quiz

Nearly 71% of the earth is covered by water, grouped into 4 oceans. The largest ocean, the Pacific Ocean, covers a third of the earth’s surface. In an ironic sense, our planet is nothing but a collection of islands and, if one considers the Arctic and Antarctic frozen ice as water, the entire earth is nothing but a massive conglomerate of archipelagos!

The deep fascia is very sensitive. Its nerve supply and of the subcutaneous periosteum (for example, tibial periosteum), is that of the overlying skin. The nerves to muscles supply the inter-muscular septa and the deep periosteum (for example, the femur). One clinical application of this is the intense pain associated with endovascular laser treatment of incompetent great and small saphenous veins, if done without antecedent tumescent anesthesia (the injection of an anesthetic into the saphenous sheath under ultrasound guidance). The sheaths are extensions of the deep fascia.

Melanocyte populations are similar in all races. In darker skinned races the melanocytes are more active and produce more pigment. There are also racial differences between melanin that can vary from yellows to browns and blacks. The change with age in hair color is due to decreasing melanocyte activity.

Apocrine glands are large sweat glands found in the axillae, areola, the genital, periumbilical, and perianal regions. Their secretions are odorless, but acquire a smell through bacterial action. The differences in body odor are due to differences in the bacterial colonies found on the human skin. The pubescent accentuation of these odors is due to increased activity of these glands that marks the onset of puberty.

The ‘rule of nines’ assigns the following proportions to the skin surface area: head 9%; upper limb 9%; lower limb 18%; front of thorax and abdomen 18%; back of thorax and abdomen 18%.

About a third of the total body water is extracellular; the remaining two-thirds is intracellular.

Sebaceous glands are small saccular structures in the dermis that open into the side of hair follicles. They produce sebum, the chemical that oils the skin. They are not innervated and are acted on locally by androgens.

Chad is a landlocked country in Central Africa. It is one of the poorest and most corrupt countries in the world and was once a French territory.

Fibrocartilage is like white fibrous tissue but has islands of cartilage cells and proteoglycan, water, and dissolved salts between dense fibrous tissue. It appears in intervertebral discs, menisci, labrum of the hip and shoulder joints, and at the ends of squamous temporal bone, the mandible and the clavicle.

Cardiac and smooth muscle cells are uninucleated, but skeletal muscle fibers are multinucleated

The shaft of the humerus develops from a primary center of ossification that appears at the 8th week of gestation; its upper and lower ends are cartilaginous at birth. In the first few years after birth, 3 secondary centers of ossification form proximally for the head of the humerus and its greater and lesser tubercles, and unite into a single bony epiphysis that fuses with the humeral shaft at about 20 years. 4 secondary ossification centers form in the lower end of the bone: the medial and lateral epicondyles and the trochlear and the capitulum. 3 of these, the trochlear, the capitulum, and the lateral epicondyle unite into a single epiphysis that fuses with the shaft at about 15 years. The medial epicondyle remains separate until 20 years, when it fuses with a downward projection of the shaft. Thus, the humerus is a single unit by age 20.

Two tuberosities and a head define the proximal humerus. The head, an incomplete sphere, and in the resting state looks up and backwards. It is 4 times the size of the scapular glenoid. At rest, its lower and anterior quarter articulate with the scapula, allowing substantial room for lateral rotation and abduction. These movements and others are effected by 7 muscles: the subscapularis (attached to the lesser tubercle), the teres major (attached to the medial lip of the intertubacular sulcus, a downward continuation of the lesser tubercle), the latissimus dorsi (attached to the floor of the intertubercular sulcus), the supraspinatus (attached to the greater tuberosisty), the infraspinatus (attached to the greater tuberosity behind the supraspinatus), the teres minor ( the greater tuberosisty, behind the infraspinatus insertion), and the pectoralis major (the lateral lip, which is the downward extension of the anterior margin of the greater tuberosisty).

The humeral radial groove (not to be confused with the radial groove on the proximal ulna that receives the radial head) is the shallow depression on the posterior mid humerus through which the radial nerve and the deep brachial artery course. It is formed by 2 ridges that give attachment to the medial and lateral heads of the triceps, respectively. The lateral ridge continues inferiorly into the lateral supracondylar ridge.

The intertubercular sulcus is the depression on the anterior proximal humerus formed by distal continuations of the margins of the lesser and greater tuberosities of the humeral head: its medial lip continues from the lesser tuberosity and its lateral lip from the greater tuberosity. The sulcus is bridged by the transverse humeral ligament and houses the long head of biceps as it leaves the shoulder joint. Rupture of the ligament, usually a component of avulsive injury to its medial lip and the tendon of the subscapularis muscle, liberates the tendon which tends to translocate medially. The floor of the sulcus receives the tendon of the latissimus dorsi; the teres major is attached to its medial lip, while the tendon of pectoralis major is attached to its lateral lip.

In 0.3% to 2.7% (roughly 3%) of normal people a bony process called “the supracondylar process” juts out the anterior humerus approximately 7 cm proximal to the medial epicondyle. A fibrous band called the ligament of Struthers, passing from the supracondylar process to the medial epicondyle creates a fibro-osseous tunnel through which the neurovascular bundle of the arm (the medial nerve, brachial artery, and brachial vein) pass. The median nerve may be compressed by the ligament resulting in numbness of the hand and weakness of the muscles of the anterior compartment of the forearm (pronator teres, flexor carpi ulnaris, flexor carpi radialis, palmaris longus, flexor digitorum superficialis).

Marrow reconversion means the recruitment of yellow marrow for hematopoiesis. It implies that the red marrow stores have exceeded their erythropoietic capacity and is caused by anemia (sickle cell disease, thalassemia, hereditary spherocytosis, and acute and chronic blood loss). It can be indistinguishable from marrow replacement by neoplastic cells and marrow response to treatment with granulocyte-macrophage colony-stimulating factor. Marrow reconversion begins in the irregular and flat bones and involves the appendicular skeleton when anemia is severe. In the long bones, it starts in the proximal metaphysis, then the distal metaphysis, and finally in the diaphysis. It is unusual in the epiphyses and apophyses of the long bones, except in severe anemia. Neoplastic marrow replacement can be focal or diffuse, but tends to begin in well-vascularized bones (the flat and irregular bones) or regions of bones (the metaphysis of long bones).

Prior to 1828, it was widely believed that living things and nonliving things belonged to 2 mutually exclusive worlds; that it was not possible to form organic materials from inorganic materials. Vitalism, the theory that governed one world, believed that all living things were driven by an inner force that opposed all physical laws and that this force kept them from dying. Mechanism, the opposing theory, taught that life is merely an amalgam of many physical and chemical laws – a breathing monumental expression of physics and chemistry. It believed that living, an organic phenomenon, required flawless operations of many inorganic processes (nonliving things). It took the formation of urea in the laboratory by the German chemist, Friedrich Wohler (1800-1882), at the age of 28, to lay the foundations for the preeminence of the mechanism theory and thus, modern medicine. He formed urea, an organic material and the chief metabolite of protein breakdown in the body, from ammonium cyanate, an inorganic compound.

The pancreas develops from dorsal and ventral buds off the endodermal lining of the duodenum. The ventral bud comprises two components that normally fuse and rotate rightward to lie inferior and dorsal to the dorsal bud, forming the uncinate process of the pancreas and the lower half of its head. Occasionally, the two halves of the ventral bud rotate in opposite directions to fuse with the dorsal bud, the right half swinging, normally, dorsal to the duodenum, while the left half swings in the opposite direction, ventral to the duodenum. This results in a constricting band of pancreatic tissue around the duodenum that causes complete duodenal obstruction.

The adult pancreas forms from ventral and dorsal endodermal buds off the duodenum. When the duodenum rotates rightward, the ventral bud swings rightward, too, and comes to lie inferior and dorsal to the dorsal pancreatic bud, explaining why the common bile duct is posterior to the first portion of the duodenum. The ventral pancreatic bud develops into the uncinate process of the pancreas and the lower half of its head, which explains why the distal common bile duct is intra-pancreatic. The duct of the distal part of the dorsal bud and the entire duct of the ventral bud form the main pancreatic duct (of Wirsung), while its proximal part either obliterates or persists as the accessory pancreatic duct of Santorini. The duct of Wirsung joins the common bile duct and enters the duodenum at the major papilla, while the accessory duct enters it at the minor papilla, proximal to the major papilla. However, in about 10% of cases, the embryologic double ductal system of the pancreas fails to fuse, resulting in pancreas divisum in which the duct of the dorsal bud enters the duodenum at the minor papilla, while the duct of the ventral bud enters it at the major papilla.

Sudden injury of the corticospinal system causes temporary depression of the anterior horn cells of the spinal cord, called neuronal shock. It manifests as paralysis accompanied at first by loss of muscle tone and absent or reduced tendon reflexes, mimicking a lower motor neuron disease. Neuronal shock is replaced by the characteristic hypertonia and hyperreflexia of upper motor neuron disease after a few hours or days.

In early in utero life, the cord filled the entire spinal canal in a 1:1 vertebral body to spinal cord segmental relationship, such that each spinal vertebral level corresponded to the segment of the cord it housed; this relationship changed with fetal growth as the trunk outgrew the cord. Thus, in the adult, the spinal segments do not correspond to the vertebrae overlying them, with the spinal cord extending from the foramen magnum to the vertebral interspace between the T12 and L1 spines, while the thecal membranes extend distally to the second sacral vertebra. To determine the spinal segment at a known vertebral body level the following guide is helpful:

For cervical vertebrae, add 1 spinal segment level; thus, the spinal segment at the C4 vertebral level is C5, and at C7 it is C8.

For T1 to T6 vertebrae, add 2 spinal segment levels; thus, the spinal segment at the T6 vertebral level is T8.

For T7 to T9 vertebrae, add 3 spinal segment levels; thus, the spinal segment at the T8 vertebral level is T11.

The arch of T10 vertebra overlies spinal segments L1 and L2.

The arch of T11 vertebra overlies spinal segments L3 and L4.

The arch of T12 vertebra protects spinal segment L5.

The arch of L1 protects the sacral and coccygeal segments.

The normal volume of cerebrospinal fluid (CSF) in humans is 150 mL of which 75 mL is around the spinal cord, 25 mL within the ventricular system, and 50 mL around the cortical sulci and in the basal cisterns. But between 450 mL and 550 mL of CSF is formed daily, 50-70% of which is formed in the choroid plexuses and the remainder around blood vessels and along the walls of the ventricles. Thus daily CSF turnover is between 3 and 3.7 times. CSF flows from the lateral ventricles across the foramina of Monro into the third ventricle, and from it through the aqueduct of Sylvius into the fourth ventricle. It then flows through the foramen of Magendie (single and medial) and the foramina of Luschka (bilateral and lateral) into the cervical subarachnoid space to bath the spinal cord. It then circulates back to sweep over the surface of the brain and is filtered across the arachnoid villi (fusions of arachnoid membrane of the endothelium of the venous sinuses) by bulk flow into the dural sinuses to return to the systemic circulation. Bulk flow of CSF across these villi is about 500 mL per day with additional small amounts absorbed by diffusion into cerebral blood vessels.

Normal lumbar CSF pressure is between 60 and 150 mm of CSF or 6 to 15 cm of CSF. The measurement of CSF pressure is frequently a component of CSF analysis and is abnormal in conditions associated with increased dural sinus pressure, increased CSF formation, or increased CSF outflow resistance. Sometimes, there is no identifiable reason for its rise as in benign essential intracranial hypertension. CSF pressure should be measured with the patient in left lateral decubitus position, the head on a pillow, at the same level as the sacrum, muscles relaxed and breathing quietly; measurements obtained in the prone position or with the patient agitated and tense are likely to be abnormal.

A 2 cm resectable non-small cell lung cancer without atelectasis, pleural effusion, nodal spread or metastasis is (T1N0M0) is a stage IA disease. We stage all malignancies to select appropriate treatment for them and divine their prognosis. The staging scheme for non-small cell lung cancers comprising adenocarcinoma, squamous cell carcinoma, and large cell carcinoma relies on the size of the tumor (T), the presence of nodal disease (N), and identification of metastasis (M), the TNM scheme. The scheme excludes small cell cancer, which typically has extrathoracic disease at presentation and is rarely resectable. Small cell cancer of the lung is said to be limited when it is confined to the thorax and extensive when there is extrathoracic spread.

In the TNM scheme, non-small cell cancers are T1 or T2 if they spare the chest wall, the diaphragm, and the mediastinum depending on their size and the presence of associated complications like atelectasis.

Nodal disease is considered with respect to the site of the tumor: N0, for no nodal spread; N1, when the ipsilateral lobar or hilar nodes are affected; N2, when there is ipsilateral mediastinal or subcarinal nodal spread; N3 when there is contralateral mediastinal or ipsilateral supraclavicular or scalene nodal spread.

When there is metastasis, the patient is said to have M1 disease, and if there is none they are classified as M0.

The stage of a patient’s disease is assigned by jointly considering their tumor, node, and metastasis status, which the tables below summarize:

Patients with central lung cancer sometimes present with segmental or lobar lung atelectasis in which the obstructing lesion is indistinguishable from the atelectatic lung on the diagnosing chest CT scan. In such situation, gadolinium-enhanced MRI of the chest may reveal the location of the mass and allow decision between the use of transbronchial or percutaneous lung biopsy to procure tissue as well as permit judgment on radiation port during radiotherapy. On T2-weighted images, the collapsed lung is brighter than the tumor because of its water content, allowing the distinction and post-gadolinium T1-weighted imaging buttresses the distinction. Other situations in the workup of primary lung cancer in which MRI is useful are the following:

1. In assessing the full extent of superior sulcus tumors.

2. In identifying and defining invasion of mediastinal vessels.

3. In identifying and defining pericardial or heart invasion.

4. In distinguishing enlarged mediastinal nodes from unopacified blood vessels when patients cannot receive radiocontrast for CT scan.

The lucid interval is classically described in relation to acute epidural hematomas though it complicates other forms of head trauma. It is the deceptive period of wakefulness following head trauma that is soon replaced by neurological deficits including lost consciousness, but occurs in only a third of patients with epidural hematoma. Its onset varies, being quick or delayed by hours or days after a head trauma. For example, it occurs soon after an acute epidural hematoma as the expanding hematoma compresses the adjacent brain, whereas it may occur days after a post-traumatic intra-parenchymal injury due to expanding hematoma.

Epidural hematomas are usually of arterial origin although venous epidural hematomas occur. Arterial epidural hematomas often occur when a skull fracture damages the middle meningeal artery. Although a skull fracture occurs in 85% to 95% of cases, the middle meningeal artery can be stretched or injured, particularly in children, without a fracture present. The resulting hematoma strips the outer dura off the endosteum of the inner table of the skull, forming a lentiform mass that only expands inwards towards the brain because the outer dura is periodically attached to the suture lines. (The only exception to this is at the vertex of the skull, where the periosteum of the inner table of the skull forms the outer wall of the sagittal sinus, allowing an epidural hematoma at this site, which is usually of venous origin, to cross the sagittal suture.) Other sites of venous epidural hematoma are the posterior cranial fossa and the anterior aspect of the middle cranial fossa, also locations of venous sinuses.

Brain herniation is a secondary manifestation of primary intracranial disease in which a process disturbs the equilibrium between the volumes of the brain, the cerebrospinal fluid, and the intracranial blood. The sum of these volumes in an intact skull is always constant and increase or decrease in one of them affects the other 2 volumes. When a primary intracranial insult overwhelms the brain’s compensatory efforts, intracranial pressure rises. Initially, such rise obliterates the subarachnoid spaces and cisterns, but if the instigating process continues unchecked, the brain begins to shift across natural apertures or weaknesses defined by the dura and the skull. These are internal brain herniations. Sometimes, the brain herniates across craniotomy defects at surgery or through traumatic skull fractures, when a cranial breach affords the swollen brain welcome avenue to decompress itself. These are external brain herniations.
Natural sites of internal brain herniation include the subfalcine space in the anterior cranial fossa, which is defined by the inferior margin of the falx crebri; the tentorial incisura, defined by the attachments of the tentorium cerebelli to the planum sphenoidale; and, the foramen magnum defined by the inferior clivus anteriorly and the medial margins of the occipital bones. Brain swollen by edema or hyperemia, or, brain pressed upon by an adjacent space-occupying mass, such as blood or tumor, decompress itself across these ‘weaknesses’. Thus, there may exist, solitarily, synchronously, or metachronously, subfalcine herniation, transtentorial herniation (descending or ascending), or transforaminal herniation. Of these herniations, the commonest is subfalcine herniation followed by descending transtentorial herniation.

No, all forms of brain herniation do not have similar characteristics or prognosis.
In subfalcine herniation, the most common form of brain herniation, the cingulate gyrus of the expanding or displaced hemisphere herniates across the midline into the opposite hemicranium, beneath the inferior margin of the falx cerebri. It may trap the ipsilateral anterior cerebral artery against the unyielding falcian edge, infarcting the territory it supplies.
In unilateral descending transtentorial herniation, the medial temporal lobe, its uncus and hippocampus, herniates into the tentorial incisura, wedging itself between the tentorial edge and the midbrain. This pushes the contralateral cerebral peduncle against the tentorial edge producing pressure necrosis, the ‘Kernohan notch’, with hemiparesis ipsilateral to the side of space-occupying disease. The herniated medial temporal lobe compresses the ipsilateral occulomotor nerve, dilating the ipsilateral pupil. The ipsilateral posterior cerebral artery is sometimes kinked or obstructed against the tentorial edge infarcting the the ipsilateral occipital lobe.
In bilateral descending transtentorial herniation, the medial temporal lobes herniate through the tentorial incisura due to increased supratentorial intracranial pressure. This obliterates the basal cisterns, causes bilateral occulomotor neuropathy, obliterates the mammilopontine angle, obstructs the aqueduct of sylvius producing hydrocephalus, and obstructs or kinks perforating arteries that supply the thalamus and basal ganglia and those that supply the midbrain and the pons, infarcting them. Hemmorrhagic infarcts produced by the latter are called Duret’s hemorrhages.
In ascending transtentorial herniation, a space-occupying lesion of the posterior cranial fossa displaces the vermis and portions of the cerebellar hermispheres into the supratentorial space across the tentorial incisura. This effaces the quadrigeminal cistern and obstructs the aqueduct of sylvius, producing hydrocephalus.
In transforaminal herniation, a mass in the posterior cranial fossa displaces the cerebellar tonsil(s) into the foramen magnum. It is the commoner of the 2 forms of posterior cranial fossa herniations and may be congenital or acquired.

Among the earliest subcellular consequences of acute occlusion of a cerebral or cerebellar artery is the disturbance of intracellular water metabolism, in which the ischemic brain cells accumulate water due to disturbed Na-K pump. The changes caused by swelling of the affected cells and interstitial edema are what are grossly depicted in cross-sectional imaging. Given its limited resolving ability, it requires substantial amount of these changes to occur before they are declared on non-contrast CT scan of the brain or on MRI sequences that depict them such as T1-weighted imaging, T2-weighted imaging, and FLAIR. On the other hand, diffusion-weighted imaging portrays these local restrictions of normal movements of the hydrogen protons in water molecules, the quintessential early event after a stroke. Infarct, DWI becomes abnormal (that is, positive) within minutes after infarction of the brain begins, well before unenhanced brain CT scan shows even subtle abnormalities of the event; it precedes hyperintensity on T2 and FLAIR sequences by 6 – 12 hours. This difference in time is crucial in modern management of acute stroke, whose outcome predicates on the time lapse between the onset of the event and the administration of systemic fibrinolytic therapy. However, unenhanced CT scan of the brain is commonly the first screening modality for acute stroke in clinical medicine because it is fast to obtain, widely available, has few restrictions to its use, and the changes it reveals in the event of a stroke help in deciding if a patient is a candidate for fibrinolytic therapy or not. When it is negative and the clinical signs of stroke equivocal, MRI should be the next port of call.

Stroke is the acute attack of neurologic deficits in the absence of trauma, “a sudden strike by invisible hands”. In nonhemorrhagic cerebral ischemia, representing 85% of cases, it results from abrupt cessation of blood flow to a region of the brain, while in the remaining 15% it is due to acute intracranial hemorrhage which, in addition to its mass effects on adjacent brain cells, deprives regional cells of blood supply too. In nonhemorrhagic cerebral ischemia, a clot may arrive a fated vessel from a distant site (the carotids, vertebrals, aortic arch, left ventricle, or, in paradoxical embolism, from the lower extremities, through a patent foramen ovale in the atrial septum), causing acute embolic stroke, or, there could develop sudden occlusion of a vessel where atherosclerosis has developed over time causing acute thrombotic stroke. The stasis of blood flow that follows the latter may produce acute coagulum of blood, a visible clot. This clot, either native or immigrant, produces changes in the blood vessel that may be seen within minutes of the obstruction, long before the ischemic changes develop. On noncontrast CT this is the ‘hyperdense artery sign’, while on MRI it is the absence of the normal flow void visible in normal arteries or the development of other manifestations of disturbed blood flow. Since in most investigations of acute stroke noncontrast CT scan of the brain is the first imaging performed, the earliest possible sign of acute nonhemorrhagic stroke is the ‘hyperdense artery sign’.

In any event, the lack of oxygenation of the ischemic brain cells leads to failure of the cellular membrane’s Na-K pump, permitting intracellular edema, or what is termed cytotoxic edema, to develop. In time, the cell membranes of the regional endothelial cells also fail and allow egress of intravascular fluid into the extravascular space, causing vasogenic edema. Thus, there is increased fluid in the ischemic region producing visible manifestations of ischemia on various modes of radiologic imaging: on CT, hypoattenuation, ‘the insular ribbon sign’, sulcal effacement, lost corticomedullary differentiation; on MRI, ‘the light bulb sign’ on DWI and T2 hyperintensity, FLAIR hyperintensity and T1 hypointensity on convensional imaging.

The abducens or cranial nerve VI lies inside the cavernous sinus, inferolateral to the internal carotid artery, and is the only cranial nerve that lies within the sinus. The other cranial nerves associated with the sinus (III, IV, V1, and V2) lie within its lateral dural wall.

Nontraumatic intraparenchymal hemorrhages of the brain cause more initial mortality than brain infarcts of equal size, because of the secondary mass effects they produce in addition to the acute assault to the brain they evoke. On recovery, however, they cause fewer neurological deficits because intraparenchymal hemorrhage displaces and shears through brain tissue and is later removed; only neurons denied perfusion when blood meant for them escapes the intravascular lumen die, while displaced neurons recover. On the other hand, acute brain infarction leaves in its wake dead neurons that never recover or replenish.

In the radiologic evaluation of intracranial abnormalities, diseases are classified as intra-axial when they arise from the brain proper and extra-axial when they do not. All the three locations alluded to in the question including the lateral ventricle are outside the brain though intracranial. This distinction is crucial to the formulation of the differential diagnosis of intracranial disease and by extension, its treatment. A useful radiologic sign in making this distinction is the “white matter buckling” sign, in which an extra-axial mass buckles the white matter of the brain, thins its fronds (the finger-like extensions of the white matter towards the gray matter), and preserves its boundary with the gray matter. Intra-axial masses do the opposite: they expand the white matter, thicken its fronds, and blur the gray matter-white matter interface. The sign, unfortunately, is useful only when present, because when an extra-axial mass is associated with intense vasogenic edema, it may expand the white matter and not buckle it.

The fetal skin is covered by an oily whitish paste called vernix caseosa (French, “cheesy varnish”), formed by secretions from sebaceous glands and degenerated epidermal cells and hair. Vernix caseosa protects the fetus from the macerating influence of amniotic fluid. It is the substance the midwife easily rubs off or washes away after birth to reveal the underlying clean pinkish skin of the baby that the mother adores. A thick layer of meconium on the fetal skin is abnormal and suggests intrauterine fetal distress. Cells destined to become melanocytes arrive the fetal epidermis in the first 3 months of life from the neural crest. They have dendritic processes through which they distribute their produce, melanin pigment, to other cells in the epidermis and cause pigmentation of the skin after birth.

The intracranial venous sinuses and their cortical venous tributaries can thrombose. Common causes of such thrombosis include dehydration (especially in children), trauma, hormonal alterations (pregnancy and oral contraceptives), and infection or inflammation (sinusitis, mastoiditis, meningitis); its uncommon causes are thrombogenic disorders (protein C disease, protein S deficiency, antiphospolipid syndrome) and vasculitis (Behcet’s syndrome). The pathology, extent, signs, and symptoms of the disease range from localized and asymptomatic disease to extensive thrombosis with parenchymal infarction, raised intracranial pressure, and altered mentation including coma. Magnetic resonance imaging (MRI) is the diagnostic imaging modality of choice when the disease is suspected and should include time-of-flight or phase contrast magnetic resonance venography in addition to conventional MRI. The chief treatment of the disease is systemic anticoagulation. Patients with complications of the disease that portend poor prognosis such as increased intracranial pressure and coma should, however, receive specific therapy such as endovascular thrombolysis in addition to systemic anticoagulation even in the presence of cerebral hemorrhage. Devices that mechanically break up clot endovascularly may be used to treat the disease though their success varies.

Blood is supplied to the brain through the internal carotid and vertebral arteries. The internal carotid arteries supply the anterior circulation, which supplies the cerebral hemispheres and their deep nuclei (the forebrain), except the occipital lobes and parts of the posterior temporal lobes that are supplied by the posterior circulation. The vertebral arteries supply the posterior circulation, which supplies the midbrain, pons, medulla oblongata, and cerebellum as well as the occipital lobes and parts of the posterior temporal lobes. The anterior circulation of one side of the brain communicates with that of the opposite side through the anterior communicating artery, while the posterior communicating artery connects the ipsilateral anterior and posterior circulations, forming the circle of Willis. Since the nutritional demands and volume of the forebrain are more than those of the rest of the brain, 80% to 85% of intracranial blood flow is through the anterior circulation. It is not surprising then that 80% of intracranial aneurysms arise from the arteries of the circle of Willis.

Yes, intracranial aneurysms may be familial. In fact, 7% to 20% of subarachnoid hemorrhages are due to ruptured intracranial familial aneurysms. Such aneurysms tend to be associated with connective tissue disorders though they can occur in their absence. The disorders include Ehlers-Danlos syndrome, Marfan’s syndrome, neurofibromatosis type-1, and aortic aneurysm or coarctation.

A giant intracranial aneurysm is one whose widest diameter is greater than 2.5 cm. Giant intracranial aneurysms rupture less frequently than smaller aneurysms, but produce mass effects on neighboring structures such as cranial nerve
palsies, seizures, and hydrocephalus. They enlarge by expansion of their walls and are prone to forming layers of mural thrombi.

Multiple intracranial aneurysms occur in 25% of patients and are commoner in females. When multiple intracranial aneurysms occur there will be 2 aneurysms in 75% of cases, 3 aneurysms in 15%, and 4 aneurysms in less than 10%. It is for this reason that when performing selective catheter angiography for intracranial aneurysms, the examiner must examine all intracranial arteries.

80% to 85% of intracranial circulation flows into the anterior circulation, while the rest flows into the posterior circulation. The anterior circulation is supplied by the internal carotid arteries, while the posterior circulation is supplied by the vertebral arteries. The internal carotids and their intracranial branches bear more stress and contribute more to the circle of Willis than the vertebral arteries and the basilar artery. Thus 80% of intracranial aneurysms are associated with the circle of Willis and occur at the branch points of the middle and anterior cerebral arteries as well as the tip of the basilar artery.

Intracranial aneurysms are commoner in females than males. Other risk factors for intracranial aneurysms include hypertension, smoking, advancing age, diabetes mellitus, and certain genetic anomalies, while conditions associated with
higher occurrence of intracranial aneurysms include fibromuscular dysplasia, glioblastoma multiforme, meningioma, adult polycystic kidney disease, arteriovenous malformations, family history of aneurysms, and connective tissue
disorders.

The visceral pleurae of the lungs form the interlobar fissures – the minor and major fissures – that separate the lungs into lobes. These lobes are aerated through lobar bronchi that branch off the main pulmonary bronchi, but which may be obstructed by intraluminal or extraluminal masses. When such obstruction is complete and the air distal to it is completely resorbed, the lobar alveoli collapse and may develop post-obstructive pneumonitis. On a chest radiograph or CT scan, the affected lung is opaque, diminished in volume, and associated with telltale signs of volume loss such as fissural and mediastinal shifts. But this ‘fissural lobarization’ of the lungs may be congenitally incomplete, allowing collateral ventilation of obstructed alveoli by air drifting in from adjacent alveoli through the pores of Kohn and the canals of Lambert across the incomplete fissure – the same communications that permit airspace (alveolar) disease to spread from one pulmonary lobe to the other. When this happens, it is possible to identify aerated lung within a lobe served by a completely obstructed bronchus.

The primary purpose of all clinical and radiologic exercises on the breast is to detect and treat breast cancer early in the ultimate hope of avoiding or delaying death from the disease. Because 10% of breast cancers come to clinical attention through breast palpation, this exercise is encouraged in all females after age 20, though its effect on breast cancer mortality is unproven. Furthermore, when a clinically-palpable lesion eludes detection by mammography and adjunctive imaging (sonography and MRI), it should be surveilled with periodic imaging or biopsied as soon as possible. Screening mammography is offered to asymptomatic women over the age of 40 because it is the only breast imaging modality scientifically proven to reduce death from breast cancer (30% reduction), though this benefit has remained stable for decades; It is also used to diagnose or clarify symptomatic breast lesions as diagnostic mammography. Mammography demonstrates early malignant lesions better than any other breast imaging technique and in its current state has a sensitivity for this purpose that ranges from 85% to 95%.  Breast sonography is not a screening tool for breast cancer, rather its chief benefit is diagnostic – the classification of breast lesions into cysts and solids, the characterization of solid lesions, and the guidance of preoperative biopsy of indeterminate or worrisome breast lesions. It is the most-used ancillary method of breast imaging because of its availability, facility, affordability and versatility. MRI’s role in investigating breast cancer has grown over the years from a diagnostic tool sometimes employed as a guide for biopsy to several specialized applications that aid the management of the disease. Indeed, in 2007 the American Cancer Society recommended annual breast MRI screening in patients whose lifetime risk for breast cancer equals or exceeds 20%.  Its effect on reducing the rate of death from cancer, like with sonography, is unproven.

There are a number of areas of the body that are overlain by layers of fat called fat pads. The “fat pad” sign describes the displacement of such fat pad over or adjacent to a joint on a plain radiograph and suggests that the joint is distended with fluid. Though popular with the elbow joint, it is a nonspecific, nonpathognomonic  descriptor that only attracts critical scrutiny of any joint for abnormality and can be caused by any joint disorder that elicits an effusion – trauma, infection, rheumatoid arthritis, and hemorrhage (in bleeding disorders). In the instance of trauma to the elbow, it suggests a supracondylar fracture in a child and a radial head fracture in an adult.

The avascular plane of Brodel lies between the territories supplied by the anterior and posterior divisions of the renal artery. It is a plane sparsely supplied by branches of these divisions of the artery and is considered a safe path for renal instrumentations such as in percutaneous insertion of a nephrostomy catheter. The anterior division of the renal artery supplies the anterior two-thirds of the kidney, while the posterior division of the artery supplies the posterior one-third of the kidney. In a patient lying prone on a procedure table for the insertion of a nephrostomy catheter, the usual position for the procedure, the plane lies 1 cm to 2 cm posterior to the lateral renal cortex or at an angle 30 to 45 degrees from the mid line. (Max Brodel (1870-1941) was a German medical artist, anatomist, and scientist, who relocated to Maryland, USA following an invitation to John Hopkins hospital. Through his medical illustrations he made major contributions to urology, gynecology, neurosurgery, and otolaryngology and also popularized an improved method of nephropexy at his time using a suture that he designed.)