Basic MR imaging

Tissue Signal Characteristics

Signal in MR images is high or low (bright or dark), depending on the pulse sequence used, and the type of tissue in the image region of interest. The following is a general guide to how tissue appears on T1- or T2- weighted images.

Dark on T1-weighted image:

• Increased water, as in edema, tumor, infarction, inflammation, infection, hemorrhage
• (hyperacute or chronic)
• Low proton density, calcification
•   Flow void

Bright on T1-weighted image:

• Fat
• Subacute hemorrhage
• Melanin
• Protein-rich fluid
• Slowly flowing blood
• Paramagnetic substances: gadolinium, manganese, copper
• Calcification (rarely)
• Laminar necrosis of cerebral infarction

Bright on T2-weighted image:

• Increased water, as in edema, tumor, infarction, inflammation, infection, subdural collection
• Methemoglobin (extracellular) in subacute hemorrhage

Dark on T2-weighted image:

·

• Low proton density, calcification, fibrous tissue
• Paramagnetic substances: deoxyhemoglobin, methemoglobin (intracellular), iron, ferritin,
• hemosiderin, melanin
• Protein-rich fluid
• Flow void

MR signal sources

When protons are placed in a magnetic field, they oscillate.The frequency at which they oscillate depends on the strength of the magnetic field. Protons are capable of absorbing energy if exposed to electromagnetic energy at the  frequency of oscillation. After they absorb energy, the nuclei release or reradiate this energy so that they return to their initial state of equilibrium. This reradiation or transmission of energy by the nuclei as they return to their initial state is what is observed as the MRI signal.

The return of the nuclei to their equilibrium state does not take place instantaneously, but rather takes place over some time. 

The return of the nuclei to their initial state is governed by two physical processes: 

o    The relaxation back to equilibrium of the component of the nuclear magnetization which is parallel to the magnetic field, and

o    The relaxation back to equilibrium of the component of the nuclear magnetization which is perpendicular to the magnetic field.

The time that it takes for these two relaxation processes to take place is roughly equal to:

o    Time T1 for the first process, and

o    Time T2 for the second process.

The strength of the MRI signal depends primarily on three parameters. 

o    Density of protons in a tissue: The greater the density of protons, the larger the signal will be.

o    T1

o    T2

The contrast between brain tissues is dependent upon how these 3 parameters differ between tissues. For most "soft" tissues in the body, the proton density is very homogeneous and therefore does not contribute in a major way to signal differences seen in an image.

However, T1 and T2 can be dramatically different for different soft tissues, and these parameters are responsible for the major contrast between soft tissues.

T1 and T2 are strongly influenced by the viscosity or rigidity of a tissue. Generally speaking, the greater the viscosity and rigidity, the smaller the value for T1 and T2.

It is possible to manipulate the MR signal by changing the way in which the nuclei are initially subjected to electromagnetic energy. This manipulation can change the dependence of the observed signal on the three parameters: proton density, T1 and T2.

Hence, one has a number of different MR imaging techniques ("weightings") to choose from, which accentuate some properties and not others.

Neuroimaging

A simplified tabulation of tissue image characteristics:

Normal Tissue 

1. Bright means high signal intensity, dark means low, and interm. means intermediate.

2. Bright means high density/high attenuation of X-rays, dark means low.

3. Grey matter appears grey, white matter white.

Abnormal Tissue

1. Blood brain barrier leak. For MR, gadolinium; for CT, iodinated contrast material.

2. Unless very fresh or very old.

3. Unless calcified.

4. Often isodense.

ECG Rhythm Interpretation-How to Analyze a Rhythm

Objectives

•          To recognize the normal rhythm of the heart - “Normal Sinus Rhythm.”

•          To recognize the 13 most common rhythm disturbances.

•          To recognize an acute myocardial infarction on a 12-lead ECG.

Steps in Analyzing a ECG rhythem

•          ECG Basics

•          How to Analyze a Rhythm

•          Normal Sinus Rhythm

•          Heart Arrhythmias

•          Diagnosing a Myocardial Infarction

•          Advanced 12-Lead Interpretation

Rhythm Analysis

•          Step 1:  Calculate rate.

•          Step 2:  Determine regularity.

•          Step 3:  Assess the P waves.

•          Step 4:  Determine PR interval.

•          Step 5:  Determine QRS duration.

Step 1:Calculate rate.

Option 1

•          Count the # of R waves in a 6 second rhythm strip, then multiply by 10.

•          Reminder: all rhythm strips in the Modules are 6 seconds in length.

Interpretation- 9 x 10 = 90 bpm

Option 2

–        Find a R wave that lands on a bold line.

–        Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc.

Step 2:  Determine regularity.

•          Look at the R-R distances (using a caliper or markings on a pen or paper).

•          Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular?

Interpretation-Regular

Step 3: Assess the P waves

•          Are there P waves?

•          Do the P waves all look alike?

•          Do the P waves occur at a regular rate?

•          Is there one P wave before each QRS?

Interpretation- Normal P waves with 1 P wave for every QRS

Step 4: Determine PR interval

•          Normal: 0.12 - 0.20 seconds.(3 - 5 boxes)

Interpretation-0.12 seconds

Step 5: QRS duration

•          Normal: 0.04 - 0.12 seconds. (1 - 3 boxes)

Interpretation-0.08 seconds

Rhythm Summary

•          Rate                                                     90-95 bpm          

•          Regularity                                          regular

•          P waves                                               normal

•          PR interval                                         0.12 s

•          QRS duration                                     0.08 s

Interpretation-Normal sinus rhythem

Denture sore mouth (DSM) and Papillary hyperplasia (PH)

DESCRIPTION:  Long treated as separate entities, there is evidence that PH and DSM may be different expressions of the same disease. Both are related to the wearing of dentures. The mildest form of denture sore mouth appears as small, localized and asymptomatic red spots on the posterior palatal mucosa. As the condition worsens, large confluent areas turn crimson red (Fig. 1) . This is the classic form of DSM. In later stages, hyperplasia of palatal mucosa occurs and produces the red, pebbly appearances of papillary hyperplasia (Fig. 2). In some cases of PH, the mucosa has a more mossy than mulberry appearance and the hyperplasia is not apparent until a gentle blast of air opens the crevices revealing the papillary nature of the lesion. Whether or not DSM.

ETIOLOGY:  The cause is unknown but there is evidence that Candida albicans is at least contributory. DSM has been called chronic atrophic candidiasis. Organisms are found more often in PH and DSM than in normal controls. Treatment with the antifungal drugs such as nystatin, clotrimazole and fluconazole have been reported to bring about remission in most cases, especially in DSM. Since organisms have been shown to colonize the tissue surface of the denture, sterilization of the denture with fungicide is indicated.

Factors other than Candida albicans seem to be involved, but it is difficult to assess the role of denture trauma and bacterial pathogens. Because the disease is limited to the area covered by the denture, it is often assumed that the patient is allergic to denture base material.. There is little evidence to support his view. Patients with palatal lesions ordinarily do not have lesions under the lower denture as would be expected if the patient were truly allergic. 

TREATMENT: We know of no effective therapy other than fungicides such as nystatin, clotrimazole, ketoconazole or fluconazole in the usual doses for oral candidiasis. Good oral and denture hygiene may help. The denture should fit well and not be worn at night. In cases of excessively redundant papillary hyperplasia, surgical reduction may provide a better denture base.

PROGNOSIS:  The condition is benign. For many years, papillary hyperplasia had the undeserved reputation of being pre-malignant. It is not.

DIFFERENTIAL DIAGNOSIS:  The disease has such a characteristic appearance that diagnosis is seldom a problem.

Aphthous stomatitis (Canker sores, recurrent aphthous stomatitis, RAS)

DESCRIPTION:   This is one of the most common oral diseases. The exact incidence is unknown, but estimates range from 20% to 60% of the population. Lesions appear as painful ulcers ranging in size from less than 1 mm to 2 centimeters. They may be single or multiple. Small lesions (less than 0.5 cm) have been referred to as minor aphthae (Fig. 1) and large lesions (more than 0.5 cm) have been called major aphthae (Fig. 2).

An uncommon presentation of this disease appears as multiple, pinpoint areas of ulceration that seldom exceed 1 mm (Fig. 3). This has been referred to as the herpetiform pattern, an unfortunate terms since herpes virus is not the cause.

Each lesion begins as a red macule, less often a papule but not as a blister. It soon ulcerates and the ulcer becomes covered by a pyogenic membrane producing the characteristic yellow-white center with surrounding erythematous flare. The shape is usually round to oval but may be elongated in natural folds such as the vestibule.

Aphthous stomatitis occurs on freely movable mucosa that does not overlie bone. The lips, cheeks, soft palate, floor of mouth, ventral and lateral tongue are often involved but attached gingival, hard palate and dorsal tongue are seldom affected.

Aphthous lesions affect all age groups from young to old but young adults and females are more affected. Elapsed time between recurrences is extremely variable; some unfortunate patients have almost continuous disease whereas others go from months to years between episodes.

ETIOLOGY:  The cause is unknown. The concept that canker sores are caused by a microbiologic agent has been superceded by theories revolving around an immunopathogenesis. The deposition of antibodies and complement within epithelium and basement membrane during the early stages of the disease suggests a humoral immune response, and the  influx  of  lymphocytes  rather  than  neutrophils  in  early  lesions  points  to  a  cellular immune reaction as well. It is yet to be learned if the immune response is directed against self (autoimmunity) or against an extrinsic antigen such as bacteria or viruses. To further cloud the issue, a variety of other factors have been implicated.

Withdrawal of certain foods such as cheese, tomato products and gluten, as well as sodium lauryl sulfate-containing tooth pastes, has been claimed to help some patients whereas in others, correction of iron, B12 and folate deficiencies have brought about a cure. Improvement of aphthous lesions during the last stages of pregnancy with exacerbation after delivery suggests that gonadal hormones may lay a role. The occurrence of canker sores during menstruation also suggests a hormonal basis. To add a final element of mystery, aphthous stomatitis has been reported to worsen when cigarette smoking is discontinued. There are too many theories for them all to be correct. Aphthous stomatitis may not be a single disease with a single cause but instead a variety of diseases all manifested by painful mouth sores.

TREATMENT:   To reduce pain, patients with few lesions may be treated with topical medications such as Orabase  ® with Benzocaine, Zilactin ®, or Soothe-N-Seal  ®. Anti-inflammatory agents such as topical steroids or Aphthasol  ® have also been shown to be effective. For severe or widespread disease, systemic prednisone such as a Medrol 4 mg Dosepak  ® is helpful. Long-term systemic steroid therapy may be associated with numerous adverse effects, including osteoporosis, asceptic necrosis, cataracts, depression, fluid retention and exacerbation of diabetes.

PROGNOSIS:  Cure is seldom achieved but palliation and long-term remission may be achieved by above mentioned treatment. Without treatment, healing time varies from 4 days for a small lesion to a month or more for major aphthae. Major aphthae may also cause scarring.

DIFFERENTIAL DIAGNOSIS:  Aphthous stomatitis must be differentiated from herpetic stomatitis, the disease with which it is most often confused. Recurrent intraoral herpes occurs almost exclusively on mucosa overlying bone. The hard palate is the most common site. Lesions indistinguishable from aphthous stomatitis have been reported in Behcet's syndrome, Reiter's syndrome, Crohn's disease and celiac disease.

Herpes simplex virus infections

DESCRIPTION:   

Oral infection with herpes simplex virus occurs in three clinical forms. The most common type consists of recurrent small blisters on the lips commonly referred to as fever blisters or secondary herpes labialis. The second type is a generalized oral infection called primary herpetic stomatitis. The third and least common form of oral herpes infection consist of small ulcers usually localized on palatal mucosa.

Herpes labialis is illustration in Figs. 1 and 2. This lesion is well known and unlikely to be  a  diagnostic  problem.  It  tends  to  be  a  recurrent  disease  in  teenagers  and  adults. Elapsed time between recurrences varies from person to person. Recurrences are thought to be triggered by exposure to sunlight, febrile diseases, physical and psychogenic trauma, and other irritants.

Generalized involvement of the oral mucous membrane is called primary herpetic stomatitis and represents the initial exposure to the virus. This is a one time infection, but the patient remains susceptible to recurrent or secondary oral herpes infections (Figs. 3 and 4).

  It  is  more  commonly  seen  in  children,  but  teenagers  and  adults  are  also  affected.

Patients initially have gingivitis with swollen and red gingiva, then small blisters may appear on other mucosal surfaces. The blisters break quickly and are seldom seen by the dentist or physician. After they break, the lesions appear as small ulcers that resemble small aphthous lesions. The primary, generalized infection is accompanied by fever, cervical lymphadenitis, and inability to eat or drink without considerable pain. Patients who suffer recurrent intraoral herpes are few. Recurrent intraoral herpes infections  tend  to  occur  as  vesicles  followed  by  small  ulcers,  mainly  on  the  hard  palate mucosa (Fig. 5) and often follow trauma to the area, such as palatal injections or periodontal therapy.

ETIOLOGY:  

Herpesvirus hominis (herpes simplex virus). Most oral lesions are caused by Type I virus but approximately 10% are thought to be caused by Type II.

TREATMENT:   

Antiviral drugs such as Acyclovir, Famciclovir, Penciclovir, Valacyclovir and over-the-counter Abreva have all shown that they can decrease the time of disease as well as help with pain management. To be beneficial, they must be started at the first sign of disease. Most studies indicate that the drugs decrease the duration of disease by about one day. Acyclovir, Penciclovir and Abreva are available in a topical ointment.

PROGNOSIS:     

Primary  infection  usually  resolves  in  10-14  days.  Once  the  virus  has entered the body, it travels through nerve trunks to the nearest ganglion where it may lie dormant  for  the  remainder  of  the  patient's  life.  Future  recurrences  are  thought  to  be brought about by the "reawakening" of the virus which retraces its steps to cause new lesions in the same general area as the original point of entry. Thus, each recurrence is not a new and different infection from the outside but a recrudescence of the original infection. The ability of the virus to remain latent in deep ganglia makes total eradication almost impossible and will likely frustrate attempts at prevention for the foreseeable future.

Patients with widespread herpetic stomatitis should drink liquids to prevent dehydration. A broad-spectrum antibiotic is commonly given to control secondary bacterial infection, but does not shorten the viral infection. Antiviral drugs may shorten the duration of the disease if they are started early.

Clinicians should be aware that the herpesvirus may cause disseminated infection including encephalitis in which case the prognosis is extremely grave.

DIFFERENTIAL DIAGNOSIS:   

Primary herpetic stomatitis may resemble oral lesions of erythema multiforme, but herpes can be diagnosed by exfoliative cytology.A characteristic multinucleated cell appears in the smear of herpes infections. Culture of the virus is possible if a viral laboratory is available. Lesions of herpangina and hand, foot and mouth disease, both caused by Coxsackievirus, may clinically resemble oral herpes virus infections. Recurrent intraoral herpes may be confused with herpes zoster. Aphthous can be differentiated since it usually does not occur over bone, does not form vesicles and is not accompanied by fever or gingivitis.