of CP is PVL. Our concept of PVL has evolved over the past 50 years. Initially, it was conceived of as an acute ischemic lesion with cavitated white matter infarcts. Now, it is a spectrum of pathology some of which is caused by chronic hypoxia-ischemia or infection and results in diffuse white matter injury and neuronal loss. A distinction is often made between HIE in premature infants, which is PVL, and HIE in mature infants, which affects predominantly the cortex and deep nuclei. This is an oversimplification. Pathological and volumetric MRI studies show that, in PVL, there is loss of neurons (and reduction in mass) in the cortex and deep nuclei, especially the thalamus. Moreover, as the picture on the left illustrates, the full range of gray matter HIE pathology that occurs at term may also develop in premature infants, usually along with white matter damage.

Subarachnoid hemorrhage A subarachnoid hemorrhage (SAH, pronounced /sbrknd hmrd/, or subarachnoid haemorrhage in British English) is bleeding into the subarachnoid spacethe area between the arachnoid membrane and the pia mater surrounding the brain. This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury. Symptoms of SAH include a severe headache with a rapid onset ("thunderclap headache"), vomiting, confusion or a lowered level of consciousness, and sometimes seizures. The diagnosis is generally confirmed with a CT scan of the head, or occasionally by lumbar puncture. Treatment is by prompt neurosurgery or radiologically guided interventions with medications and other treatments to help prevent recurrence of the bleeding and complications. Surgery for aneurysms was introduced in the 1930s, but since the 1990s many aneurysms are treated by a less invasive procedure called "coiling", which is carried out by instrumentation through large blood vessels. SAH is a form of stroke and comprises 17% of all strokes. It is a medical emergency and can lead to death or severe disabilityeven when recognized and treated at an early stage. Up to half of all cases of SAH are fatal and 1015% die before reaching a hospital, and those who survive often have neurological or cognitive impairment.

Classification There are several grading scales available for SAH. The Glasgow Coma Scale is ubiquitously used for assessing consciousness. Three specialized scores are used to evaluate SAH; in each, a higher number is associated with a worse outcome. These scales have been derived by retrospectively matching characteristics of patients with their outcomes. The first scale of severity was described by Hunt and Hess in 1968: Grade 1 2 3 4 5 Signs and symptoms Asymptomatic or minimal headache and slight neck stiffness Moderate to severe headache; neck stiffness; no neurologic deficit except cranial nerve palsy Drowsy; minimal neurologic deficit Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances Deep coma; decerebrate rigidity; moribund Survival 70% 60% 50% 20% 10%

The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan. This scale has been modified by Claassen and coworkers, reflecting the additive risk from SAH size and accompanying intraventricular hemorrhage.

Grade 1 2 3 4

Appearance of hemorrhage None evident Less than 1 mm thick More than 1 mm thick Any thickness with intraventricular hemorrhage or parenchymal extension

The World Federation of Neurosurgeons (WFNS) classification uses Glasgow coma score (GCS) and focal neurological deficit to gauge severity of symptoms. Grade 1 2 3 4 5 GCS 15 1314 1314 712 <7 Focal neurological deficit Absent Absent Present Present or absent Present or absent

A comprehensive classification scheme has been suggested by Ogilvy and Carter to predict outcome and gauge therapy. The system consists of five grades and it assigns one point for the presence or absence of each of five factors: age greater than 50; Hunt and Hess grade 4 or 5; Fisher scale 3 or 4; aneurysm size greater than 10 mm; and posterior circulation aneurysm 25 mm or more.

Basal ganglia The basal ganglia (or basal nuclei) are a group of nuclei of varied origin (mostly telencephalic embryonal origin, with some diencephalic and mesencephalic elements) in the brains of vertebrates that act as a cohesive functional unit. They are situated at the base of the forebrain and strongly connected with the cerebral cortex, thalamus and other brain areas. The basal ganglia are associated with a variety of functions, including voluntary motor control, procedural learning relating to routine behaviors or "habits," eye movements, and cognitive, emotional functions. Currently popular theories implicate the basal ganglia primarily in action selection, that is, the decision of which of several possible behaviors to execute at a given time. Experimental studies show that the basal ganglia exert an inhibitory influence on a number of motor systems, and that a release of this inhibition permits a motor system to become active. The "behavior switching" that takes place within the basal ganglia is influenced by signals from many parts of the brain, including the prefrontal cortex, which is widely believed to play a key role in executive functions.

What is a hypo dense lesion of the right occipital lobe of the brain? a hypodense lesion is any lesion in the brain of density lesser than the normal tissue.it can be any fluid collection such as pus, blood or cyst or any low grade tumors with cystic changes.occipital region is a region in the backside of the brain. so hypodense lesion in occipital region denotes any of the above lesions in that region.to find out the exact lesion clinical correlation is needed.