GI differential Diagnoses

GI differential Diagnoses

ESOPHAGUS

Diverticular disease: pharyngocele, Zenker, Killian Jamieson, traction, pulsion, pseudodiverticula, epiphrenic
Luminal narrowing: webs, Plummer-Vinson, vascular ring, Schatzki ring, strictures (reflux, meds, skin lesions, tumor, mets, radiation, eosinophilic gastroenteritis, Crohn’s, lye, Barrett’s, infection, NGT, achalasia, scleroderma, Chagas), extrinsic compression (aorta, left bronchus, left atrium, mediastinal tumor)
High stricture: Barrett’s, radiation, caustic ingestion, CA, mets, meds, skin dz, Crohn’s
Low stricture: peptic stricture, lower esophageal ring, Barrett’s
Nodules/plaques: diffuse - reflux, Candida, glycogenic acanthosis; localized – Candida, superficial spreading CA, Barrett’s

Ulcers: distal – reflux, Crohn’s; small, mid – herpes, medications (tetracycline, doxycycline, KCl, iron, quinidine, NSAIDs, vit C, Fosamax), Crohn’s; giant – CMV, HIV

Megaesophagus: achalasia, scleroderma, distal narrowing from tumor or stricture, Chagas

Contrast extravasation: esophagitis, tumor, vomiting (MW tear, Boerhaave), TE fistula, foregut duplication cyst with communication to esophagus, iatrogenic, trauma

Solitary filling defects: intraluminal – food impaction, foreign body, fibrovascular polyp, spindle cell tumor, leiomyosarcoma, adenocarcinoma; tumor – leiomyoma, fibrovascular polyp, duplication cyst, papilloma, fibroma, hemangioma, SCC, adenocarcinoma, spindle cell tumor, lymphoma, mets (breast, lung, KS, melanoma, RCC); varices – uphill (portal HTN), downhill (SVC obstruction); extrinsic – lymph nodes, engorged vessels, aneurysms, cysts

Thickened folds: esophagitis, lymphoma, varicoid carcinoma, varices
Air-fluid level: hiatal hernia, esophageal diverticulum, CA, achalasia, scleroderma
Feline esophagus: reflux, motor disorders
Corkscrew esophagus: diffuse esophageal spasm, presbyesophagus

STOMACH
Gastritis: H pylori, erosive gastritis (corrosives, alcohol, stress, NSAIDS), granulomatous (Crohn’s, sarcoid, TB, histo, syphilis), eosinophilic, hypertrophic (Menetrier’s, ZE syndrome), recurrent gastric ulcer (ZE syndrome, PUD, drugs), radiation, emphysematous
Target lesions: gastritis (aphthoid type) – erosive (NSAID, alcohol), Crohn’s, infection (Candida, herpes, CMV); submucosal mets (large ulcer) – melanoma, KS > breast, lung, lymphoma; solitary giant bullseye (very large ulcer) – leiomyoma, sarcoma, CA, solitary met, ectopic pancreas, benign ulcer

Filling defect: bezoar, adenocarcinoma, lymphoma, leiomyosarcoma, mets, KS, endometriosis, carcinoid, leiomyoma, lipoma, polyps (hyperplastic #1), varices, ectopic pancreas, extrinsic compression from spleen/pancreas/liver
Giant rugal folds: lymphoma, Menetrier’s, ZE syndrome, gastritis, eosinophilic gastroenteritis, radiation, infection, Crohn’s, mets, varices (mimic)

Linitis plastica: scirrhous CA (#1), lymphoma, mets (esp breast), pancreatic CA (direct invasion), radiation, Crohn’s, eosinophilic gastroenteritis, corrosive ingestion, TB, sarcoid, syphilis

Antral lesions: adenocarcinoma, lymphoma, mets, Crohn’s, PUD, TB, sarcoid, HPS, pylorospasm, antral web, ectopic pancreas, erosive gastritis, caustics

Double pylorus: lesser curve antral ulcer, Crohn’s, lymphoma

Gastroenteric fistula: PUD, Crohn’s, CA, iatrogenic, surgery
Free air: surgery and laparoscopy, perforated ulcer, perforated distal bowel (IBD, diverticulitis, tumor)

UGI surgery: plication defect, marginal ulcer, bezoar, chronic gastritis, leak, obstruction, intussusception (jejunogastric), gastric CA, afferent loop syndrome, malabsorption

DUODENUM
Filling defects: benign (often 1st portion, asx) – adenoma, leiomyoma, lipoma, villous adenoma, ectopic pancreas; malignant (often distal to 1st portion, sx) – adenocarcinoma at or distal to papilla, leiomyosarcoma, lymphoma, mets (melanoma, breast, KS, carcinoid); bulb – ectopic gastric mucosa, prolapsed antral mucosa, Brunner gland hyperplasia, varices, duodenitis, Crohn’s, lymphoma, sprue, CF, polyposis, benign tumors; distal – benign lymphoid hyperplasia, ectopic pancreas, annular pancreas, ampulla of Vater, tumor, edema with impacted or passed gallstone, choledochocele; soft and changing – choledochocele, lipoma, duplication cyst

Target lesion: leiomyoma, leiomyosarcoma, met (melanoma, KS, breast, lung, lymphoma), ulcer, ZE syndrome

Luminal outpouchings: ulcer, diverticulum, choledochoduodenal or cholecystoduodenal fistula
Reverse figure 3 sign: pancreatitis, pancreatic CA
Notched duodenum: annular pancreas, post-bulbar ulcer, Crohn’s, post-op, pancreatitis, pancreatic CA

Postbulbar narrowing: adenocarcinoma, lymphoma, mets, postbulbar ulcer, duodenitis, Crohn’s, pancreatitis (extrinsic), pancreatic CA, annular pancreas, intramural diverticulum, duodenal duplication cyst, duodenal hematoma, aortic aneurysm, SMA syndrome (seen in scleroderma, lymphoma)

Papillary enlargement: >15mm; normal variant, choledochocele, papillary edema (pancreatitis, acute duodenal ulcer, impacted stone), ampullary CA

JEJUNUM AND ILEUM

Adynamic ileus: postoperative (#1); inflammatory (often sentinel loop) – pancreatitis, appendicitis, cholecystitis, diverticulitis, peritonitis; metabolic – low K+, Ca++, Mg++; medication – morphine

Mechanical SBO: adhesion, hernia, tumor, gallstone, inflammation with strictures
alabsorpmtion patterns: dilatation, dilution, delay; predominantly thick/irregular folds – Whipple’s, MAI, Strongyloides (proximal), amyloid, Giardia (jejunum), GVH, Cryptosporidium (jejunum), lymphoma, lymphangiectasia, mastocytosis, eosinophilic gastroenteritis; predominantly dilated loops and normal folds – sprue (#1), obstruction, ileus, scleroderma, medication

Thick folds without malabsorption pattern: criteria – folds >3mm, uniformly thickened if diffuse, nodular thickening (pinkyprinting) if focal with stack of coins appearance; submucosal edema – ischemia, infection, radiation, hypoproteinemia, GVH; submucosal tumor – lymphoma, leukemia, submucosal hemorrhage – Henoch-Schonlein purpura, hemophilia, anticoagulation

Tubular bowel: Cryptosporidium, sprue (proximal), lymphoma, GVH, radiation, ischemia, Strongyloides (proximal)

Nodules: mastocytosis, nodular lymphoid hyperplasia, lymphoma, mets, polyps, Crohn’s, eosinophilic gastroenteritis, TB, infection, amyloid, lymphangiectasia, Whipple’s, Waldenstrom’s macroglobulinemia

Diffuse tiny nodules: lymphoid hyperplasia (#1), hypogammaglobulinemia, Giardia, Whipple’s, Waldenstrom’s

Small bowel tumors: benign – adenoma (#1), leiomyoma (#2), lipoma, hemangioma, neurogenic tumors, Brunner gland hyperplasia, heterotopic pancreatic tissue; malignant – mets (melanoma, RCC, breast, KS), lymphoma, carcinoid (#1 primary tumor), leiomyosarcoma (large ulcerating), adenocarcinoma; polyposis syndromes

Small bowel stricture: Crohn’s, lymphoma, mets, infection, radiation, ischemia, adenoCA, extrinsic compression, NSAIDs; focal stricture with shouldering – adenoCA (#1), breast mets, TB

Coiled spring: intussusception, intramural hematoma

Large ulcerated mass (endoexoenteric): lymphoma, leiomyosarcoma, mets (melanoma), interloop abscess

Diverticula: small bowel, Meckel’s

Intraluminal filling defects: parasites (Ascaris, tapeworm), bezoar, foreign body, gallstone, lipoma

Enteric fistulas: Crohn’s, diverticulitis, CA, TB, radiation, surgery, iatrogenic

Serosal: carcinoid, serosal mets, diverticulitis, appendicitis, endometriosis

Mesenteric bowel ischemia: occlusive – emboli (afib, LV aneurysm), arterial thrombosis (atherosclerosis), venous thrombosis (portal HTN, pancreatitis, tumor, hypercoagulable state, drugs); nonocclusive – low flow state

Shortened transit time: anxiety, hyperthyroid, medication (reglan), partial SBO

COLON

Crohn’s: fold thickening, wall thickening, nodular pattern (cobblestone), string sign, aphthoid ulcers, filiform polyps, sinus tracts and fistulas, mesenteric fat stranding, creeping fat, lymphadenopathy, separated bowel loop (omega sign), pseudosacculations, strictures, asymmetric, skip lesions

UC: ahaustral, granular mucosa, filiform polyps, starts in rectum, continuous spread, backwash ileitis, crypt abscesses, strictures (worrisome)

Mass lesions: normal lymphofollicular pattern, pneumatosis coli, colitis cystica profunda, amyloid, endometriosis, ischemic colitis, polyps, polyposis syndromes, lipoma, leiomyoma, hemangioma, villous adenoma, adenocarcinoma, mets, lymphoma, hemorrhoids

Polypoid filling defects: polyps - hyperplastic (#1), adenomatous (#2), hamartomatous, post-inflammatory; polyposis – FAP, Peutz-Jeghers, juvenile polyposis, Turcot, Cronkhite-Canada, Cowden; lymphoma; pneumatosis

Carpet lesion: villous adenoma, adenoCA, polyposis, endometriosis, varices

Colonic urticaria: herpes, Yersinia, allergy, Crohn’s, ischemia

Aphthoid ulcers: Crohn’s, amebiasis, Behcet’s, CMV, herpes, TB, Yersinia (TI)

Deep ulcers: UC, Crohn’s, Behcet’s, infectious (amebiasis, TB, Salmonella, Shigella, histo, Candida, herpes, CMV), ischemic colitis, radiation

Bowel wall thickening (thumbprinting): hemorrhage – ischemia, Henoch-Schonlein purpura, hemophilia, anticoagulation; tumor – lymphoma, leukemia; edema – infectious (pseudomembranous colitis, CMV, E Coli, Salmonella, Shigella, amebiasis, typhlitis), IBD

Circumferential (apple core) or asymmetric narrowing: tumor – adenocarcinoma, serosal mets (stomach, ovarian, colon, pancreas); inflammation – diverticulitis, IBD, TB, amebiasis; other – endometriosis, pelvic abscess, epiploic appendagitis; multifocal – lymphoma, serosal mets, TB, amebiasis, Crohn’s, endometriosis

Long segment narrowing: scirrhous adenocarcinoma, lymphoma, UC, Crohn’s, ischemic stricture, radiation

Ahaustral colon: cathartic abuse (usu R colon), UC, Crohn’s, amebiasis, aging (usu L colon), scleroderma, radiation, prior ischemia

Pseudosacculations: Crohn’s, scleroderma, ischemia

Obstruction: CA, diverticulitis, volvulus, impaction, hernia

Megacolon: toxic megacolon – pseudomembranous colitis, UC, Crohn’s, amebiasis; acute distension – obstructive CA, ileus, volvulus; chronic – laxative abuse, Ogilvie syndrome, congenital Hirschsprung’s, Chagas, neuromuscular disorders (Parkinson, DM, scleroderma, amyloid), hypothyroid

Adult intussusception: usually ileoileal; tumors – polyps, lipoma, mets, lymphoma, carcinoid; idiopathic, Meckel’s diverticulum, feeding tube; no lead point consider sprue, scleroderma, Whipple’s

Pneumatosis coli: pneumatosis cystoides – COPD, asthma, CF, iatrogenic, CVD, steroids; pneumatosis intestinalis – infarcted bowel, NEC, toxic megacolon, typhlitis

Coned cecum: Crohn’s, lymphoma, mets, TB, amebiasis, typhlitis

Ileocecal deformities: Crohn’s, UC, amebiasis (spares TI), TB, typhlitis, lymphoma, adenocarcinoma, carcinoid, intussusception

Enlarged ileocecal valve: >3cm; lipomatous infiltration (#1), lipoma, Crohn’s, lymphoma, prolapsing ileal neoplasms

Cecal filling defect and nonfilling appendix: carcinoid, appendicitis, appendix stump, mucocele

Fat containing mass adjacent to colon: epiploic appendagitis, omental infarction

Proctitis: Condyloma acuminata, lymphogranuloma venereum, GC, UC, Crohn’s, HIV, herpes

Rectal involvement: serosal mets, TOA, radiation, appendicitis, diverticulitis, endometriosis

Presacral space widening: >2cm; rectal inflammation (colitis, radiation), infection, tumor, pelvic lipomatosis, edema hemorrhage

LIVER

Solid masses: hemangioma, FNH, adenoma, HCC, mets, regenerating nodules, focal fatty deposition, lymphoma

Cystic masses: infectious – pyogenic abscess, amebiasis, Echinococcus; benign – simple cysts, ADPKD, biliary cystadenoma, biloma, intrahepatic GB; malignant – necrotic tumors, cystic mets, cholangioCAcreased density: hemochromatosis, glycogen storage disease, Wilson’s, amiodarone, chemotherapy, thorotrast, anemia, regenerative nodules in cirrhosis (low T2)

Decreased density: fatty liver – obesity, alcohol, DM, steroids, chemotherapy; radiation-induced

Mottled density without focal mass: passive congestion, Budd-Chiari, geographic fatty infiltration, hepatoma, lymphoma

Hypervascular: hemangioma, hemangioendothelioma, cholangioCA, HCC, mets (islet cell, melanoma, carcinoid, RCC, thyroid, breast, sarcoma)

Hyperechoic: round – hemangioma, hyperechoic mets (hypervascular and calcified mets), HCC, fibrolamellar HCC, focal fat, lipoma, AML, Gaucher’s; linear – pneumobilia, PV gas, biliary ascariasis; multiple punctate foci – hepatitis, granulomatous infection, PCP, biliary hamartomas, pneumobilia, PV gas, vascular calcs

Multiple hypoechoic: tumor – mets, lymphoma, HCC; infection – pyogenic, amebic, Echinococcus, Candida, Schistosomiasis; other – regenerative nodules in cirrhosis, sarcoid, extramedullary hematopoiesis, hematomas, hemangiomas

Hepatic hemorrhage: iatrogenic, trauma, adenoma, HCC, pregnancy

Gas in liver: pneumobilia – ERCP, surgery, penetrating ulcer, gallstone ileus, CA, bowel obstruction; PV air – bowel necrosis > IBD, abscess, obstruction, ulcer, NEC, iatrogenic, liver transplant; abscess; emphysematous cholecystitis

Delayed retention of contrast: cholangioCA, hemangioma, fibrous tumor, scar (FNH, adenoma, fibrolamellar HCC, hemangioma)

BILIARY SYSTEM

Extrahepatic biliary dilatation: intrapancreatic (#1) – pancreatic CA, calculus, chronic pancreatitis; suprapancreatic – cholangioCA, metastatic lymph nodes; portal – cholangioCA, GB CA, surgical strictures, hepatoma; choledochal cyst


Types of obstruction: tumor – abrupt termination of duct, mass adjacent to duct; pancreatitis -–smooth, long tapering; lithiasis-related – calculus visible, meniscus sign, intrahepatic dilatation; cholangitis – sclerosing, AIDS, oriental; Caroli’s; biliary cystadenoma

Double duct sign: dilated BD and PD; pancreatitis, pancreatic CA, stone impacted in ampulla, cholangioCA, duodenal or ampullary CA

Filling defects in bile duct: stone, blood clot, parasite, sludge, tumor

Hemobilia: iatrogenic, tumor, trauma, infection

Strictures on ERCP: hilum – cholangioCA, porta hepatis nodes, GB CA; 1cm from ampulla – pancreatic CA, cholangioCA, mets; long segment – chronic pancreatitis, lymphoma; CHD at cystic duct region – Mirizzi’s, GB CA, cholangioCA; multiple intrahepatic – sclerosing cholangitis, HIV, ischemic, primary biliary cirrhosis, liver mets (rare); multiple intrahepatic and extrahepatic -–sclerosing cholangitis, HIV, ischemia

Irregular wall and filling defects: cholangitis – HIV, oriental, ascending

Pancreatic duct: stricture – pancreatic CA, chronic pancreatitis; cystic dilatation and side branches – chronic pancreatitis, IPMT; variants - annular pancreas, pancreas divisum

Cholecystectomy leaks: cystic duct remnant, duct of Luschka

GB wall thickening: >3mm; diffuse – nonfasting GB, acute cholecystitis, chronic cholecystitis, portal HTN, hypoalbuminemia, hepatitis, AIDS (cryptosporidium, CMV, MAI), ascites; focal – GB CA, mets (melanoma), cholesterol polyps, adenomyomatosis, tumefactive sludge, AIDS

GB wall hyperechoic foci: calculus, polyp, cholesterol, emphysematous cholecystitis, porcelain GB

Dense gallbladder: vicarious excretion of contrast, calculi, milk of calcium, oral cholecystogram, hemorrhage

Biliary enteric fistula: cholecystitis (gallstone ileus), PUD, tumor, trauma, surgery, Crohn’s

PANCREAS

Focal pancreatic signal abnormality: tumor, focal pancreatitis, adenopathy

Pancreatitis: causes - biliary stones, alcohol, drugs, hyperlipidemia, infection, trauma; complications – fluid collection, pseudocyst, abscess, necrosis, splenic artery pseudoaneurysm, splenic vein thrombosis

Cystic lesions: tumor – microcystic adenoma, mucinous cystadenoma, IPMT, solid/cystic and papillary epithelial neoplasm, cystic islet cell tumor; cyst – simple, pseudocyst, ADPKD, VHL, duct ectasia; abscess

Hyperechoic pancreas: CF, pancreatic lipomatosis

Hypervascular: islet cell tumor, hypervascular mets

Hypovascular: adenocarcinoma, focal chronic pancreatitis

SPLEEN

Anatomic variations: accessory spleen, lobulations, wandering spleen, polyspenia, asplenia, splenosis (s/p trauma)

Focal splenic lesions: tumor – mets (lymphoma, melanoma), hemangioma, lymphangioma, hamartoma; infection (often calcified) – abscess, Candida, TB, MAI, Schistosomiasis, PCP; other – infarct, septic emboli, hematoma, cyst (simple, hydatid) pancreatic pseudocyst, fatty nodules in Gaucher’s

Microabscess pattern: Candida, MAI, TB, PCP, bacterial, fungal, Gaucher’s, sarcoid, KS, lymphoma, mets

Scalloped contour: infarcts, septic emboli, hematoma, metastatic implants, pseudocyst

Splenic cyst: primary – congenital, true; secondary – calcified, false, prior infarct, trauma, infection, echinococcus, pancreatic pseudocyst

Splenic calcifications: TB, histo, PCP, phleboliths, hemangioma

Splenomegaly: tumor – lymphoma, leukemia; infection – infectious mono, histo, sarcoid; metabolic – Gaucher’s, amyloid, hemochromatosis; trauma; vascular – portal HTN, hematologic disorders

PERITONEAL CAVITY

Peritoneal mets: ovarian, stomach, colon, pancreas

Pseudomyxoma peritonei: mucinous cystadenoCA from ovary or appendix, mucocele

Peritoneal fluid collections: ascites, urinoma, biloma, seroma, lymphocele, pseudocyst, CSFoma; complex – abscess, hematoma, pseudomyxoma peritonei, pancreatic necrosis

Intraperitoneal calcifications: arterial calcs, appendicolith, mesenteric node, gallstone, pancreatic calcs, porcelain GB, renal/ureteral stone, nephrocalcinosis, old hematoma, abscess, fibroid, fetal skeletal part, phlebolith, teratoma, echinococcal cyst, mucinous tumor

MISC

General GI DDx: Crohn’s, lymphoma, TB (infection), mets, CA, radiation, ischemia
Mucosal: acute angle, absence of normal mucosal pattern, irregular fuzzy margin

Submucosal: obtuse angle, presence of normal mucosal pattern, smooth distinct margin

Extrinsic: spiculation, tethering

AIDS: infection – CMV, Candida, herpes, Cryptosporidium, MAI; tumor – KS, lymphoma; esophagus – ulcers (Candida, CMV, herpes, HIV), sinus tracts (TB, Actinomycosis); proximal small bowel – ulcers (cryptosporidium), nodules (KS, lymphoma, MAI); distal small bowel – enteritis (TB, MAI, CMV); colon – colitis (CMV, pseudomembranous), typhlitis; rectum – herpes, lymphoma; biliary – strictures (CMV, Cryptosporidium); liver and spleen – KS, lymphoma, Candida, TB, MAI, PCP

Abdominal trauma: liver laceration (#1), splenic lac, renal trauma, bowel hematoma, pancreatic fx, GB injury, adrenal hemorrhage

Abdominal complications after cardiac surgery: GI hemorrhage, cholecystitis, pancreatitis, perforated peptic ulcer, mesenteric ischemia, perforated diverticulitis

Low density lymph nodes: TB, MAI, lymphoma, testicular tumor, mucinous adenoCA, Whipple’s

Cystic abdominal mass: abscess, loculated ascites, panc pseudocyst, ovarian cyst or tumor, lymphocele, cystic lymphangioma, enteric duplication cyst, cystic teratoma

Mesenteric mass: lymphoma, mets, carcinoid, mesenteric fibromatosis, mesothelioma

Large LUQ mass: stomach (leiomyosarcoma), pancreas (pseudocyst, nonfunctioning islet cell tumor, mucinous tumor), adrenal (carcinoma), spleen (lymphoma), kidney (RCC, lymphoma)

RLQ inflammation: appendicitis, Crohn’s, cecal diverticulitis, perforated cecal CA, mesenteric adenitis, PID

Volvulus: gastric (organoaxial, mesenteroaxial), midgut, colon (sigmoid, cecal)

Hernia: paraesophageal, paraduodenal, inguinal, umbilical, Spigelian, lumbar, Richter’s, incisional

Abdominal wall: mets (melanoma, NF, iatrogenic seeding), rectus sheath hematoma (trauma, anticoagulation)

Ascites: cirrhosis, mets, CA, hypoalbuminemia, CHF, pancreatitis

Gasless abdomen: obstruction with fluid-filled bowel, severe vomiting, high obstruction, achalasia, impaired swallowing, continuous NG suction

MR MORPHOLOGY IN INTRACRANIAL TUBERCULOMAS

MR Morphology of Intracranial Tuberculomas


Dr. H. S. Das, Dr. N. Medhi, Dr. B. Saharia, Dr. S. K. Handique


Introduction:

Tuberculomas represent a common neurological disorder in developing countries, forming 12-30% of all intracranial masses – (1,2). Furthermore the incidence of intracranial TB in patients with AIDS is also increasing, the highest incidence recorded being 2.3% - (3,4) in one study to 18% in another – (5). Prompt diagnosis is mandatory since any delay in increased morbidity and mortality. Unfortunately the diagnosis is not always possible on the basis of clinical and epidemiological data, since clinical manifestations are nonspecific – (7,8) and objective evidence of systemic tuberculosis or exposure to the disease may be absent in upto 70% of the cases – (9). The role of CT in diagnosis of CNS tuberculomas in well established, nevertheless CT findings should be interpreted with caution since neoplastic, fungal or parasitic diseases may cause similar changes on CT – (10). Recently Magnetic Resonance (MR) Imaging has shown advantage over CT in the detection of intracranial pathology – (11) and its value in the diagnosis of infections diseases of the central nervous system (CNS) has been reported – (12,13). Although tubercular meningitis can not be differentiated from other meningitides on the basis of MR findings; but intraparenchymal tuberculomas show characteristic T2 shortening not found in most other space occupying lesions – (14). Thus in the appropiate clinical setting tuberculomas should be considered. Here, we report our experience in using MR for the evaluation of patients with intracranial tuberculoma.

Patients and Methods:

10 Patients with intracranial tuberculomas were evaluated with MR in our institution between August ’95 to August’ 99. 8 males and 2 females between 5-45 years (Mean 22.9 years) were included in this study. MRI was performed on a 1-tesla super conductive magnet. Standard spin echo techniques were used to obtain multiplanar T1 and T2 weighted images. Contrast was used in 6 patients. The diagnosis of CNS tuberculosis was made after proper integration of data from the surgical and medical findings. Data included positive biopsy in 2 patients; analysis of blood and CSF (elevation in 2 cases); positive response to anti tubercular drugs in 6 patients and MR findings. Initial CT was done upon admission to the hospital in all ten cases. MR was done to visualize the full extent of the lesion, to differentiate these lesions from other diseases affecting the brain and to delineate the contents (necrotic centre, capsule and surrounding edema). None of the patients tested positive for HIV.

Results:

Tuberculomas were supratentorial in 9 patients and infratentorial in 1. All but one patient had single lesions, which were located at the cortico-subcortical junction of the cerebral hemispheres and in the brainstem in 2 patients. 1 patient had a cerebellar tuberculoma. On MR intracranial tuberculoma caused prolongation of the T1 relaxation time which was most marked at the centre of the lesion. 5 patients had lesions hypointense to normal brain; 4 patients had lesions isointense and 1 patient had a mixed signal with hypointensity predominating on T1 weighted images. On the T2 weighted sequences the MR appearance varied. In six patients the centre of the lesion gave hypointense (dark) signal while the periphery gave a hyperintense (bright) signal relative to the brain parenchyma due to surrounding oedema. In 2 patients the centre of the lesion was hyperintense with a hypointense rim surrounded again by diffuse hyperintensity due to edema.

Follow up CT in 6 patients during the course of antituberculous drugs showed reduction in the six of the lesion as well as the oedema as a result of therapy. 2 patients positive biopsy while 2 patients were lost to follow up. Following contrast infusion in 6 patients ring enhancing lesions were observed in 4 patients, disc enhancing lesion size of less than 1 cm, 3 patients had lesion size of more then 2 cms while the lesion size varied between 1-2 cms in the rest of the 6 patients. 2 out of the 10 patients presented with meningitis, which shows diffuse thick meningeal contrast enhancement presumably due to granulation tissue. These 2 patients also had different degrees of hydrocephalus.


Discussion:

Tuberculomas develop in the brain when the initial Rich’s focus does not rupture into the meninges but expands locally within the parenchyma due to greater resistance of host tissues to the infecting organism (5). Meningitis can cause borderline encephalitis resulting in direct infiltration of the brain parenchyma and multiple small tuberculomas which coalesce to form mature tuberculomas – (16).

Tuberculomas have different appearances on T2 weighted images depending on their stage of evolution. At an early stage of formation of tuberculomas, an inflammatory reaction occurs; the mass has an abundance of giant cells and a capsule poor in collagen. At this stage the mass is isointense on T1 and T2 weighted images. At a later stage, the capsule becomes rich in collagen. When small tuberculomas coalesce to become larger lesions they give low signal on T2 weighted images because of fibrosis, scar tissue and free radicals produced by macrophages during active phagocytosis – (17).

22 of the 27 cases (84%) of NCS tuberculoma in the literature clearly showed low signal on T2 weighted images – (8, 18, 19, 20). 5 (16%) had lesions with central high signal thought to represent caseating pathologic examination revealed tuberculoma with dense reactive fibrosis.

In another study out of 97 patients presumed to harbour cerebral tuberculomas (of which 11 were confirmed by biopsy and 73 showed a therapeutic response to AKT) the lesions were either homogenously hypointense or revealed a central hyperintense nidus within the hypointense lesion on T2 weighted images (21).

Based on a histopathological grading of 7 proven tuberculomas, Gupta et al (22) concluded that the signal intensity on T2 weighted images is variable and dependant on the relative proportion of macrophages, cellular infiltrates and fibrosis. Granulomas, which were frankly hyperintense on T2 weighted images, exhibited increased cellular infiltrates, scantly macrophages and little fibrosis; while the hypointense lesions showed grater numbers of macrophages; more fibrosis and gliosis – (22). Large amounts of lipids were reported to contribute to the T2 shortening in 2 of the granulomas analysed by localized proton spectroscopy – (22). MR is of value to visualize the full extent of the lesion, in differentiation of the lesion with other diseases of the CNS (e.g. fungal granuloma, haemorrhagic metastases and “granulo-nodular” stage of neurocysticercosis) and to delineate the different components of the lesion (necrotic center, capsule and surrounding oedema), which is not always possible with CT.

References:
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2. Laitha VS, Marker FE, Dastur DK, tuberculosis of the Central Nervous System. Neurology (India) 1980; 28: 197-201.
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16. Dastur DK, (1983) Neurosurgically relevant aspects and pathognesis of intracranial and intraspinal tuberculomas. Neurosurg Rev. 6 : 103-110.
17. Chang KH, Han MH, Roh JK et al (1990): Gd-DTPA enhanced MR Imaging in intracranial tuberculosis. Neuroradiology 32: 19-25.
18. Gupta RK, Jena A, Sharma A, Guha DK (1988) MR imaging of intracranial tuberculoma, J. computer Assist Tomong. 121: 280-285.
19. Salgado P, Del Brutto OH, Talamas O, Zenteno MA, Rodriguez Carbajal J, Neuroradiology (1989) 31 : 299-302. Intracranial tuberculoma: MR imaging.
20. Dastur HM (1983) Diagnosis and neurosurgical treatment in tuberculous diseases of the CNS. Neurosurgery 6: 11-113.
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22. Gupta RK, Pandey B, Khan EM, Mittal P, Gujral RB, Chhabra DK. Intra cranial tuberculomas: MRI signal intensity correlation with histopathology and localized proton spectroscopy. Mag. Res. Imaging (1993), 11: 443-449.

HEAD & NECK NODAL IMAGING

Cervical Nodes

Variable size. Typically, as many as 75 nodes are located on each side of the neck. Nodes contain a sub capsular sinus below a prominent capsule, into which lymphatic fluid drains. This capsule is often the first site of metastatic growth. The fluid permeates into the substance of the node (composed of a cortex and a medulla) and exits through the hilum to enter more lymphatic vessels. These nodes are located between the superficial cervical and prevertebral fascia and, thus, are very amenable to surgical removal. The lymphatic fluid eventually enters the venous system at the junction of the internal jugular and subclavian veins. Many nodal descriptions exist today; Rouvière's is the classic model.

The occipital nodes are in the superficial group, which includes 3-5 nodes. This group of nodes is localized between the sternocleidomastoid (SCM) and trapezius muscles, at the apex of the posterior triangle. These nodes are superficial to the splenius capitis. The deep group includes 1-3 nodes. This group of nodes is located deep to the splenius capitis and follows the course of the occipital artery. These nodes drain the scalp, the posterior portion of the neck, and the deep muscular layers of the neck.

The postauricular nodes vary in number from 2 to 4; they are located in the fibrous portion of the superior attachment of the SCM muscle to the mastoid process. Postauricular nodes drain the posterior parietal scalp and the skin of the mastoid region.

The parotid nodes can be divided into intraglandular and extraglandular groups. The extraglandular parotid nodes are located outside but adjacent to the parotid gland, where they drain the frontolateral scalp and face, the anterior aspects of the auricle, the external auditory canal, and the buccal mucosa. Embryologically, the lymphatic system develops before the parotid gland, which surrounds the intraglandular nodes as it develops. The intraglandular nodes drain the same regions as the extraglandularnodes, to which they interconnect and then drain into the upper jugular group of lymph nodes. As many as 20 parotid nodes may be found.

The submandibular nodes are divided into 5 groups:

Preglandular, postglandular, prevascular, postvascular, and intracapsular. The preglandular and prevascular groups are located anterior to the submandibular gland and facial artery, respectively. The postglandular and postvascular groups are posterior to these structures. Differing from the parotid gland in embryological development, there is no true intraglandular node; however, occasionally, a node has been identified inside the capsule of the gland. The submandibular nodes drain the ipsilateral upper and lower lip, cheek, nose, nasal mucosa, medial

canthus, anterior gingiva, anterior tonsillar pillar, soft palate, anterior two thirds of the tongue, and submandibular gland. The efferent vessels drain into the internal jugular nodes. For the submental nodes, 2-8 nodes are located in the soft tissues of the submental triangle between the platysma and mylohyoid muscles. These nodes drain the mentum, the middle portion of the lower lip, the anterior gingiva, and the anterior third of the tongue. The efferent vessels draininto both the ipsilateral and contralateral submandibular nodes or into the internal jugular group.

The sublingual nodes are located along the collecting trunk of the tongue and sublingual gland and drain the anterior floor of the mouth and ventral surface of the tongue. These nodes subsequently drain into the submandibular or jugular group of nodes.

The retropharyngeal nodes are divided into a medial and lateral group, located between the pharynx and the prevertebral fascia. The lateral group, located at the level of the atlas near the internal carotid artery, consists of 1-3 nodes, which may extend to the skull base. The medial group extends inferiorly to the postcricoid level. This group drains the posterior region of the nasal cavity, sphenoid and ethmoid sinuses, hard and soft palates, Nasopharynx, and posterior pharynx down to the postcricoid area. Management of these nodes must be considered if any Malignancy arises from the mentioned drainage areas.

The anterior cervical nodes are divided into the anterior jugular chain and the juxtavisceral chain of nodes. The anterior jugular chain nodes follow the anterior jugular vein, located superficial to the strap muscles. These nodes drain the skin and muscles of the anterior portion of the neck, and the efferent vessels empty into the lower internal jugular nodes. The juxtavisceral nodes are separated into the prelaryngeal, parathyroid, pretracheal, and paratracheal nodes. Prelaryngeal nodes are located from the thyrohyoid membrane to the cricothyroid membrane and drain the larynx and the thyroid lobes. A single Delphian node is often found overlying the thyroid cartilage.

The pretracheal group consists of nodes between the isthmus of the thyroid gland down to the level of the innominate vein. Varying from 2-12 in number, these nodes drain the region of the thyroid gland and the trachea and receive afferent flow from the prelaryngeal group. The pretracheal efferents empty in the internal jugular group and the anterior superior mediastinal nodes.

The paratracheal nodes lie near the recurrent laryngeal nerve and drain the thyroid lobes, parathyroid glands, subglottic larynx, trachea, and upper esophagus. The efferent vessels travel to the lower jugular group or directly toward the junction of the internal jugular vein and theSubclavian vein. The anterior nodes drain bilaterally because the midline of the neck has no division. Treatment must be planned accordingly when a tumor is located in subjacent draining areas.

The lateral cervical nodes are divided into superficial and deep groups. The superficial group follows the external jugular vein and drains into either the internal jugular or transverse cervical nodes of the deep group. The deep group forms a triangle bordered by the internal jugular nodes,the spinal accessory nodes, and the transverse cervical nodes. The transverse cervical nodes, forming the base of the triangle, follow the transverse cervical vessels and may contain as many as 12 nodes. These nodes receive drainage from the spinal accessory group and from collecting trunks of the skin of the neck and upper chest. The spinal accessory chain follows the nerve of the same name and may account for as many as 20 nodes. This chain receives lymph from the occipital, postauricular, and suprascapular nodes and from the posterior aspect of the scalp, nape of the neck, lateral aspect of the neck, and the shoulder.

The internal jugular chain consists of a large system covering the anterior and lateral aspects of the internal jugular vein, extending broadly from the digastric muscle superiorly to the subclavian vein inferiorly. As many as 30 of these nodes may exist, and they have beenarbitrarily divided into upper, middle, and lower groups. The efferents of these nodes eventually pass into the venous system via the thoracic duct on the left and multiple lymphatic channels on the right. These nodes drain all the other groups mentioned. Direct efferents may be present from the nasal fossa, pharynx, tonsils, external and middle ear, Eustachian tube, tongue, palate, laryngopharynx, major salivary glands, thyroid, and parathyroid glands. Although fairly consistent, these drainage patterns are subject to alteration with malignant involvement or after radiotherapy. In such cases, rerouting is possible, with metastases arising in unusual sites.Metastases have also been shown to skip first-echelon nodes and manifest in the lower internal jugular group.

The most widely accepted terminology was originally described by a group of head and necksurgeons at Memorial Sloan-Kettering Hospital. This classification uses neck levels or zones and divides each side of the neck into 6 separate regions. Level I is bordered by the body of the mandible, anterior belly of the contralateral digastric muscle, and anterior and posterior bellies of the ipsilateral digastric muscle. Two nodal subgroups are found. The submental group (Ia) is found in the submental triangle (anterior belly of the digastric muscles and the hyoid bone), and the submandibular group (Ib) is found within the submandibular triangle (anterior and posterior bellies of the digastric muscle and the body of the mandible).

The nodes found in level II are located around the upper third of the internal jugular vein, extending from the level of the carotid bifurcation inferiorly to the skull base superiorly. The lateral boundary is formed by the posterior border of the SCM muscle; the medialboundary is formed by the stylohyoid muscle. Two subzones are also described; nodes located anterior to the spinal accessory nerve are part of level IIa, and those nodes posterior to the nerve are located in level IIb. The middle jugular lymph node group defines level III. Nodes are limited by the carotid bifurcation superiorly and the cricothyroid membrane inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. Level lV contains the lower jugular group and extends superiorly from the omohyoid muscle to the clavicle inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. The lymph nodes found in level V are contained in the posterior neck triangle, bordered anteriorly by the posterior border of the SCM muscle, posteriorly by the anterior border of the trapezius, and inferiorly by the clavicle. Level V includes the spinal accessory, transverse cervical, and supraclavicular nodal groups. Level VI lymph nodes are located in the anterior compartment. These nodes surround the middle visceral structures of the neck from the level of the hyoid superiorly to the suprasternal notch inferiorly.

Evaluating neck metastases based on physical examination findings has been the classic method for patients with new tumors in the head and neck. The single most important factor in determining prognosis is whether nodal metastasis is present. Survival rates decrease by 50% when nodal metastases are present. Furthermore, the presence of cervical adenopathy has been correlated with an increase in the rate of distant metastasis. During the clinical evaluation, carefully palpate the neck, with specific attention to location, size, firmness, and mobility of each node. Direct attention to nodes that appear fixed to underlying neurovascular structures or visceral organs or that demonstrate skin infiltration. The description of each node becomes an important part of the medical record, which can be used to assess the response to treatment or the progression of the disease.

Unfortunately, clinical palpation of the neck demonstrates a large variation of findings among various examiners. Although both inexpensive to perform and repeat, palpation findings are generally accepted as inaccurate. Both the sensitivity and specificity are in the range of 60-70%, depending on the tumor studied. Because of the known low sensitivity and specificity of palpation, a neck side without palpable metastases is at risk of harboring occult metastasis, with the risk determined by the characteristics of the primary tumor. The incidence of false-negative (occult) nodes based on physical examination findings varies in the literature from 16-60%. Before the introduction of diagnostic imaging, particularly CT scan, clinical palpation was shown to be inadequate for detecting cervical metastasis. Soko et al reported that only 28% of occult cervical metastases were found by clinical palpation. Martis reported a 38% prevalence of occult metastasis based on clinical examination findings

Debate persists over the relative merits of imaging in the evaluation of the neck for metastatic disease. Studies that correlate radiologic and histopathologic findings show that early microscopic metastases can be present in nodes smaller than 10 mm that demonstrate no stigmata of neoplasia (i.e., central necrosis, extracapsular spread). Evidence of early metastatic disease in clinically occult nodes is minimal and may evade the efforts of the pathologist and radiologist.

Ultrasound :

Ultrasound is reported superior to clinical palpation for detecting lymph nodes and metastases. The advantages of ultrasound over other imaging modalities are price, low patient burden, and possibilities for follow-up.

Sonographs of metastatic lymph node disease characteristically find enlargement with a spherical shape. Commonly, nodes are hypo echoic, with a loss of hilar definition. In cases of extranodal spread with infiltrative growth, the borders are poorly defined. Common findings of metastases from squamous cell carcinoma are extranodal spread and central necrosis together with liquid areas in the lymph nodes. Lymph node metastases from malignant melanoma and papillary thyroid carcinoma have a nonechoic appearance that mimics a cystic lesion. Sonography also is useful for assessing invasion of the carotid artery and jugular vein. Because lymph nodes of borderline size cannot be reliably diagnosed using ultrasound alone, ultrasound-guided fine-needle aspiration and cytologic examination of the nodes in question can be easily performed. The result of the aspirate examination depends on the skill of the ultrasonographer and the quality of the specimen (ie, harboring an adequate number of representative cells). Using this technique, most studies report that a sensitivity of up to 70% can be obtained for the N0 neck.

CT scans

Since its debut in the 1970s, CT scans have been an invaluable tool in all fields of medicine, including the evaluation of head and neck cancer. Since the advent of high-resolution systems and specific contrast media, fine-cut CT scanning has allowed the detection of pathological cervical nodes of smaller size that may be missed by clinical examination. CT scanning is now used routinely for the preoperative evaluation of the neck because, presumably, it helps decrease the incidence of occult cervical Lymphadenopathy. Introduced in 1998, multiple-spiral CT scanning promises further improvement of temporal and spatial resolution (in the longitudinal axis). This technique permits rapid scanning of large volumes of tissue during quiet breathing. The volumetric helical data permit optical multiplanar and 3-dimensional reconstructions. Improvement of the assessment of tumor spread and lymph node metastases in arbitrary oblique planes is another advantage of the spiral technique.

Criteria for the identification of questionable nodes are also evolving as technology advances. Central necrosis remains the most specific finding suggestive of nodal involvement, but its absence does not exclude metastasis. Unfortunately, metastasis is usually quite rare or not visible in small lymph nodes, where detection would be crucial. Because of the higher imaging resolution, various studies have reduced the traditional values of 10-15 mm for a node to be suggestive. Many authors have proposed a minimal axial diameter of 11 mm for the submandibular triangle and 10 mm for the rest of the neck. Other criteria include the presence of groups of 3 or more borderline nodes and the loss of tissue planes.

Magnetic resonance imaging

The value of MRI is its excellent soft tissue resolution. MRI has surpassed CT scanning as the preferred study in the evaluation of cancer at primary sites such as the base of the tongue and the salivary glands. The sensitivity of MRI exceeds that of clinical palpation in detecting occult cervical lymphadenopathy. Size, the presence of multiple nodes, and necrosis are criteria shared by CT scanning and MRI imaging protocols. Most reports indicate that CT scanning still has an edge over MRI for detecting cervical nodal involvement. Advances in MRI technology (eg, fast spin-echo imaging, fat suppression) have not yet surpassed the capacity of CT scanning to identify lymph nodes and to define nodal architecture. Central necrosis, as evaluated by unenhanced T1- and T2-weighted images, has been shown to provide an overall accuracy rate of 86-87% compared with CT scanning, which has an accuracy rate of 91-96%. The use of newerContrast media, especially supramagnetic contrast media agents, hopefully will improve the sensitivity of MRI.

Positron emission tomography and single-photon emission computed tomography

Some studies have demonstrated that positron emission tomography may be able to detect nodal metastases in lymph nodes that are negative for disease based on CT scan or MRI findings. Single-photon emission computed tomography imaging with fluorodeoxyglucose or thallium also reportedly detects nodal metastases. The use of positron emission tomography in combination with immunoimaging using monoclonal antibodies might further enhance accuracy.

None of the currently available imaging techniques can help depict small tumor deposits inside lymph nodes. Characteristics of metastatic lymph nodes that can be depicted are the size and presence of noncontrast-enhancing parts inside metastatic lymph nodes caused by tumor necrosis, tumor keratinization, or cystic areas inside the tumor. Only rarely does tumoral tissue enhance more than reactive lymph node tissue; in these rare cases, the tumor can be visualized within a reactive lymph node.

Patients who need an evaluation for a possible nodal malignancy require a comprehensive multidisciplinary evaluation of all potential sites of drainage to that node to identify its primary source. This includes a thorough evaluation of potential primary sites using endoscopic techniques. When appropriate, include laryngoscopy, esophagoscopy, bronchoscopy, and examination of the nasopharynx. If no primary source is identified, taking blind mucosal biopsy samples of the most likely head and neck subsites is essential. Complete documentation of nodal characteristics by clinical examination and palpation guide the examiner in using adjunctive radiological tools to exclude occult nodal metastasis

References:

Chen Z, Malhotra PS, Thomas GR, et al: Expression of proinflammatory and proangiogenic cytokines in patients with head and neck cancer. Clin Cancer Res 1999 Jun; 5(6): 1369-79[Medline].

Curtin HD, Ishwaran H, Mancuso AA, et al: Comparison of CT and MR imaging in staging of neck metastases. Radiology 1998 Apr; 207(1): 123-30[Medline].

Haor SP, Ng SH: Magnetic resonance imaging versus clinical palpation in evaluating cervical metastasis from head and neck cancer. Otolaryngol Head Neck Surg 2000 Sep; 123(3): 324-7[Medline].

Merritt RM, Williams MF, James TH, Porubsky ES: Detection of cervical metastasis. A meta-analysis comparing computed tomography with physical examination. Arch Otolaryngol Head Neck Surg 1997 Feb; 123(2): 9-52[Medline].

Safa AA, Tran LM, Rege S, et al: The role of positron emission tomography in occult primary head and neck cancers. Cancer J Sci Am 1999 Jul-Aug; 5(4): 214-8[Medline].

Southwick, HW, Slaughter, DP, Trevino, ET: Elective neck dissection for intraoral cancer. Arch Surg 1960; 80: 905-9.

Stacker SA, Caesar C, Baldwin ME, et al: VEGF-D promotes the metastatic spread of tumor cells via the lymphatics. Nat Med 2001 Feb; 7(2): 186-91[Medline].

Van den Brekel MW: Lymph node metastases: CT and MRI. Eur J Radiol 2000 Mar; 33(3): 230-8[Medline].

MAGING IN CEREBRAL VASCULAR PATHOLOGIES: EVOLUTION OF INTRACRANIAL HEMATOMA

IMAGING IN CEREBRAL VASCULAR PATHOLOGIES:

EVOLUTION OF INTRACRANIAL HEMATOMA

1. Immediate
- liquid with 95% O2 saturated Hb, T2 hyper, T1 iso within seconds platelets thrombi form & cells aggregate

2. Hyper acute stage -

4-6 hrs, fluid serum begins to disperse

Protein clot retracts, red cells become spherical,

Early peripheral edema begins, T2 iso, T1 iso

OxyHb is diamagnetic with no unpaired electrons,

CT - isodense for 1-3hrs, then becomes dense, 60-100HU

3. Acute stage
- 7-72 hrs, red cells begin to compact, deoxyhb

Central portion T2 hypo, T1 iso

DeoxyHb is paramagnetic with 4 unpaired electrons, T2 shortening

Sheilded from H2O by globin, prevents T1 shortening

No proton-electron relaxation enhancement can occur

Edema pronounced in periphery

Dense on CT, window width of 150-250 best

4. Subacute stage -

1-4 wks, methemoglobin starts day 4

Begins at periphery & progresses towards anoxic center

Cells begin to lyse at 1 week releasing metHb, decrease in edema

Perivascular inflammatory reaction begins with macrophage at periphery

Ring Enhancement caused by this process

T1 BRIGHT due to 5 unpaired electrons exposed by globin change

Proton-electron relaxation enhancement does occur

Periphery affected 1st, middle remains iso initially

T2 HYPO early when methemoglobin still in RBC

BRIGHT once the cell breaks down & Hb diluted in water

CT attenuation decreases approx 1.5HU per day

CT is NOT an accurate indicator of age, due to variable Hb etc

5. Early Chronic stage

- >4wks, edema & inflammatory reaction subside

Vascular proliferation encroaches on haematoma decreasing its size

Dilute uniform pool of extracellular metHb with vascular walls

Macrophage contain ferritin & hemosiderin at periphery

T2 hypo due to strong magnetic susceptibility

T1 iso due to fact that hemosiderin is water insoluble

Hypodense on CT unless rebleeding has occurred

6. Late Chronic stage -
cystic or collapsed with dense capsule

Vascular proliferation gradually forms fibrotic matrix with macrophage

Infants may resolve completely

Ferritin laden scar persists for years in adults

10% calc with residual hypodense focus in 40%

Gradient echo is helpful in detecting Haem in low field MRI's

OVERVIEW OF HEMORRHAGE CAUSES

Underlying cause often hidden by the bleed. Intraventricular extension associated with 10% mortality

1. Neonatal Hemorrhage - germinal matrix hemorrhage secondary to prematurity

thin walled, proliferating vessels in subependyma of lateral caudothalamic groove

involution occurs at 34 wks when all cells have migrated

No hemorrhage in utero or beyond first 28 days post birth

Grade I - Hemorrhage confined to germinal matrix, can be bilateral

Grade II - rupture into normal size ventricles

Grade III - intraventricular hemorrhage with Hydrocephalus

Grade IV - extension to adjacent hemispheric white matter

Can be seen by US in acute & subacute, lucent if chronic

Term Infants - Hemorrhage usually secondary to trauma, subdural mostly

Asphyxia & infarction most commonly in non-traumatic cases

Posterolateral lentiform nuclei & ventral thalamus most susceptible

2. Hypertension – Most common cause of nontraumatic bleed in adult

Lenticulostriate & Pontine vasculatures mostly involved, penetrating branches of MCA

Usually spontaneous in elderly patients, basal ganglia mostly

Vessels often abnormal, ruptured microanuerysms etc

50% have hemorrhage dissection into ventricles, poor prognosis

Lobar white matter hemorrhage in 20%, cerebellum 10%, midbrain & brainstem rare

Originates along perforating branches near dentate nuclei

Active bleeding usually lasts <1hr

Edema progresses for 24-48hrs, 25% die in this period

Hypertensive Encephalopathy - occurs secondary to elevated BP

Toxemia (Most common) - autoregulation overwhelmed especially in posterior aspect

Overdistention of arteriole leads to BBB breakdown

Reversible vasogenic edema results, frank hemorrhage rare

Cortical petechia & subcortical hemorrhage possible, especially in occipital regions

Increased T2 in external capsule & basal ganglia more common

Chronic renal Diseases, TTP, & Hemolytic-Uremic syndrome other causes

3. Hemorrhagic Infarction

Arterial Infarction - hemorrhage when endothelium reperfused

Occurs in 50%, but only seen in 10%, sensitivity: MRI>CT

Cortex & basal ganglia from MCA distribution most commonly, 24-48hrs later

Pseudolaminar Cortical Necrosis - generalized hypoxia

Middle layers usually effected, gyriform hemorrhage

Nonhemorrhagic ischemic changes can occur, gyri calcification possible

Venous Infarction - usually associated with dural sinus thrombosis

Dura around sinus will enhance, clot stays hypodense (empty delta sign)

More likely to effect white matter than cortex

4. Aneurysms - 90% of nontraumatic subarachnoid hemorrhage

Headache common presenting sign for aneurysm, CT best for acute SAH

Blood usually fills ambient cisterns & sylvian first

90% of blood cleared from CSF in 1wk

MRI better for subacute or chronic SAH, dirty CSF

Superficial siderosis - hemosiderin deposit on meninges

Cerebellum brainstem & cranial nerves also coated - neurological dysfunction

Giant aneurysms >2.5cm often have intramural hemorrhage

most from carotid, cavernous portion most common, all ages

75% have calc if thrombosed, none otherwise

Charcot-Bushard Aneurysm - secondary to HTN

5. Vascular Malformations -

AVM & Cavernous Angioma commonly

Most bleed into parenchyma rather than subarachnoid space

Arteriovenous Malformation - pial, dural or mixed, No cap bed

Pial AVM's - hemorrhage @ 2% per year, often in previously normal young pts

70% bleed by 1st exam, repeated hemorrhage can simulate neoplasm

Central nidus with gliosis & encephalomalacia

Dural AVM's - no central nidus, SAH or subdural

hemorrhage rare unless drainage through cortical veins

Cavernous Angioma - bleed @ .5% per year, freq repeated bleeds

Popcorn like with mixed signal foci & hemosiderin ring

Venous Angiomas - bleed rare, similar hematoma of other malformations

Medusa like collection of dilated medullary veins

Capillary Telangiectasias - usually small & clinically silent

may see multiple small foci of hemosiderin on T2

INTRACRANIAL ANEURYSMS & VASCULAR MALFORMATIONS

Charcot-Bushard Aneurysm - secondary to Hypertension

20% multiple, higher incidence in females.

Look for familial causes such as Polycystic Kid Disease

SACCULAR ANEURYSMS

Berrylike out pouching from arterial bifurcation

Include intima & adventitia, media ends with normal vessel

1. Etiology - hemodynamic induced injury, abnormal shear forces most commonly

Trauma, infection, tumor, drug abuse & AV malformations

Berry Aneurysms - associated with polycystic kidney Diseases & aortic coarctation

2. Incidence - 1% of angios & 5% of postmortems

Multiple in 20%, esp in females & polycystic kidney Diseases

Bilateral in 20%, esp at cavernous sinus, Pcom & MCA trifurcation

Occur age 40-60 unless traumatic or mycotic,

3. Associated Conditions - occur at anomalous vessels & AVM

Inc pressure ie HTN & aortic coarctation

Systemic Diseases - Marfan’s, fibromuscular dysplasia, polycystic kidney diaeases

4. Location - 30% at anterior communicating, 30% at posterior communicating, 20% MCA origin

10% in post circulation especially basilar artery bifurcation

traumatic or mycotic occur anywhere

5. Clinical Presentation - asymptomatic until rupture or giant >2.5cm

1-2% risk of rupture per year, 3.5% risk of surg

No different risk with HTN, age, sex or multiplicity

All should be repaired if >3yr life expectancy

Subarachnoid Hem - clinical grade by Hunt & Hess scale I-V

Vasospasm most common cause of morbidity, 30% die

highest bleed rate in 1st 24hrs, 50% rebleed in 2wk

CT - shows SAH in >80% of ruptured aneurysms

Cavernous sinus aneurysms can compress Nerves III-VI

TIA, Seizures & embolic ischaemia less common

Giant Aneurysms - most from supraclinoid carotid, all ages

Fibrous vascular walls, rarely rupture, Symptoms secondary to mass effect

Partially Thrombosed Aneurysms - 75% have curvilinear calcification

CT most specific for these with target seen

NO calc if not thrombosed

D/D - Meningioma, both erode sella & lat sphenoid

aneurysm has no associated hyperostosis or atherosclerosis

6. Appearance of Saccular Type - catheter angiography definitive

asses for relation to vessel, adjacent branches & vasospasm

essential in assessment of nontraumatic SAH

Thrombosed aneurysm will have no finding, 15%

may see mass effect if large

irregularity or local vasospasm can indicate rupture

D/D vascular loops & infundibuli (embryonic funnel <2mm)

CT may show bone erosion in long standing case

Patent aneurysms enhance intensely w contrast

Location of SAH can be prognostic indicator

Ambient cisterns anterior to brainstem probably just venous rupture

No repeat angio needed

Suprasellar cistern to lateral sylvian fissure

more aneurysmal pattern, must do F/U angio

MRI dependent on pattern of flow, turbulence & clot

may have wall enhancement with gadodiamide, laminated with thrombosis

7. Traumatic Aneurysm - <1%,>

nonpenetrating usually occur at skull base, or shear

hyperextention stretches ICA over lat C1

8. Mycotic Aneurysms - Secondary to infection of arterial wall, rare <10%

adventitia & muscularis disrupted, thoracic aorta commonly

Angio - occur dist to usual location, 2nd branch MCA commonly

most common cause of multiple MCA aneurysms

usually small, staph & strep most common, inc in child

bleed into parenchyma or SAH equal incidence

Medical Treatment usually sufficient to control, surgery if enlarge on angio

Mucor & Aspergilla invade direct from nasopharynx cause thrombosis & infarct more often than aneurysm

9. Oncotic Aneurysms - usually extra cranial, exsanguinate freq

tumor may implant or cause emboli, primary or metastatic

10. Flow-Related Aneurysms - seen with AVM's in 30%

distal ones most likely to hemorrhage

11. Vasculopathies - rare but seen with SLE, infarct & TIA commonly

Takayasu's Arteritis - 9:1 female, inflammation & stenosis most commonly

prox arch vessels, L subclavian commonly, often occludes

Fibromuscular Dysplasia - up to 50%, dissection & A-V fistula, 65% bilateral

Cocaine - 50% with CNS symptoms have SAH, may be secondary to HTN treatment

several drugs cause vasculitis .

FUSIFORM ANUERYSMS

Etiology - atherosclerosis, exaggerated arterial ectasia

media damaged, stretches & elongates, frequent mural thrombus

Vertebrobasilar Dolichoectasia - Common site, older patient

often thrombus producing brainstem infarcts

can also compress local stem causing nerve palsies

Imaging - enhances if patent, hyperintense if thrombosed

curvilinear calcification pathognomonic, may cause skull base erosion

DISSECTING ANEURYSMS

Etiology - intramural blood from tear in intima

may narrow or occlude lumen, may distend subadventitia

do not confuse with Pseudoaneurysm, a encapsulated hematoma

Presentation - usually extracranial unless severe trauma

Commonly in midcervical ICA & vertebral from C2 to skull base

Catheter angio remains procedure of choice for assesment

INTRACRANIAL VASCULAR MALFORMATIONS

1. Parenchymal AVM - congenital, dilated arteries & veins without capillary bed

98% solitary, multiple in Osler-Weber-Rendu & Wyburn-Mason

Incidence - 85% supratentorial, peak 20-40y, 25% children

Hemorrhage in 85% with 3% per year risk, seizure 25%, deficit 25%

Size not predictive, deeper & smaller ones bleed more

Parenchymal commonly, also common cause of SAH if <20yrs,>

Vascular Steal - atrophy due to vasculopathy of feeding vessel

atrophic low density regions & hematoma with high density

Overlying meninges thick & hemosiderin stained

Angio - shows feeding arteries & tortuous veins

often wedge shaped, possible to appear Normal if thrombosed

GBM may simulate but usually has tissue between vessels

10% have aneurysms in feeding arteries, can bleed

Cryptic AVM's - not seen by angio, 10%

CT - often absent w/o contrast, 25% have mild curvilinear calcification

mixed increased & decreased density if seen, Mild mass effect possible

Enlarged post venous sinuses but not cavernous sinus

Calcification seen in <1/3,>

MRI - honeycomb of flow voids, increased signal if thrombosed

hemorrhage in different stages often present

No significant intervening brain tissue, D/D : GBM

TX - resection if unruptured, must be completely removed

Aneurysms must be treated separately, increased risk for bleed

2. Dural AVM's & Fistulae - form within a venous sinus

no discrete nidus, multiple microfistulae, occluding sinus frequent

Follow recanulation of thrombosed sinus, 10% of all AVM's

Transverse or Sigmoid sinus commonly, Bruits & headache most common

Cavernous sinus AVM - proptosis, retro orbital pain, proptosis

SAH common if reflux flow forced into cortical veins

Carotid-Cavernous fistula related, follow trauma

Occipital & Meningeal branch of ext carotid #1 feeders

CT often N, MRI may show dilated cortical veins

3. Mixed - 15%, if parenchymal AVM recruits arteries from dural supply

4. Capillary Telangiectasias - multiple nests of dilated capillaries

Common in pons & Cerebellum, usually incidental

Gliosis of adjacent brain & hemosiderin staining from hem possibly

Cavernous Angiomas assoc or simply the extreme form

Osler-Weber-Rendu - hereditary hemorrhagic Telangiectasias

25% have brain abnormalities, most are true AVM's

Visceral angio dysplasia with scalp & mucous membrane telangiectasia

2nd most common lesion to venous angioma at autopsy

Not visualized by angio, may present with epistaxis

CT may faintly enhance, faint on MRI

5. Cavernous Angiomas - Hemangioma or cavernoma

Circumscribed nodule of honeycomb sinusoidal vascular spaces

separated by fibrous bands but no intervening neural tissue

frequently MULTIPLE HEMATOMAS at different stages, reticulated core of vessels

Supratentorial 80% but can occur anywhere, 50% multiple

Most Common vascular lesion identified, 20-40y/o

Seizure, deficits & bleed most common presenting features

Angio does NOT visualize, possible faint blush in early venous

CT shows freq Calc, variable enhancement, can simulate neoplasm

MRI - popcorn like appearance on T2 due to multiple hem

multiple areas of signal drop-out due to hemosiderin

VENOUS MALFORMATIONS

1. Venous Angioma - dilated anomalous veins converge on central vein

Etiology - remnant embryonic venous system, usually solitary

assoc with migrational abnormalities & cavernous Angiomas in 30%

Asymptomatic, Hemorrhage very rare unless from associated cavernous angioma

CT - may show linear tuft of vessels post contrast

located in deep White Matter of cortex or Cerebellum, commonly adjacent to frontal horn

MRI - shows stellate tributary veins into prominent collector vein

gliosis or hemorrhage seen in only 15%

Angio - the only vascular malformation with a single draining vein

Medusa head appearance on venous phase of angio

2. Vein of Galen Aneurysm - enlargement of Galenic system

Secondary to arteriovenous fistulae from choroidal arteries

AVM in thalmus or midbrain can also cause this

Present at birth with high-out put cardiac failure, cranial bruit +

Macrocephaly with obstructive hydrocephalus, deficits & ocular symptoms

US shows bi-directional flow in vein of Galen

Angio demonstrates either choroidal artery or thalmoperforating feeder

dilation to venous varix with or without distal stenosis

if stenosed distally will often thrombose

CT - large enhancing midline mass posterior to 3rd ventricle

Hydrocephalus frequent but hemorrhage rare

enhancing serpentine vessels in thalamic region

3. Venous varix - assoc with several intracranial vascular abnormalities

Enlarged & thin veins resulting in SAH, hydrocephalus & increased ICP

Sinus Pericranii - venous haemangioma adherent to outer skull, deep to galea

supplied from intracranial sinus & blood returns to sinus

present with enlarging fluctuant soft tissue mass, enlarge with crying

often secondary to trauma, often resolved with prolonged compression

Frontal commonly, parietal next, most near sagittal sinus, can be very lateral

Skull Film - usually sharp margins, vascular honeycombs possible

CT - shows strong uniform enhancement

MRI - well delineated ovoid or fusiform areas w variable signal

Venous Cavernoma - subcutaneous lesions of scalp

blood supply from external carotid, drain to external jugular

4. Orbital Venous Varix - rare vascular malformation in orbit

Causes intermittent proptosis & diplopia with valsalva & bending over

Disappear completely with axial views, use tourniquet on jugular vein

NEONATAL HEMORRAGE

Caudothalamic groove - between head of caudate & thalamus

both make up lateral wall of lateral ventricle, terminates in Monroe

Foramen of Monroe - divides frontal & body portions of ventricles

thalmus entirely posterior, caudate head anterior, choroid enters it

1. Subependymal Hemorrhage - preterm infants <32wks

Correlates with size of germinal matrix at birth, largest 24-32wks

involutes & is absent by 40wks, last in inferior lateral wall of frontal

lies inferior to ependyma, superior to head of caudate & anterior to thalmus

Usually occurs in first 3 days, always by 7-8 days

Grade 0 – Normal

Grade I - Subependymal alone

Grade II - intraventricular with no ventriculomegaly

Grade III - Hydrocephalus,

Grade IV - intraparenchymal

grade does not predict ultimate outcome, may progress

Serial studies required, only applies to germinal matrix hemorrhage

2. Parenchymal Hemorrhage - extends farther lateral than germinal matrix

can be "grade IV", but not all secondary to germinal matrix bleed

most extend from SHE(Subependymal haemorrhage) to frontal or parietal lobes

Hypoxia & Hypercapnia implicated as etiology

stress causes vessels to dilate & burst

Phase 1 - echogenic like SEH for 1-2wks

Phase 2 - central Hypoechoic, bright peripheral rim 2-4wks

Phase 3 - retracts & settles into dependent position

Phase 4 - necrosis & phagocytosis complete, encephalomalacia

Cerebellar hematoma best scaned in coronal behind ear

assoc with mortality of 50%.

3. Choroidal Hemorrhage - usually grade II or III

Second cause of intraventricular hemorrhage not caused by SEH

Difficult to discern from normal choroid on US

asym scanning can show marked asym in choroid size

isolated choroid hematoma simulates ventricular hematoma with no hydrocephalus

Myelomeningocele assoc with pedunculated choroid

CT more reliable than US for Dx

D/D - Choroid Papilloma, very rare, consider if CSF clear on tap

all assoc with hydrocephalus, enhance intensely on CT

HEMORRHAGIC NEOPLASMS & CYSTS

1. Malignancy Related Coagulopathy - esp with leukemia & chemotherapy

systemic neoplasms can be assoc with term coagulopathy

2. Intratumoral Hematomas - 10%, malignant , Astrocytoma’s are most common.

Neovascularity, central necrosis, plasminogen activators etc contribute

Heterogeneous, incomplete hemosiderin ring, edema persist

multiple lesions & min edema suggests nonneoplastic cause

Cysts & slow growing cystic neoplasm like cranio rarely bleed

Oligodendroglioma, neuroectodermal & teratoma hemorrhage frequently

Ependymoma & choroid tumors - frequent SAH & hemosiderosis

Pituitary Adenoma - may bleed more frequently than astrocytoma

Lymphoma rarely bleed unless with AIDS

Renal cell Ca, chorio Ca, melanoma, thyroid & lung mets, 15%

3. Nonneoplastic Hemorrhagic Cysts -rare, colloid cysts never bleed

Rathke cleft cysts & Arachnoid cysts more commonly bleed

Arachnoid cysts bleed secondary to trauma, bridging vessels rupture

sometimes assoc with subdural hematoma

MISCELLANEOUS CAUSES OF BENIGN INTRACRANIAL HEMORRHAGE

1. Amyloid Angiopathy – Most common cause of bleed in elderly patient with no HTN

nonbranching fibrillar protiens form beta-pleated sheets

Deposit is Cortical & leptomeningeal vessels

extend from small vessels to brain parenchyma

Contractile elements replaced by the crystals

Multiple hematomas frequent & occurs at cortico medullary junction

basal ganglia & brainstem not affected

2. Infection & vasculitis - rare, increased chance if immuncompromised

septic emboli - mycotic aneurysms & hemorrhagic infarct

10% of Infective endocarditis have SAH or parenchymal

Aspergillosis & other fungi directly invade vessel

Thrombosis, infarction & hem result

Herpes Simplex II - the only encephalitis assoc with hematoma

3. Recreational Drugs - 50% have preexisting AVM or aneurysm

Cocaine can induce an acute hypertensive episode, vasospasm

also enhances platelet aggregation, dural sinus thrombosis

amphetamine & PCP also associated with hemorrhage

endothelial damage & necrotizing vasculitis

4. Blood Dyscrasias & Coagulopathies - iatrogenic or acquired

Vit K deficiency, hepatocellular diseases, antibody against clot, DIC

Anticoagulants, thrombolytics, aspirin, Etoh abuse, chemo

15% of all intracranial hemorrhage on anticoagulants

Supratentorial, intraparenchymal bleeds most common

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