A Few Thoughts Before You Go...

The start of your clinical rotations provides you with an opportunity to finally get involved with patient care and begin in earnest the process of becoming a doctor. You'll be amazed at the speed with which you move from outsider to functioning participant amidst the swirl of activity that is clinical medicine. It is, unfortunately, quite easy to lose your sense of perspective while working in this very intense environment. In fact, you'll recognize this as a common problem among many in the medical field. A few things to think about before you get started (and perhaps refer back to as you make your journey):

1. Treat patients as you would want yourself or a family member to be cared for. This should cover not only the technical aspects of health care but also the quality and nature of your interpersonal interactions.

2. Try to avoid viewing the medical training process as a means to an end. As medical education is a life long undertaking, you've got to enjoy the journey. If not, stop and think why.

3. Do the right thing. This applies to patient care and your dealings with colleagues and other health care workers. If something feels wrong, it probably is! The rules which govern your behavior in the world outside of medicine still apply, regardless of what others say or how they might act! This can be challenging, particularly when you are fatigued, in a subordinate position or working with others who don't have the same interests.

4. Mistakes will happen. The oft referred to: "Primum Non Nocere (first do no harm)" probably sets an unreasonable expectation. You will all do harm to someone at various points in your careers. Those who claim otherwise have either not taken care of enough patients or are not being truthful. We are all human and thus all fallible. When errors occur, acknowledge them, discuss them with colleagues and the patient, make efforts to correct the fall out, and move on. Above all, try to learn from what happened and don't allow yourself to forget any relevant lessons (without at the same time torturing yourself unnecessarily). This should help you to maintain a healthy dose of humility and become a better doctor. Remember also that anyone can be a genius in retrospect. Using this information in a manner that promotes education and growth requires a sensitive touch.

5. Never be afraid to ask questions. If those that you are currently working with are unreceptive, make use of other resources (e.g. house staff, students, nurses, health care technicians, staff physicians). You can learn something from anyone.

6. There is no substitute for being thorough in your efforts to care for patients. Performing a good examination and obtaining an accurate history takes a certain amount of time, regardless of your level of experience or ability. In addition, get in the habit of checking the primary data yourself, obtaining hard copies of outside studies, mining the old records for information, re-questioning patients when the story is unclear, and in general being tenacious in your pursuit of clinically relevant material. While this dogged search for answers is not too sexy, it is the cornerstone of good care.

7. Learn from your patients. In particular, those with chronic or unusual diseases will likely know more about their illnesses then you. Find out how their diagnosis was made, therapies that have worked or failed, disease progression, reasons for frustration or gratitude with the health care system, etc. Realize also that patients and their stories are frequently more interesting then the diseases that inhabit their bodies.

8. Become involved (within reason) in all aspects of patient care. Look at the x-ray, examine the sputum, talk with the radiologist, watch the echo being performed. This will allow you to learn more and gain insight into a particular illness/disease state that would not be well conveyed by simply reading the formal report. It will also give you an appreciation for tests and their limitations. Caring for patients is not a spectator sport. As an active participant in the health care process (rather then simply a scribe who documents events as they occur) you will not only help deliver better medical care but will also find the process to be more rewarding and enjoyable.

9. Follow up on patients that you care for in the ER, are transferred to other services, seen by sub-specialists or discharged from the hospital. This should give you a better sense of the natural history of some disease processes and allow you to confirm (or adjust) your clinical suspicions. This is particularly relevant today as patients are shuttled through the system with great speed, affording us only snap shot views of what may be complex clinical courses.

10. Keep your eyes open for other interesting things that might be going on elsewhere in the hospital/clinic. If there is a patient on another service with an interesting finding, go over and investigate, assuming it doesn't interfere with your other responsibilities and is OK with the patient and their providers. This will give you the opportunity to expand your internal library of what is both normal and abnormal.

11. Pay particular attention when things don't seem to add up. Chances are someone (you, the patient, the consultant) is missing something, a clue that the matter needs further investigation. Challege yourself and those around you by continually asking "Why... ?"

12. Before deciding that another provider is an "idiot" for adopting what seems an unorthodox or inappropriate clinical approach, assume that it is you that are short some important historical data. Give others the benefit of the doubt until you've had an opportunity to fully explore all the relevant information. And in those instances when it becomes apparent that mismanagement has occurred, focus on communication and education rather then derision and condescension.

13. Become comfortable with the phrases, "I don't know" and "I need help."

14. Try to read something medical every day. This will help you to stay abreast of new developments and provide an opportunity to become reacquainted with things that you've learned and forgotten. Medicine is less about achieving mastery then it is about reinforcing old lessons. Our individual "knowledge tanks" leak information on a daily basis. There is no way to plug the hole. Instead, you must continually replenish by adding to the top.

15. Realize that, ultimately, you are responsible for you. The quality of care that you provide is a direct result of the time and effort that you invest in the process. The distinction between good and bad medicine is generally not a function of oversight by the patient, colleagues, or the legal system. For the most part, it's dependent on your willingness to push and police yourself.

16. You are not automatically endowed with the historical wisdom of a particular institution merely by walking through its doors. Nor does this knowledge necessarily arrive with your white coat, degree or other advanced title. Rather, this is something that's learned and earned, often on a daily basis.

17. Every once in a while, push yourself to become an expert in something. First hand knowledge is a powerful tool, one that is available to anyone willing to take the time to read through the primary data. Become informed by delving into the original literature pertaining to a particular subject. You may find that the data is robust and the rationale for a clinical approach or treatment well grounded. As frequently, I suspect you'll find instances where the data is rather shaky, and the best path not as clear as guidelines or expert opinion might suggest.

18. Be kind... to others and yourself.

19. Have fun! Remember why you went into medicine. Keep this first and foremost in your mind and periodically readjust your course so that this is always in your sites.

There is magic in medicine. It does not, however, derive solely from technology, testing, or diagnostic aptitude. Rather it more often comes from your interactions with patients, a touch on the sleeve, sitting at the bedside and treating them (if only for a few minutes) as a fellow human being and not as, "That guy with Lupus." You are all capable, right now, without additional training, of being magicians. The challenge lies in not losing track of this as you make your way in the coming years.

Clinical Decision Making

Clinical decision making is the process by which we determine who needs what, when. While not exactly arbitrary, this exercise can be quite subjective. Each clinician compiles their own data (hence the emphasis on learning to perform an accurate H&P) and then constructs an argument for a particular disease state based on their interpretation of the "facts." The strength of their case will depend on the way in which they gather and assemble information. There may then be no single, right way of applying diagnostic and therapeutic strategies to a particular case. Of course, not every situation is a clinical quandary. A patient with a known history of coronary artery disease presenting with 3 hours of crushing chest pain, an EKG with 4mm ST segment elevations across the precordial leads, and an initial Troponin-I of 50 is having a myocardial infarction. That is a diagnostic slam dunk. More commonly, however, there exist elements of uncertainty. Medicine involves playing the odds, assessing the relative chance that a patient is/is not suffering from a particular illness. Codifying the way in which clinicians logically approach problems and deal with this uncertainty is a difficult task. What follows is my take on diagnostic and therapeutic decision making. It incorporates the following series of questions in a more or less step-wise fashion:

1. Does this particular clinical situation, on the basis of the H&P, seem familiar to me (i.e. does it fit any pattern of disease that I have seen/read about)? Is there a single answer which explains even a multitude of complaints/findings? Referred to as Occam's Razor this, in essence, is the search for the simplest possible explanation.
2. What other explanations exist? This is known as the "differential." Rather then long, it should be logical. The list is arranged from most to least likely and highlights those conditions that I absolutely do not want to miss (i.e. conditions that would result in significant morbidity/mortality if not promptly identified). When searching for explanations, remember that common things occur commonly. While patients do contract unusual illnesses, these are rather rare events. Thus, strange symptoms and findings are still more likely to represent an uncommon presentation of a common problem then to be due to an altogether uncommon illness. I didn't make this up, but have found it to be a clinical truism. However, fear not Great Lupus Hunters, unusual illnesses do occur. Simply make sure that you really rule out the more run-of-the-mill stuff first!
3. What (if anything) do I need to do to rule out the "really bad things" and how quickly does this need to be done? Can it be achieved as an outpatient or will hospitalization be required? This type of evaluation frequently produces a list of things that the patient does not have without ever reaching a definitive diagnosis, which is quite acceptable.
4. Of the remaining potential explanations, do I need to make use of additional tests or am I comfortable enough with the available information to make a presumptive diagnosis and proceed on that basis alone?

   Note: A test should only be obtained if the result will in some way affect your decision making. That is, if you are going to embark on a particular strategy regardless of the results, why obtain it in the first place? Furthermore, if you don't understand the operating characteristics of a test (e.g. it's sensitivity and specificity and thus how the results will affect your view of the candidate diagnosis), don't order it.

5. If the diagnosis is still unclear, can I use the passage of time as a diagnostic test (i.e. perhaps with time the process will more closely resemble a pattern of disease that will be recognizable to me� or simply fade away without explanation)? I like to think of every patient as living on their own curve, with "wellness" measured along the Y axis, and time on the X axis. Curves, of course, cannot be plotted on the basis of a single point. Similarly, it may take several observations separated by time before I can begin to determine a patient's clinical direction (i.e. getting better, worse or staying the same).
6. Does this condition require specific therapy? If so, do I first need to have an established diagnosis (see above)? Can the patient wait for this diagnosis to be made before initiating treatment or does their clinical situation mandate the beginning of empirical therapy while a diagnosis is simultaneously being sought? Can the treatment be administered as an outpatient or will it require hospitalization (either because of its complexity, compliance issues, patient's compromised clinical condition, need to assess efficacy on a frequent basis, etc.)? What will I do if the treatment fails to have the desired effect?
7. Is the patient on board with this plan? Do they understand the rationale for the approach that I have chosen as well as their role?

Elements of uncertainty are wound into almost every case that you will see. Students and the public are surprised (and perhaps disappointed) to learn that, despite the abundance of technology that currently exists, physicians are still "reduced" to using their judgment when making clinical decisions (e.g. is a cold viral or bacterial? Should antibiotics be administered or withheld? etc.). The trick lies in knowing when its OK to be parsimonious with the use of testing and which situations demand a no-holds-barred pursuit of an answer. Lets look at a few examples:

Case 1: A 24 year old otherwise healthy male presents with a 3 day history of cough productive of green sputum, fever, chills and slight shortness of breath associated with right sided chest pain. Exam is remarkable for a temperature of 102 F with otherwise normal vital signs. The patient looks well (i.e. not distressed). A few crackles are noted in the right base on lung exam. No other abnormalities are apparent.

Discussion: Following the above question template, we can reason through the case as follows:

1 & 2: This clinical situation seems most consistent with a well compensated bacterial pneumonia. Other possibilities might include:

viral infection
asthma flair
pulmonary embolism (P.E.)
other

Each, however, either cannot explain all of the findings present or is not supported by the objective data. A viral infection, for example shouldn't cause a focal lung exam; asthma can cause a cough and shortness of breath, but wheezing should be present; while a pulmonary embolism can cause shortness of breath, cough and chest pain, it should not result in fever, chills or sputum production. Furthermore, P.E.s generally occur in patient's who have risk factors for this illness, none of which were present in this case. "Other" includes the list of unlikely diagnoses (e.g. eosinophilic pneumonitis, histoplasmosis, malignancy etc.) that would only be considered if the patient's course deviated markedly from expected and/or could not be explained on the basis of those things higher on the differential.

3&4: Many clinicians would feel comfortable enough at this point (based on their clinical impression) to proceed without obtaining any additional tests to either support the candidate diagnosis or rule out other possibilities. Other approaches would also be acceptable. For example, another clinician may have seen a similar case in the past, treated the patient for a bacterial process, and found out later that they had actually had a P.E. Because of this experience, they might be uncomfortable proceeding without first obtaining a CXR (to confirm the presence of an infiltrate), CBC (to identify a leukocytosis c/w a bacterial infection), D-Dimer (clot breakdown product elevated in DVTs/PEs), and an EKG (to look for stigmata of a P.E.). This approach would not necessarily be incorrect. It's driven by a particular provider's anecdotal experience, which for obvious reasons has a powerful impact on future decision making. This is generally helpful, as long as it is based on logic and not fear. You might then wonder, "Why not obtain confirmatory tests whenever possible?" Remember, tests come at a cost (in terms of dollars, time and patient discomfort). You need to be able to justify, at least in your own mind if not that of the insurance company, the expense. Furthermore, the expected value of any test is dependent on the situation in which it is being applied. In general, as few tests in medicine have 100% sensitivity and specificity (i.e. correctly identify those with and without disease all of the time), the likelihood that a result is correct is dependent on how strongly you already feel about the candidate diagnosis. That is, if you are certain that someone is suffering from a particular disease (on the basis of history, exam and other findings) and you order an additional test "just to make sure" then the results of the test aren't likely to have a significant impact on your decision making (i.e. if it confirms your suspicions, so what; if it conflicts, you'll ignore it, treating the result as a false negative). The same principles apply in the reverse situation (i.e. if you are certain that someone does not have a particular illness). Tests have their greatest value when applied to situations where you're truly on the fence about a particular diagnosis. An in depth discussion of this subject can be found in any text under Baysean Analysis.

5: In this setting, I would probably not be comfortable waiting for the process to "play out" any further without initiating therapy. Bacterial processes tend to worsen unless they are treated, even in otherwise healthy 23 year olds.

6: Therapy in this case could be initiated on an outpatient basis with an antibiotic directed against Strep and H. Flu, the pathogens most commonly associated with respiratory infections in this age group. Treatment would last for a total of 7 days (a somewhat arbitrary number) and the patient instructed to return for re-evaluation on the last day of therapy to insure that the infection was completely treated and that the antibiotics could be discontinued. In addition, they would be told to contact me if they felt worse. If this, in fact, occurred I would have to consider why things did not go as I had anticipated. Did the patient have an atypical infection (e.g. Legionellosis)? Were they non-compliant with medications? Had they developed a complication (e.g. empyema)? Were they suffering from a particularly virulent strain of bacterium? Or was the initial diagnosis (e.g. infectious process) correct in the first place? The only way to make this determination (and catch the rare zebra) would be through re-evaluation of the patient, applying additional tests in a logical and ordered fashion.

Example 2, by design, is a bit more murky.

Case 2: A 55 year old male with history of Chronic Obstructive Pulmonary Disease (COPD), Coronary Artery Disease (CAD), and past Pulmonary Embolism (P.E.) presents with several hours of chest pain radiating to his left arm associated with shortness of breath and diaphoresis. This is somewhat reminiscent of his past myocardial infarction, but is also similar to past admissions for COPD and his P.E.�. he's just not sure. Exam is remarkable for a pale gentleman who looks quite distressed, sweating profusely. Vital signs remarkable for Temp 99 P 110 BP 180/100 RR 30 Sat 91%. JVP is at 8cm. Lung exam is remarkable for diffuse wheezing. Patient has bilateral lower extremity edema (1+ to the mid shin) with the right leg slightly more swollen then the left, which he says has been present since his DVT and subsequent PE several years ago.

Discussion: We will approach this case in the same way as the previous example.

1&2: An exacerbation of any of this patient's underlying conditions could explain his presentation. On the basis of the history and examination, recurrent cardiac ischemia, a flair of his COPD or another P.E. are all possible. Additionally, this could represent new Congestive Heart Failure (CHF), perhaps associated with ongoing cardiac ischemia. Although he has never had this before, I know that CHF tends to occur in patients with CAD (which this patient does have) and can cause a clinical picture similar to that presented above. A bacterial infection (either bronchitis or pneumonia) is usually accompanied by additional symptoms (e.g. fever, chills, sputum production), but remains a possibility, particularly as I know that COPD flairs usually occur in association with such an infection. Bringing up the rear would be "other" which would include, but not be restricted to, the initial presentation of a lung cancer or a pneumothorax. These processes do occur in patients with COPD but tend to present with other exam/historical findings (e.g. malignancy is often associated with weeks-to-months of weakness, fatigue, weight loss and a focal lung exam; pneumothorax causes decreased/absent breath sounds on the affected side). Ordering these possibilities from most to least likely, I would put coronary ischemia/CHF and P.E. 1 and 2, followed by COPD flair, pneumonia and "other." In this case, I am impressed by the acuity of the presentation, which has increased my suspicion for the first 2 processes. The others, however, remain reasonable diagnostic possibilities which cannot be ruled out on a clinical basis.

3&4: All of the above conditions carry significant morbidity and/or mortality. In addition, treatment strategies for each are quite different, and may themselves carry risk. Anti-coagulation with heparin, for example, would be useful in patients with PEs but has no role in the treatment of a COPD flair, and would unnecessarily expose the patient to the risk of bleeding. There is also a sense of urgency that surrounds the need to make the diagnosis and begin treatment as:

1. the patient appears ill, with clear potential for further deterioration
2. some of the treatments are only effective if applied within a narrow window of opportunity (e.g. thrombolytics can open an occluded coronary artery and save downstream myocardium only if they are given soon after the onset of ischemia).

The following tests, essentially performed simultaneously, are necessary in order to rapidly make a diagnosis:

1. EKG� to assess for evidence of acute myocardial infarction or stigmata of PE
2. CXR� to evaluate for signs of CHF, PE, infiltrate� will also identity pneumothorax or evidence of malignancy
3. CBC� to asses for anemia which could be a precipitant for cardiac ischemia or shortness of breath; might also suggest a bacterial process if the white blood cell count is elevated.
4. Chem 7 (includes electrolytes, BUN, Creatinine, Glucose)� might be helpful in determination of volume status; also useful if patient will need diuretic therapy if diagnosed with CHF.
5. Arterial Blood Gas� to define Alveolar-arterial gradient and degree of gas exchange abnormality
6. CK-MB, Cardiac Troponins� will be elevated if patient has suffered a myocardial infarction.
7. D-Dimer...elevated in cases of DVT/PE
8. BNP (B-type naturetic peptide)...elevated in cases of CHF

The test results are as follows:
EKG remarkable for sinus tachycardia at 110, non-specific ST segment changes in the inferior and precordial leads.
CXR consistent with moderate emphysema; no evidence infection, pneumothorax or malignancy; ? upper zone vascular redistribution consistent with CHF
Chem 7 and cardiac enzymes all normal.
CBC� mildly elevated White Blood Cell Count (14 thousand) with normal differential; normal hematocrit
ABG� PO2 50, PCO2 30, PH 7.5� c/w hypoxemia and acute respiratory alkalosis
D-Dimer...600 (moderately elevated)
BNP 300 (mildly elevated)

The diagnosis still remains in doubt. The data does not support an acute myocardial infarction, though unstable angina without myocardial necrosis is still a possibility. There is nothing to suggest a pneumonia, pneumothorax or malignancy, which we thought were unlikely. I would now re-order my differential, placing pulmonary embolism at the top followed by COPD exacerbation, CHF and unstable angina. I still need to press on and make use of additional tests in order to identify the correct diagnosis and institute appropriate therapy. In this case I would obtain a radiologic test known as a CT-angiogram of the chest to assess for evidence of a pulmonary embolism. If this were negative, I would then be left with a diagnosis of COPD, CHF or unstable angina. Further treatment would be based on the clinical course, response to therapy, and if, in fact, there were any additional means of distinguishing between these possibilities.

5&6: Because this patient is rather ill, treatment should occur in concert with the diagnostic evaluation and would include:

1. Oxygen: The patient is hypoxemic and would benefit from oxygen, regardless of the underlying cause.
2. Heparin: As it may take some time before the CT scan is performed, I would elect to begin therapy with heparin while waiting to obtain the study. This decision is based on my high clinical suspicion that the patient has had an embolous. Because he already appears pretty sick and compromised, I would be uncomfortable withholding therapy that could prevent additional (and perhaps catastrophic) emboli. Furthermore, anti-coagulation would also be used as first-line treatment for unstable angina, which is #2 on my differential. Only in the setting of COPD flair (#3) would heparin be inappropriate. In this case, I have decided that the potential benefit of heparin out weighs the short term risk of bleeding.
3. Aerosolized Albuterol (a beta-2 agonist): I would also give the patient a breathing treatment with nebulized albuterol to see if it relieved any of his bronchospasm.
4. Lasix: This would help improve hypoxemia in the event that some component of the patient's illness is caused by CHF. While I have no way of knowing definitively that he does have pulmonary edema and would therefore benefit from diuresis, there are few other therapeutic options that would have a rapid, dramatic impact on his gas exchange. He certainly does not appear intravascularly depleted, a situation where Lasix would be dangerous. By my calculations then, the potential benefits of this treatment outweigh its risks.
5. Steroids: Another therapeutic option would be to give him a dose of intravenous steroids for his possible COPD. A single dose of steroids has little downside. I also know that it takes a while (at least several hours) to have an effect. Thus, particularly if it will take some time to get the V/Q scan, I would probably opt to initiate steroid therapy, which could always be discontinued if the results were consistent with a P.E.
6. Antibiotics: Since COPD remains high on my list, and COPD flairs are most frequently precipitated by bacterial infections, it's logical to treat for this potential problem as well.

Thrombolytics are not indicated. Nor would I initiate therapy with any of the more potent platelet inhibiting agents (the 2a/3b receptor antagonists), as these carry a higher risk of bleeding (at least until that point when unstable angina was more clearly the leading diagnosis). As additional data became available, I would need to continually re-evaluate all of these decisions.

There are a few themes that are common to both cases and help guide decision making in general:

1. Patient substrate along with the clarity of presentation will have a significant impact on our willingness to accept clinical uncertainty. Healthy patients who present with "classic" complaints/findings can generally be managed comfortably on the basis of data acquired from the H&P alone. These patients have significant physiologic reserves and can tolerate incorrect treatments/diagnoses, affording us the opportunity to redirect our efforts in the event of a diagnostic/therapeutic misstep without having them suffer significantly. As patients accrue baseline illnesses, however, there is a marked increase in "background chatter," making it difficult to pinpoint the etiology of an illness solely on the basis of the history and physical. Furthermore, the patient's ability to tolerate additional insults becomes quite limited. Thus, we become both less capable of making diagnoses on clinical grounds alone and less comfortable proceeding without the utilization of diagnostic tests. That is, our willingness to accept uncertainty diminishes dramatically.
2. Therapies that carry significant risk are generally reserved for more serious illnesses. They are administered only when there is some reasonable certainty that the patient is suffering from the disease or are doing so poorly that it's felt to be worth the risk. Treatments that carry less risk are initiated with relative impunity, although obviously even these options have downsides.
3. Patients with significant baseline organ dysfunction often have little reserve and therefore tolerate additional insults poorly. This imparts a sense of urgency to the process which is generally absent when caring for healthier patients. While tests are being obtained to define the nature/extent of a clinical problem, empirical therapies directed against several of the most likely illnesses are initiated in an effort to prevent further deterioration. If no tests are available that can accurately distinguish between several diagnoses, a number of different therapeutic strategies may be pursued in parallel. These patients frequently require very close monitoring (i.e. in-hospital treatment) so that appropriate adjustments can be made and clinical down-turns rapidly addressed. This everything-but-the-kitchen-sink mentality is certainly less appealing and elegant then focused therapy where interventions are initiated individually, enabling the clinician to clearly gauge their efficacy and minimize any associated therapeutic risk. Unfortunately, it is often impossible to identify the exact limb of the system that is broken, forcing the use of multi-modality approaches.
4. Clinicians listen, ask, examine and then try to use the information obtained to put patients into known diagnostic categories. The differential diagnosis is a list of these possibilities and can be thought of as a group of boxes of various shapes and sizes. The quantity and variety of these containers is a function of the way in which providers combine historical information and exam findings with clinical experience and their understanding of pathophysiology. Frequently there is an imperfect fit between what we find and what we know. Instead of trying to cram patients into ill suited spaces we should recognize that these instances indicate a need to either expand our knowledge base, change our approach to a patient's complaint, or gather additional data. Remember also that there is no shame in admitting that we can't explain a particular finding or symptom. In fact, knowing what something is not has as much value as providing a specific label for a complaint or condition.
5. Clinical decision making is based on the expectation that the human body will respond to illness in a predictable way. Disease states which alter this behavior wreak havoc on logical decision making. Illnesses which decrease normal immune function (e.g. HIV infection), medications that blunt the response to infection (e.g. steroids, chemotherapy), or advanced age (which frequently leads to an impaired physiologic response to stress) are a few examples. When caring for these patients, providers are forced to cast a wide net, relying on the initiation of empirical therapies while multiple diagnostic avenues are pursued.
6. There will always be some element of non-modifiable uncertainty in clinical medicine (unless, of course, someone actually invents Star Trek-type Tricordors!). Technological advances have succeeded in improving both diagnostic and therapeutic accuracy. However, they are almost never correct all of the time. Reliance on the less-then-perfect information that these tests provide without in some way taking into account clinical judgment can have serious consequences for the patient.

The Oral Presentation

The purpose of the oral presentation is to provide other clinicians with patient information. This must be done in such a way that it tells the patient's story in a logical, clear and complete fashion yet is neither cumbersome nor too long. It is a difficult skill to master and is made more complicated by the fact that different clinical situations demand different types of presentations. For example, presentations given during morning work rounds (the time when the medical team briefly visits with each patient to review their clinical course and determine the plan for the day), are not the same as those given at formal patient management conferences. The first situation requires a focused presentation, with emphasis placed on reviewing new facts and data (e.g. test results, vital signs, changes in clinical course, etc.) and outlining the care plan. The second example calls for a much more detailed discussion. The presenter, then, must take into account the "environmental" factors which determine the type of presentation that is required. These include:

1. The audience to which you are presenting. A group of cardiologists, for example, are going to be most interested in the cardiac history.
2. The purpose of the presentation (e.g. is it for work rounds, teaching conference, clinic etc.?).
3. Time available to give the presentation. The longest, most complete presentation should take no longer then 5-7 minutes while shortened versions can be given in as little as 15 to 30 seconds.
4. Your familiarity with the case as well as associated pathophysiology.

For the purposes of this discussion, we will focus on the formal/complete presentation as it is probably the form which is most complicated and intimidating. You will find, however, that once you grasp the logic and organization of this process and have an opportunity to practice, your presentations will become both more effective and less anxiety provoking. Tips for presenting during work rounds are provided in the "Inpatient Medicine" section of the Clinical Guide.

In the discussion that follows, illustrative examples are frequently included and have been set off from the text by means of quotation marks and italics.

The Formal Presentation

Chief Complaint/Chief Concern:
The presentation begins with a one sentence description of the patient and the reason prompting their evaluation (i.e. the Chief Complaint). This is a teaser that sets the tone for the information to follow. It should not be too inclusive.

"Mr. H is a 50 year old male with AIDS who presents for the evaluation of fever, chills and a cough over the past 3 days."

History of Present Illness (HPI):
The HPI is presented in both a problem based and chronological fashion. That is, the dominant problem/complaint serves as the centerpiece of the history. If there is more then one problem, the presenter may try to link them together when appropriate. Information related to this main theme is presented in chronological order. This requires that the presenter go back far enough in time to cover any historical data that is relevant to the patient's main complaint. Your ability as a presenter to know which past information is important and which superfluous will be based on both your clinical experience and understanding of pathophysiology. At the current time, this might be quite limited. For the above patient, a thorough description would include:

"Mr. H has been HIV + since 1987; his CD4 count in June of '97was 150 and viral load approximately 50,000. Past opportunistic infections have included: PCP pneumonia 12/95; CMV retinitis 1/96; and Kaposi's Sarcoma first noted on his skin 1/96. He currently takes 3TC, AZT, and Indinavir, all of which he has been receiving for approximately one year. He also takes Bactrim Single Strength tablets on a daily basis, along with Fluconazole troches PRN for thrush. He claims to be 100% compliant with all of his medication. He is homosexual though he is currently not sexually active. He has never used intravenous drugs."

This information is not, in a strict sense, part of the present illness. However, it providescritical information that will have a direct bearing on the listener's interpretation of this patient's active problem. Your ability to determine which background to incorporate into your HPI will improve with time and exposure. The details of the patient's acute problem are then presented:

"Until 1 week ago, Mr. H had been quite active, walking up to 2 miles a day without feeling short of breath. Approximately 1 week ago, he began to feel dyspneic with moderate activity. This progressed to the point that, 1 day ago, he was breathless after walking up a single flight of stairs. 3 days ago, he began to develop subjective fevers and chills along with a cough productive of rust-colored sputum. There was associated nausea but no vomiting. He has spent most of the last 24 hours in bed. He denies head ache, photophobia, stiff neck, focal weakness, chest pain, hemoptysis, abdominal pain, diarrhea or other complaints. There is no know history of asthma, COPD or chronic pulmonary condition. His current problem seems different to him then his past episode of PCP."

This section documents the course of the patient's most active problem. It concludes with a list of "pertinent negatives" that are meant to exclude, on the basis of history, other possible diagnoses that are known to have a similar symptom complex. In a patient with an HIV related illness, this review might actually be much more extensive than that provided above due to the diffuse, multi-organ system involvement that occurs with this disease. Note that the patient's baseline functional status is described, allowing the listener to gain some sense of the degree of impairment caused by the acute medical problem. If a patient is a poor historian, confused or simply unaware of all the details related to their illness, state this and move on. Historical information can be obtained from family, friends, etc. If this is the case, make sure that you note the source.

If, for example, a patient complains of both chest pain and shortness of breath, they may well be secondary to a single underlying process such as myocardial ischemia resulting in heart failure. When the problems are completely unrelated, the "dominant issue" (as determined by the presenter) is treated first, followed by a discussion of the secondary complaint. This can get quite complicated when multiple problems exist in parallel.

Review of Systems: The critical positive and negative findings discovered during a review of systems are generally incorporated at the end of the patient's history, as was done above. These questions are designed to uncover illnesses which might "travel with" the main problem and attempt to identify commonly occurring complications (e.g. hemoptysis can be a sequelae of pulmonary infection). The listener needs this information to help them put the remainder of the history in appropriate perspective. Any positive responses to a more inclusive ROS that covers all of the other various organ systems are then noted. The extent to which this is repeated is left to the discretion of the presenter. If it is completely negative, it is generally acceptable to simply state, "ROS negative."

Past Medical History: Note is made of any other past medical problems which the patient has that are not related to the current complaint. Those items mentioned above are not repeated.

"The patient's past medical history includes:

1. Hypertension x 10 years
2. Gastro-Esophageal Reflux Disease
3. Degenerative Joint Disease of the Right Knee"

Past Surgical History: Any prior surgeries (along with the year in which they occurred) are noted.

"Past surgical history is remarkable for:

1. Status Post Cholycystectomy 1990
2. Status Post Appendectomy 1985
3. Status Post open repair and internal fixation of left femur fracture, 1983"

Medications/Allergies: All current medications (along with dose, route and frequency) are mentioned:

"The patient takes the following medications:

AZT 300 mg, 1 PO, BID
Indinavir 750 mg, 2 PO, TID
3TC 150 mg, 1 PO, BID
Lansoprazole 20 mg, 1 PO, BID
Lopressor 50 mg, 2 PO, BID
Clotrimazole Troches 100 mg, 1 PO TID PRN
Naprosyn 250 mg, 1-2, PO, BID PRN
He has no allergies"

Smoking and Alcohol (and any other substance abuse): Cigarettes and alcohol are highlighted because their use is so widespread and the deleterious effects associated with prolonged exposure well documented. Any additional substance abuse (e.g. cocaine use, intravenous drugs, etc.) should also be mentioned.

"Mr. H smokes 1 pack of cigarettes per day and has done so for 20 years. He drinks approximately 1 glass of wine per week. He denies any other drug use."

Social/Work History: This includes a brief description of the patient's work and home environments. Sexual history, if relevant to the oral presentation would also be presented here. Any unusual work-related exposures should be noted.

"Mr. H works as an accountant for a large firm in Boston. He lives alone in an apartment in the city."

Family History: Emphasis is placed on the identification of illnesses within the family (particularly among first degree relatives) that are known to be genetically based and therefore potentially inherited by the patient. This would include: history of coronary artery disease, diabetes, certain neoplasms, etc.

"Both of the patient's parents are alive and well (his mother is 78 and father 80). He has 2 brothers, one 45 and the other 55, who are also healthy. There is no family history of heart disease or cancer."

Physical Exam: This begins with a one sentence description of the patient's appearance along with their vital signs. In general, only '+' findings are noted. It is also reasonable to mention the absence of certain things that the listener will find helpful in excluding particular diagnoses. If, for example, a patient has shortness of breath secondary to asthma, the presenter might mention that rales, elevated jugular venous pressure and an S3 were not present, indicating that congestive heart failure is an unlikely diagnosis. Some listeners expect the entire physical examination to be recounted, including "normal findings," particularly if the presenter is a student. The following exam is listed in more detail then is necessary. However, it should give you an idea of how abnormalities as well as "normal findings" are reported.

"Mr. H was seated on a gurney in the ER, breathing comfortably through a face mask oxygen delivery system. Breathing was unlabored and accessory muscles were not in use.

• Vital signs were: Temp 102 Pulse 90 BP 150/90 Respiratory Rate 20 O2 Sat (on 40% Face Mask) 95%
• Head, Eyes, Ears, Nose, Throat: Pupils equal, round and reactive to light; Tympanic membranes pearly gray with cone of light well seen; Sclera anicteric; No thrush was noted; Mucosa was dry and without lesions; There was no appreciable adenopathy; Thyroid non-palpable; JVP was less then 5 cm.
• Lungs: Crackles and Bronchial breath sounds noted at right base. E to A changes present. No wheezing or other abnormal sounds noted over any other area of the lung. Dullness to percussion and increased fremitus was also appreciated at the right base.
• Cardiac: Rhythm was Regular. Normal S1 and S2. No murmurs or extra heart sounds noted.
• Abdomen: Symmetric appearing; soft, flat, non-tender; no palpable masses; well healed Right upper and lower quadrant incisions at sites of prior apppendectomy and cholycystectomy.
• Rectal Exam: Brown stool in rectal vault, guiac negative; no masses; prostate small, smooth and non-tender.
• GU: Testes descended bilaterally; no masses; no hernia; penis without lesions.
• Extremities: No evidence of clubbing, cyanosis or edema; Dorsalis Pedis and Posterior Tibial pulses 2+ and equal bilaterally.
• Skin: a 2x3 cm raised, purplish, non-tender, non-blanching area noted on left mid-shin; no other skin abnormalities identified.
• Neurologic Exam:

  Mental Status: Awake, alert, appropriate and completely oriented.
  Cranial Nerves: 2 thru 12 tested and intact.
  Motor: Strength 5/5 all extremities.
  Cerebellar: Finger to nose well done.
  Reflexes: 2+ at ankles, knees, biceps and triceps
  Sensation: Intact to light touch and pin prick bilaterally; proprioception normal; vibration normal.
  Ambulation: Normal gait; negative Romberg."

Lab results, Radiological Studies, EKGs: In general, only lab values which are abnormal are mentioned. Similarly, if the interpretation of radiological studies and EKGs are directly relevant to the case, they are discussed.

"Mr. H's lab work was remarkable for: White count of 18 thousand with 10% bands; Normal Chem 7 and LFTs. Room air blood gas: pH of 7.45/ PO2 of 55/PCO2 of 30. Sputum gram stain remarkable for an abundance of polys along with gram positive diplococci. CXR showed a dense right lower lobe infiltrate without effusion."

Impression and Plan: This is your opportunity to summarize the important aspects of the history, physical exam and supporting lab tests and formulate a differential diagnosis as well as a plan of action that addresses both the diagnostic and therapeutic approach to the patient's problems.

"Mr. H is an HIV + male with a low CD 4 count and high viral load who presents with an acute pulmonary process. The rapid progression, focality of findings on lung exam and radiography, along with the sputum gram stain suggest a bacterial infection, in particular Streptococcal pneumonia. Other pathogens to consider include H Flu and, less commonly, Legionella. While he is certainly at risk for PCP, his presentation, compliance with PCP prophylaxis and statement that his current illness seems different then past PCP infection would argue against this as the etiologic agent. Mycobacterial infection also seems unlikely. Viral infections and neoplastic processes like CMV or Kaposi's Sarcoma of the lung do not generally give this clinical presentation. Furthermore, the data does not support the existence of either a primary cardiac or noninfectious pulmonary process.
The Current plan then is:

1. Follow up on cultures of sputum and blood.
2. Obtain sputum for silver staining to r/o PCP
3. Begin treatment with IV cefuroxime; Hold off on empiric treatment for PCP.
4. Continue O2,with goal to keep sats greater then 92%
5. IV fluid replacement with Normal Saline at 125cc/H for next 24 hours to correct mild hypovolemia, with plan to reassess volume status at that time
6. If patient does not show improvement (or worsens) and cultures are unrevealing, consider bronchoscopy as a means of making more definitive diagnosis."

A Few Practical Tips:

1. Practice, Practice, Practice. Mastering the oral presentation takes time and experience. This will not occur overnight. Early on in your careers, try to avoid presenting "on-the-fly" as it is obviously quite difficult to rapidly assimilate all of the relevant data and present it in a clear and cogent fashion. It's O.K. to use notes, though with practice and experience, this will eventually become unnecessary.

2. Prior to presenting, think about what sort of picture you are trying to paint and then practice (while at home, walking to the hospital, in front of friends, etc.) doing this. Ask yourself and those listening to you whether the information that you have provided is in synch with the impression that you are trying to create. Are your listeners able to generate an accurate mental image along with a reasonable list of diagnostic possibilities?

3. Listen to others when they present. Try to identify which elements distinguish concise presentations from those that are confusing or ineffective.

4. Think about the clinical situation in which you are presenting so that you can provide a summary that is consistent with the expectations of your audience. Work rounds, for example, are clearly different from conferences and therefore mandate a different style of presentation. Some services, in particular, general surgery and surgical sub-specialties, have very regimented presentation formats that are used for all patients. This is driven by the time constraints and high patient volumes seen on these services. Alternatively, some listeners demand that the presenter, particularly if that person is a student, recount the history in exquisite detail. They may, for example, expect you to list the entire physical exam, including both normal and abnormal findings, as well as the results of an extensive ROS. The only way for you to know what is expected is to ask beforehand.

5. Try to be thorough without at the same time being long-winded or too detail oriented. Knowing what constitutes the "right amount" of relevant information will obviously take some practice and experience.

6. Ask for feedback from your listeners. This will allow you to correct errors and improve subsequent presentations.

Write Ups

The written History and Physical (H&P) serves several purposes:

1. It is an important reference document that gives concise information about a patient's history and exam findings at the time of admission. In addition, it outlines a plan for addressing the issues which prompted the hospitalization/visit. This information should be presented in a logical fashion that prominently features all data immediately relevant to the patient's condition.
2. It is a means of communicating information to all providers who are involved in the care of a particular patient.
3. It allows students and house staff an opportunity to demonstrate their ability to accumulate historical and examination based information, make use of their medical fund of knowledge, and derive a logical plan of attack.
4. It is an important medical-legal document.

The H&P is not:

1. An instrument designed to torture Medical Students and Interns.
2. Meant to cover unrelated bits of historical information.
3. Should neither require the killing of more then one tree nor the use of more then one pen to write!

Knowing what to include and what to leave out will be largely dependent on experience and your understanding of illness and pathophysiology. If, for example, you were unaware that chest pain is commonly associated with coronary artery disease, you would be unlikely to mention other coronary risk-factors when writing the history. Until you gain experience, your write-ups will be somewhat poorly focused. Not to worry; this will change with time and exposure. Several sample student write-ups can be found at the end of this section.

Chief Complaint or Chief Concern (CC):
One sentence that covers the dominant reason(s) for hospitalization. While this has traditionally been referred to as the Chief Complaint, Chief Concern may be a better description as it is perhaps less pejorative/confrontational sounding.

"Mr. Smith is a 70 year old male admitted for evaluation of increasing chest pain."

History of Present Illness (HPI):
The HPI should provide enough information without being too inclusive. Traditionally, this covers all events leading to the patient's arrival in the ER (or the floor, if admission was arranged without an ER visit). Events that occurred after arrival are covered in a separate summary paragraph that follows the pre-hospital history. Some HPIs are rather straight forward. If, for example, you are describing the course of an otherwise healthy 20 year old who presents with 3 days of cough, fever, and shortness of breath, you can focus on that time frame alone. It gets a bit more tricky when writing up patients with pre-existing illness(es) or a chronic, relapsing problem. In such cases, it is important to give relevant past history "up front," as having an awareness of this data will provide contextual information that will allow the reader to better understand the most recent complaint. If, for example, a patient with a long history of coronary artery disease presents with chest pain and shortness of breath, it might be written as follows:

"Mr. S is a 70 yr old male with known coronary artery disease who is:
-Status Post 3 vessel CABG in 4/82.
-Suffered recurrent chest pain in 12/93 which ultimately lead to catheterization and stent placement in a mid-LAD lesion.
-Recathed in 1/95 for recurrent chest pain at rest; at that time there was no significant change compared to cath of 12/93; patient was therefore continued on medical therapy.
-Known to have an Ejection Fraction of 30% with inferior and lateral akinesis by echo in 2/96
-No prior episodes of heart failure.
-Last Exercise Tolerance Test was performed in 1/97 and showed no ischemia at 10 METS of activity.

Mr. S was well until last week (9/97), when he began to experience recurrent episodes of chest pain, exactly like his past angina, after walking only one block. This represented a significant change in his anginal pattern, which is normally characterized as mild discomfort which occurs after walking vigorously for 8 or 9 blocks. In addition, 1 day prior to admission, the pain briefly occurred while the patient was reading a book. He has also noted swelling in his legs over this same time period and has awakened several times in the middle of the night, gasping for breath. In order to breathe comfortably at night, Mr. S now requires the use of 3 pillows, whereas in the past he was always able to lie flat on his back without difficulty. Mr. S is known to have poorly controlled diabetes and hypertension. He currently smokes 2 packs of cigarettes/day. He denies fevers, chills, cough, wheezing, nausea vomiting or other complaints."

That's a rather complicated history. However, it is obviously of great importance to include all of the past cardiac information "up front" so that the reader can accurately interpret the patient's new symptom complex. From a purely mechanical standpoint, note that historical information can be presented as a list (in the case of Mr. S, this refers to his cardiac catheterizations and other related data). This format is easy to read and makes bytes of chronological information readily apparent to your audience. While this data is technically part of the patient's "Past Medical History," it would be inappropriate to not feature this prominently in the HPI. Without this knowledge, the reader would be significantly handicapped in their ability to understand the patient's current condition. Knowing which past medical events are relevant to their area of current concern takes experience. In order to gain insight into what to include in the HPI, continually ask yourself, "If I was reading this, what historical information would I like to know?" Note also that the patient's baseline health status is described in some detail so that the level of impairment caused by their current problem is readily apparent to the reader.

The remainder of the HPI is dedicated to the further description of the presenting complaint. As the story teller you are expected to put your own spin on the write-up. That is, the history is written with some bias. You will be directing the reader towards what you feel is the likely diagnosis by virtue of the way in which you tell the tale. If, for example, you believed that the patient's chest pain was of cardiac origin, you would highlight features that supported this notion (e.g. crushing chest pain with activity, relieved with nitroglycerin, preponderance of coronary risk factors etc.). These are referred to as "pertinent positives." This is not misleading; all of the details written are based on facts and no important features have been omitted. The reader retains the ability to provide an alternative interpretation of the data if he/she so wishes. A brief review of systems related to the current complaint is generally noted at the end of the HPI. This also includes "pertinent negatives" (i.e. symptoms which the patient does not have). If present, these symptoms might lead the reader to entertain alternative diagnoses. Their absence, then, lends support to the candidate diagnosis suggested in the HPI.

Occasionally, patients will present with two (or more) dominant, truly unrelated problems. First, spend some extra time and effort assuring yourself that they are truly unconnected and worthy of addressing in the HPI. That being the case, present them as separate HPIs, each with its own paragraph.

Past Medical History (PMH):
This should include any illness (past or present) for which the patient has received treatment. Items which were noted in the HPI (e.g. the cardiac catheterization history mentioned previously) do not have to be re-stated. You may simply write "See above" in reference to these events. All other historical information should be listed. Detailed descriptions are generally not required. If, for example, the patient has hypertension, it is acceptable to simply write "HTN" without giving an in-depth report on the duration of this problem, medications used to treat it, etc. (unless this has been a dominant problem, requiring extensive evaluation...as might occur in the setting of Secondary Hypertension resulting from Renal Artery Stenosis). Also, get in the habit of looking for the data that supports each diagnosis that the patient is purported to have. It is not uncommon for misinformation to be perpetuated when past write-ups are used as the template for new H&Ps. When this occurs, a patient may be tagged with (and perhaps even treated for) an illness which they do not have! For example, many patients are noted to have Chronic Obstructive Pulmonary Disease (COPD). This is, in fact, a rather common diagnosis but one which can only be made on the basis of Pulmonary Function Tests (PFTs). While a Chest X-Ray and smoking history offer important supporting data, they are not diagnostic. Thus, it is not unusual to see "COPD" repeatedly appear under a patient's PMH on the basis of a suggestive CXR and known smoking history, despite the fact that they have never had PFTs! So, maintain a healthy dose of skepticism when reviewing old records and get in the habit of checking on the primary information yourself.

Past Surgical History (PSH):
All past surgeries should be listed, along with the rough date when they occurred.

Medications (MEDS):
Includes all currently prescribed medications as well as over the counter and non-traditional therapies. Dosage and frequency should be noted.

Allergies/Reactions (All/RXNs):
Identify the specific reaction that occurred with each medication.

Social History (SH):
This is a broad category which includes:

• Alcohol Intake: Specify the type and quantity.
• Cigarette smoking: Determine the number of packs used per day and the number of years which the patient has smoked. When multiplied this is referred to as "pack years." If they have quit, make note of when this occurred.
• Other Drug Use: Specify type, frequency and duration.
• Marital Status:
• Sexual History:
• Work History (type, duration, exposures):
• Other (e.g. travel, pets, hobbies):

Family History (FH):
This includes history of illnesses within the patient's immediate family. In particular, seach for a history of cancer, coronary artery disease or other heritable diseases among first degree relatives.

Obstetrical History (where appropriate):

Review of Systems (ROS): As mentioned previously, the most important ROS questioning (i.e. pertinent positives and negatives related to the chief complaint) is generally noted at the end of the HPI. The responses to a more extensive review which covers all organ systems are placed in this "ROS" area of the write-up. In actual practice, most providers do not document such an inclusive ROS. The ROS questions, however, are the same ones that, in a different setting, are used to unravel the cause of a patient's chief complaint. Thus, at this stage of your careers it is probably a good idea to practice asking all of these questions as well as noting the responses so that you will be better able to use them for obtaining historical information when interviewing future patients.

Physical Exam:
Generally begins with a one sentence description of the patient's appearance.
Vital Signs:
HEENT: Includes head, eyes, ears, nose, throat, oro-pharynx, thyroid.
Lymph Nodes:
Lungs:
Heart:
Carotids:
Abdomen:
Rectum:
Genitalia/Pelvic:
Extremities, Including Pulses:
Neurologic:

• Mental Status
• Cranial Nerves
• Motor Strength
• Sensation (light touch, pin prick, vibration and position)
• Reflexes, Babinski
• Cerebellar Function, Observed Ambulation

Lab Results, Radiologic Studies, EKG Interpretation, Etc.:

Assessment and Plan:

It's worth noting that the above format is in no way written in stone. When you're exposed to other styles, think about whether the proposed system is logical and readily comprehensible. Then incorporate those elements that make sense into your future write-ups.

SAMPLE WRITE UP #1

01/27/98 MEDICAL SERVICE STUDENT ADMISSION NOTE
Location: A-GM
Mr. "B" is a 72 yo man with h/o CHF and CAD, who presented with increasing lower extremity edema and weight gain.

HPI: Mr. "B" has a long history of CHF subsequent to multiple MI's last in 1991. Cardiac cath at that time revealed occlusions in LAD, OMB, and circ with EF of 50%. ECHO in 1996 showed a dilated LV, EF of 20-25%, diffuse regional wall motion abnormalities, 2+MR and trace TR. His CHF has been managed medically with captopril, lasix, metolazone, and digoxin. Over the past 6mos he has required increasing doses of lasix to control his edema. He was seen 2 wks ago by his Cardiologist, at which time he was noted to have leg, scrotal and penile edema. His lasix dose was increaed to 120 bid without relief of his swelling.

Over the past week he and his wife have noticed an increase in his LE edema which then became markedly worse in the past two days. The swelling was accompanied by a weight gain of 10lb in 2 days (175 to 185lb) as well as a decrease in his exercise tolerance. He now becomes dyspneic when rising to get out of bed and has to rest due to SOB when walking on flat ground. He has 2 pillow orthopnea, denies PND. His chronic cough has worsened and is now productive of "transparent" sputum with no hemoptysis. He has occ audible wheeze. Denies CP/pressure/palpitations/diaphoresis. Occ nausea/no vomiting. He eats limited quantities but does not salt or fluid restrict--eating canned soup and drinking 6-8 glasses liquid/day. He has increased urinary freq. but decreased amount. He states he has been taking all prescribed medications.

PMH:	CHF: as above MI Afib: on coumadin Pacemaker placed in 3/93 for afib/flutter and slow ventricular response HTN Chronic renal insufficiency: BUN/Cr stable on 1/21/98, 52/1.4 DM: controlled with glyburide. Admitted for hypoglycemia in 9/97.
PSH:	Tonsillectomy
MED:	Lasix 120 mg BID Metolazone 5 mg gd Captopril 50 mg TID Digoxin 0.125 mg qd KCl coumadin 4mg qd Glyburide 2.5 mg BID Colace 100 mg BID
ALLERGIES:	No Known Drug Allergies
SMOKING	None
ALCOHOL	None
OTHER SUBSTANCE USE	None
SOCIAL HISTORY:	Married for 45 years, sexual active with wife. Three children, 2 grandchildren, all healthy and well; all live within 50 miles. Retired school teacher. Enjoys model car building. Walks around home, shopping but otherwise not physically active.
FAMILY HISTORY	+ sister and mother with DM, father with CAD, age onset 50. Brother with leukemia.
ROS	If written, would be present here.
PE:	VS: T 97.1, P65, BP 116/66, O2Sat 98% on 2L NC GEN: elderly man lying in bed with head up, NAD HEENT: NCAT, multiple telangiectasias on face and nose, EOMi, PERRL, OP-benign NECK: thyroid not palpable, no LAD, carotic pulse 2+B, no bruits, no JVD RESP: +dullness to perc at right base, +ant wheezes, +crackles 1/2 way up chest bilat. COR: rrr, +2/6 holosystolic murmur at apex radiating to axilla, no gallops ABD: +BS, distended, nontender, no HSM, liver percussed to 9cm at MCL PULSES: 2+femoral B, 1+ PT/DP B EXT: 3+ edema to lower back, abdomen including genitals, hyperemia over ant., legs bilat, warm, non-tender; non clubbing, cyanosis SKIN: 4 cm ulcer on R buttock with central scabbing, non-tender, no discharge NEURO: AOX3; difficulty remembering events, dates; remainder of exam nonfocal
LABS/ DATA:	Na 138, C1 96, BUn 59, Glu 92, K 4.4, CO2 40.8, CR 1.4, WBC 7.9, PLT 349, HCT 43.9, pulses P73 L16 E3 B0 Alk phos 72, Tot prot 5.6, Alb 2.5 T Bili 0.5, AlT 17, AST 52, LDH 275, CPK 229 CXR: mildly prominent vessels. Minimal interstitial congestion. Cardiomegaly, no infiltrates. ECHO 1/27: 1. LV mild dilated (ED=6.0 cm) severaly depressed global systolic function with EF 20-25%. Extensive area thinning and akinesis: anterior, anteroseptal, anterolateral c/w old infarct 2. Mod 2-3/4 MR. LA size nl 3. No AS/AI 4. RV dilated with preserved fxn. 2-3/4 TR. PA pressure 36+ RA pressure.
ASSESSMENT/ PLAN	72 year old man with h/o CHF following MI, chronic renal insufficiency and venous stasis admitted with worsening edema and DOE. His symptoms are most consistent with incrasing CHF-biventricular-which would account for both his pulmonary congestion as well as his peripheral edema. His renal disease is a less likely explanation for his extensive edema as his BUN/Cr have remained stable throughout. However, his low albumin which could contribute to his edema may be due to renal losses. So if his edema is due to CHF, why has it become gradually and now acutely worse? Possibilities include: 1) worsening LV function, 2) another MI, 3) worsening valvular disease, 4) poor compliance with medications or 5) excess salt and water intake. His ECHO today shows no change in his EF, but there is marked wall motion abnormalities with akinesis. There is no evidence in his history, EKG, or enzymes for current ischemia/infarct. He does have MR and TR and his valvular disease may in part account for his worsening symptoms though his estimated PA pressure is unchanged and his LA is not dilated. The most likely precipitant of his failure is a combination of poor compliance with medication and fluid overload from excessive intake. We will continue to investigate the possibility of a structural precipitant for his deterioration and treat his current symptoms. Pulm: his wheezing, crackles, and oxygen requirement are all likely due to pulmonary congestion from LV dysfunction. He has no signs, symptoms of pulm infection. 02 to maintain sat greater than 95% treat cardiac disease as below Cardiac: As above his picture is consistent with CHF with no clear precipitant. Will continue to evaluate structural disease as precipitating factor and treat fluid overload. Strict I/O's. Daily weights Fluid restriction to 1.5L Low salt diet Lasix 80mg IV with IV Metolatzone now and Q8.. With goal diuresis of 2-3 L/day Increase digoxin to 0.25mg qd Continue captropril 50mg TID Check electrolytes, renal fxn and digoxin level in am Education about appropriate diet Repeat Echo and compare with old film Consider Cardiology consult if fails to improve, needs invasive hemodynamic monitoring or cath GI Continue colace Renal: We will continue to evaluate whether he could be losing protein from his kidney leading to his increasing edema. Check urine prot/cr ratio UA DM: His sugars have been well-controlled on current regimen Continue glyburide ADA 2100 calorie diet FS BS qac and qhs Signed by:

SAMPLE WRITE-UP #2

01/19/98, 21:44 MEDICAL SERVICE STUDENT ADMISSION NOTE
Location: A-GM
Mr. "S" is a 65 year old man with a history of Atrial Fibrillation, S/P Distant stroke, who has been off anticoagulation for 4 mos during evaluation of slow GI Bleed. He presents with 2 complaints:

1. Acute eye pain with difficulty seeing.

2. Several day history of a cough.

HPI: 1. Visual changes: Patient has a known history of atherosclerotic and hypertensive cerebrovascular disease: workup for dizziness/?TIA's in 94/95 revealed critical carotid stenosis and old R basal ganglia and L occipital infarcts on CT. A cerebral angiogram was complicated by a CVA manifested as R arm weakness with resolution. He subsequently had a R CEA in 1995 and no further TIA's.

Patient has had PAF for past 2+ years. ECHO in 1996 showed nl EF and marked LA enlargement (6cm) with mild-mod MR. Hehad been anticoagulated with coumadin until last summer. Developed GIB and chronic iron def. anemia. Coumadin d/c'd prior to colonscopy in Sept. and has not been restarted.

Yesterday morning while eating lunch patient had the sudden onset of sharp, R eye pain accompanied by decrease in vision. Pain was worse with coughing, unchanged by position, unrelieved by tylenol, aspirin or percocet. When the pain started, he "couldn't see the clock." He also had difficulty determining the numbers on the telephone. No blurred vision or diplopia. Vision is the same whether he covers right or left eye. He had nausea and vomiting x2--NB/NB at the onset of the pain. Was unable to give niece directions to hospital--unable to decide whether to make right or left turns. Pain and visual changes persisted through the night. No photophobia. No dizziness, weakness, dysarthria, CP, palpitations.

2. Cough: Patient has history of COPD with 60+ pack year smoking history and most recent PFT's showing mild deficits. Over the past few days he has noted increased dyspnea, wheezing, and sputum production. Sputum still clear, no hemoptysis and no fevers noted. No orthopnea or PND.

PMH:	PAF ? CAD: ETT 7/96 6 min Bruce HR 134 showed 1mm upsloping ST seg depressions and MIBI with lg fixed anteroapical and anterinf defect Carotid stenosis CVA Seizure disorder - though patient does not recall last event or details of evaluation GI Bleed: Intermittent heme + stools. Colonscopy on 9/97 showed 2 cm polyp. Biopsy showed adenoma. Patient declined polypectomy. COPD HTN GERD Anemia: Extensive workup consistently shows iron deficinecy anemia with last HCT 12/97 at 30. H/O asbestos exposure Bilateral shoulder bursitis.
PSH:	R CEA R orchiectomy at age 5 for traumatic injury Cataract s/p removal and implant placement on right
MEDS:	Ecotrin 325 mg po qd Verapamil SA 180 po qd Lansoprazole 15 po qd Dilantin 300 po qhs Atrovent 4 puffs QID Vanceril 4 puffs BID Colace 100 mg po BID
ALLERGIES:	No Known Drug Allergies
SMOKING	60 pack year hx, now 1 pack per day.
ALCOHOL	Heavy use in past, quit 5 years ago. None current.
OTHER SUBSTANCE USE	None
SOCIAL HISTORY:	Lives with roommate in Rockland, MA. Heterosexual, not currently active. Never married, no children. Worked in past as architect, though currently on disability. Enjoys walking and reading.
FAMILY HISTORY	Brother and father with CAD. Brother with CABG at age 55. Father with multiple strokes. Mother with DM.
PE:	VS: T 100.2, P89, irreg irreg BP 139/63, RR 35 O2 Sat 98% RA GEN: Obese, pale man turning his head side to side to see us with labored breathing. HEENT: NCAT, pupils L larger than R. Both reactive to light. Discs sharp. EOMI. Left Homonymous hemianopia. Temporal arteries nontender. Conjunctiva clear. Decreased hearing of high freq on left. OP-benign NECK: CEA scar on right. No LAD. No JVD. Carotic pulse 2+ on right, 1+ on left. RESP: CTP. + audible wheeze. Good aearation. Occ. Wheezes on ausc throughout. Coarse insp crackles at bases CAR: PMI at L lower sternal border. nl s1/s2. II/VI systolic crescendo-decrescendo murmur at LUSB. ABD: Obese + nl BS. Soft. Nontender. Liver nonpalpable. Liver 10cm at MCL. RECTAL: OV neg in ER MS: Decreased ROM at shoulders PULSES: Fem R 2+ L +1. DP 2+ B. PT 1+ B EXT: ? clubbing, no cyanosis. No edema. Warm, well-perfused. NEURO: AOX3; Able to see clock, unable to tell time. Unable to give directions from home to grocery store. Speech intact. Naming intact. Drawing clockface required prompting to put in numbers on left side. Min neglect for left side. CN: II: as above III, IV, VI: as above V: decreased light touch on right, MM 5/5 B VII: muscles of facila expression intact IX, X: palate symmetric XI: SCM, Trap 5/5 XII: Tongue midline Motor: Strength 5/5:biceps, triceps, grip, quad, hamstring, plantarflex, dorsiflex. F-N slight int. tremor on left. RAM: slowed on left. ? pronator drift on left. Gait: unsteady. Able to walk on heels not toes. Sensory: Slightly decreased light touch on right. Romberg neg. Reflexes: Biceps/triceps/brachio: 1+ B. Knee/ankle: 0 Toes equivocal.
LABS/ DATA:	Labs 1/19. Na 138, C1 106, BUn 13, Glu 99, K 4.5, CO2 25.4, CR 0.7, WBC 12.2, PLT 597, HCT 22.4, MCV 72.5, pulses P73 L16 E3 B0 Alk phos 72, T prot 7.2, Alb 3.1, ALT 9, AST 14, Alk phos 75, LDH 123, TB 0.5, Dilantin Less than 2.5, PT 13.5, INR 1.3, PTT 21.1 Head CT: new well-demarcated infarct in R occipitoparietal region. Old lacunar infarcts and L occipital infarct. No evidence hemorrhage. No shift in midline.
ASSESSMENT/ PLAN:	65 year old man with h/o PAF, HTN, CVA now presents with visual field deficits and spatial perception difficulty. Story of the sudden onset of neurologic deficits while awake, eating lunch in the setting of chronic intermittent atrial fibrillation is most consistent with embolic stroke. Infarction was confirmed with CT showing lesion in R PCA distribution. Patient has multiple risk factors for cardiogenic embolization from afib: h/o previous stroke, hypertension, age over 65, increased LV size, and valvular disease. Given his carotid disease artery-artery embolization is possibility but less likely becasue 1) less common than cardiac embolization and 2) his current infarct is in the posterior curculation. Visual disturbances could also be caused by temporal arteritis: though he does have a temporal headache, he has no tenderness and his visual defect is a bilateral loss of the left visual fields which is consistent with a cortical as opposed to a retinal injury. Neuro: story and imaging consistent with ischemic stroke to R PCA. Currently no signs of cerebral edema increased ICP. Head of bed elevated 30 degrees Given duration of symptoms and location of infarction would not anticoagulate immediately. Will discuss when to restart coumadin to preent further embolization. Continue aspirin Monitor level of consciousness Monitor electrolytes for signs SIADH Consult occupational therapy for assistance with managing deficits Continue dilantin for ?seizure disorder Tylenol for headache OOB with assistance only Pulm: Currently febrile and with increased SOB and cough, all suggestive of Bronchitis/COPD flare. Continue inhalers Bactrim DS 1 tab bid Prednisone 60 mg qd Re-evaluate CXR this am. Consider change to IC abx if clear infiltrate Encourage to stop smoking while in hospital CVS Continue verapamil for hypertension A Fib well rate controled Anti-coagulation as discussed above and below GI Arrange for Colonoscopy/EGD during this evaluation to complete evaluation GIB. Can use this information to make most informed decision about safety of reinitiating anti-coagulation Continue lansoprazole Guaiac all stools and follow for signs/sx ongoing GI bleeding HEME: Longstanding anemia now significantly worse. Given cerebral infarction and worsening dyspnea will transfuse for HCT over 30.. Transfuse two units PRBC's Start multivitamin Check CBC in am ID: Currently febrile. Likely due to COPD flare. Start bactrim Rheum: Shoulder pain consistent with subacromial bursitis. Offer subacromial steroid injection. Signed by:

Putting It All Together

How do you perform the examination in a way that is complete, makes sense and yet is not awkward or prolonged? Is it OK to mix together different areas of the exam or should each system be explored as a block? As I am sure you've already recognized, these and many other related questions are not easy to answer. Putting together a smooth exam is, in fact, quite challenging. There is no single right way to perform a complete physical. The goal is to generate a method that works for you. Any technique, however, should:

1. Cover all aspects of the examination such that you have a reasonable chance of identifying any pathology that might in fact be present.
2. Be readily reproducible, allowing you to perform the exam the same way all the time.
3. Keep patient gymnastics to a minimum (i.e. limit the number of times that the patient has to get up and down).
4. Link together sections which, although disconnected physiologically, are connected spatially. It makes sense, for example, to integrate the cranial nerve and head and neck examinations as both involve the same region of the body.
5. Allow you to be efficient and perform the exam with an economy of movement (i.e. minimize the number of times that you pick up and put down instruments, move from one side of the patient to the other, etc.).

It may take a fair amount of time, thought and practice before you come up with a system that works for you. I encourage you to experiment while choreographing your own moves.

What follows is not an in-depth review detailing the specifics of each area of the exam. Rather, it is simply an outline of the "mechanical events" that make up a complete physical.

1. Wash your hands.
2. Have the patient change into a hospital gown and take a seat at the end of the examining table. If possible, spend a few minutes simply watching them.
3. Determine the blood pressure in both arms.
4. Count the pulse. Measure this at both radial arteries simultaneously. Following this, examine the hands and fingers.
5. Respiratory rate is noted while counting the pulse. Temperature is measured at the same time.
6. Feel for axillary lymph nodes.
7. Examine the scalp and head for any superficial abnormalities.
8. Feel for lymph nodes in the head and neck.
9. Have patient raise eyebrows, wrinkle forehead, close their eyes and smile (CN 7).
10. Check sensation to touch on face; Feel temporal and masseter muscles when jaw clenched (CN 5).
11. Assess extra occular movements (cranial nerves 3, 4, & 6).
    Check visual fields and acuity (CN 2) if appropriate.
12. Using ophthalmoscope, check pupillary response to light (direct and indirect). Look for red reflex. Examine external structures of the eye.
13. Perform fundoscopy. When examining the left eye you will have to walk to the left side of the body.
14. Examine the outer and inner ears. You will again have to walk to the left side of the body to look at the left ear. Use your otoscope to view the tympanic membrane and associated structures.
15. Examine the nose.
16. Ask the patient to show their teeth and stick out their tongue. Using the otoscope and tongue depressor, examine the oral cavity. (CN 9, 10, 12).
17. Check hearing acuity, Weber, and Rinne (CN 8) if appropriate.
18. Have the patient shrug their shoulders and turn their head from side to side (CN 11).
19. Walk behind the patient and feel the thyroid gland.
20. Palpate the spine.
21. Observe, palpate, percuss and auscultate the posterior lung fields as well the right middle lobe and the lingula.
22. Walk around to the front, ask the patient to lie down, and listen to the anterior lung fields.
23. Look at the cardiac area of the chest. Then feel for the point of maximal cardiac impulse.
24. Auscultate the heart.
25. Have the patient turn their head to the left and assess for jugular venous distention.
26. Palpate the carotids.
27. Listen over the carotids.
    *Note....Steps 19 thru 25 can be performed without ever removing your stethoscope from your ears.
28. Observe, auscultate, percuss and palpate the abdomen.
29. Feel for inguinal adenopathy and asses femoral and then popliteal pulses.
30. Examine the feet, looking for edema, ulcers, discoloration, etc. Check for dorsalis pedis and posterior tibial pulses.
31. Ask patient to sit up.
32. Assess muscle bulk, tone and strength in lower extremities.
33. Assess muscle bulk, tone and strength in upper extremities.
34. Check sensation to pin prick, light touch, vibration, and position sense in feet and lower extremities if appropriate.
35. Check sensation in upper extremities, as described for lower extremities, if appropriate.
36. Check biceps, triceps and brachioradialis reflexes.
37. Check achilles and patellar reflexes.
38. Assess for Babinski.
39. Assess cerebellar function with finger to nose and heel to shin testing.
40. Have patient stand and then walk. Observe gait. Check for Romberg's Sign.
41. For male patients, perform genital and rectal exam while they are standing.
42. For female patients, perform pelvic exam.
43. Wash your hands.

I have omitted the formal joint examination. If indicated, this can be done in concert with assessment of extremity strength towards the end of the exam.

This approach keeps the movement of the examiner to a minimum, limits the frequency with which the patient has to get up and down, allows exploration of neighboring areas of the body even if they are part of different organ systems, and is reasonably logical, thorough and efficient. There is a lot of room for flexibility.

The Neurological Examination

Cranial Nerves

Sensory and Motor Examinations

Reflex Testing

Cerebellar Testing

Gait Testing

Making Sense of Neurological Findings

Introduction

The goals of the neurological examination are several:

1. For patients presenting with symptoms suggestive of a neurological problem, the examination should:
1. Determine, on the basis of an organized and thorough examination, whether in fact neurological dysfunction exists.
2. Identify which component(s) of the neurological system are affected (e.g. motor, sensory, cranial nerves, or possibly several systems simultaneously).
3. If possible, determine the precise location of the problem (e.g. peripheral v central nervous system; region and side of the brain affected etc.).
4. On the basis of these findings, generate a list of possible etiologies. Unlikely diagnoses can be excluded and appropriate testing (e.g. brain and spinal cord imaging) then applied in an orderly and logical fashion.

2. Screening for the presence of discrete abnormalities in patients at risk for the development of neurological disorders. This is appropriate for individuals who have no particular subjective symptoms suggestive of a neurological problem, yet have systemic illnesses that might put them at risk for subtle dysfunction. Diabetic patients, for example (particularly those with long standing poor control), may develop peripheral nerve dysfunction. This may only be detected through careful sensory testing (see below under Sensory Testing), which would have important clinical implications.

3. Cursory screening/documentation of baseline function for those who are otherwise healthy. In patients with neither signs nor risk factors for neurological disease, it's unlikely that the detailed exam would uncover occult problems. Simply observing the patient during the course of the usual H&P (i.e. watching them walk, get up and down from the exam table, etc.) may well suffice. Many examiners incorporate some aspects of the neuro exam into their standard evaluations. Cranial Nerve testing, for example, can be easily blended into the Head and Neck evaluation. Deciding what other aspects to routinely include is based on judgment and experience.

The major areas of the exam, covering the most testable components of the neurological system, include:

1. Mental status testing (covered in a separate section of this web site)
2. Cranial Nerves
3. Muscle strength, tone and bulk
4. Reflexes
5. Cerbellar Function
6. Sensory Function
7. Gait

Real and imagined problems with the neurological examination:

The neurological examination is one of the least popular and (perhaps) most poorly performed aspects of the complete physical. I suspect that this situation exists for several reasons:

1. This exam is perceived as being time and labor intensive.
2. Students and house staff never develop an adequate level of confidence in their ability to perform the exam, nor in the accuracy of their findings. This, in turn, probably translates into poor performance later in their careers.
3. Exam findings are often quite subjective.Thus, particularly when the examiner does not have confidence in their abilities (see above), interpretation of the results can be problematic.
4. Understanding/Interpretation of some neurological findings requires an in depth understanding of neuroanatomy and pathophysiology. As many clinicians do not see a large number of patients with neurological disorders, they likely maintain a limited working understanding of this information.
5. There is an over reliance on the utility of neuro-imaging (e.g. CT, MRI). These studies provide an evaluation of anatomy but not function. Thus, while extremely helpful, they must be interpreted within the context of exam findings. Careful examination may make imaging unnecessary. Also, exam findings can make a strong case for the presence of a pathologic process, even if it is not seen on a particular radiological study (i.e. there are limits to what can be seen on even the most high tech imaging).

The above are not meant to lower expectations with regards to how well a physician should be expected to learn and perform the neurological examination. Rather, I mention these points to highlight some of the real and imagined obstacles to clinical performance. Like all other aspects of the physical exam, there is a wealth of information that can be obtained from the neurological examination, provided that it is done carefully and accurately.This is, of course, predicated on learning how to do it correctly. A few practical considerations/suggestions:

1. In general, the neurological examination is not applied in its entirety to asymptomatic, otherwise healthy people as the yield (i.e. likelihood of identifying occult disease) would be quite low. It is, however, a good idea to practice the exam early in your careers, even when working with normal patients.This will improve the facility with which you perform the exam, provide you with a better sense of the range of normal, increase the accuracy of the results generated, and give you confidence in the meaning of findings identified when evaluating other patients.
2. It is sometimes appropriate to perform only certain parts of the neurological examination (e.g. just cranial nerves; or only motor testing)These situations will become apparent with experience.
3. The testing described below is still rather basic. There are many additional aspects of the exam that should be applied in specific settings. They are beyond the scope of this text, but can be found in other references.
4. Take advantage of those opportunities when a more experienced clinician examines one of your patients. When possible, watch them perform their exam. Then go back alone and verify the findings.

Like any other aspect of the exam, the neurological assessment has limits. Testing of one system is often predicated on the normal function of other organ systems. If, for example, a patient is visually impaired, they may not be able to perform finger to nose testing, a part of the assessment of cerebellar function (see below). Or, a patient's severe degenerative hip disease will prevent them from walking, making that aspect of the exam impossible to assess. The interpretation of "findings" must therefore take these things into account. Only in this way can you generate an accurate picture. Doing this, of course, takes practice and experience.

Cranial Nerve (CN) Testing

CN2

CN3, 4, 5

CN6

CN7

CN8

CN9, 10

CN11

CN12

Many practitioners incorporate cranial nerve testing with their complete examination of the head and neck (see the Head and Neck section of this web site for details). A detailed description of the CN assessment is provided below. As each half of the body has its own cranial nerve, both right and left sides must be checked independently.

Cranial Nerve 1 (Olfactory): Formal assessment of ability to smell is generally omitted, unless there is a specific complaint. If it is to be tested:

1. Each nostril should be checked separately. Push on the outside of the nares, occluding the side that is not to be tested.
2. Have the patient close their eyes. Make sure that the patient is able to inhale and exhale through the open nostril.
3. Present a small test tube filled with something that has a distinct, common odor (e.g. ground coffee) to the open nostril. The patient should be able to correctly identify the smell.

If you wish to test olfaction and don't have any "substance filled tubes" use an alcohol pad as a screening test. Patients should be able to identify its distinctive odor from approximately 10 cm .

Alcohol Pad Sniff Test

For more information about CN1, see the following links:

Yale University Cranial Nerve Review Site

Uniform Services School of Medicine Cranial Nerve Review Site

Cranial Nerve 2 (Optic): This nerve carries visual impulses from the eye to the optical cortex of the brain by means of the optic tracts. Testing involves 3 phases (also covered in the section of this site dedicated to the Eye Exam):

1. Acuity:
1. Each eye is tested separately. If the patient uses glasses to view distant objects, they should be permitted to wear them (referred to as best corrected vision).
2. A Snellen Chart is the standard, wall mounted device used for this assessment. Patients are asked to read the letters or numbers on successively lower lines (each with smaller images) until you identify the last line which can be read with 100% accuracy. Each line has a fraction written next to it. 20/20 indicates normal vision. 20/400 means that the patient's vision 20 feet from an object is equivalent to that of a normal person viewing the same object from 400 feet. In other words, the larger the denominator, the worse the vision.

Snellen chart for measuring visual acuity
3. There are hand held cards that look like Snellen Charts but are positioned 14 inches from the patient. These are used simply for convenience. Testing and interpretation are as described for the Snellen.
Hand held visual acuity card
4. If neither chart is available and the patient has visual complaints, some attempt should be made to objectively measure visual acuity. This is a critically important reference point, particularly when trying to communicate the magnitude of a visual disturbance to a consulting physician. Can the patient read news print? The headline of a newspaper? Distinguish fingers or hand movement in front of their face? Detect light?Failure at each level correlates with a more severe problem.

2. Visual Field Testing: Specific areas of the retina receive input from precise areas of the visual field. This information is carried to the brain along well defined anatomic pathways. Holes in vision (referred to as visual field cuts) are caused by a disruption along any point in the path from the eyeball to the visual cortex of the brain. Visual fields can be crudely assessed as follows:
   1. The examiner should be nose to nose with the patient, separated by approximately 8 to 12 inches.
   2. Each eye is checked separately. The examiner closes one eye and the patient closes the one opposite. The open eyes should then be staring directly at one another.
   3. The examiner should move their hand out towards the periphery of his/her visual field on the side where the eyes are open. The finger should be equidistant from both persons.
   4. The examiner should then move the wiggling finger in towards them, along an imaginary line drawn between the two persons.The patient and examiner should detect the finger at more or less the same time.
   5. The finger is then moved out to the diagonal corners of the field and moved inwards from each of these directions. Testing is then done starting at a point in front of the closed eyes. The wiggling finger is moved towards the open eyes.
   6. The other eye is then tested.

Meaningful interpretation is predicated upon the examiner having normal fields, as they are using themselves for comparison.

If the examiner cannot seem to move their finger to a point that is outside the patient's field don't worry, as it simply means that their fields are normal.

Interpretation: This test is rather crude, and it is quite possible to have small visual field defects that would not be apparent on this type of testing. Prior to interpreting abnormal findings, the examiner must understand the normal pathways by which visual impulses travel from the eye to the brain.

For more information about visual field testing, see the following links:

Washington University, review of visual field of testing and pathology

University of Arkansas, gross anatomy of visual pathway

3. Pupils: The pupil has afferent (sensory) nerves that travel with CN2. These nerves carry the impulse generated by the light back towards the brain. They function in concert with efferent (motor) nerves that travel with CN 3 and cause pupillary constriction. Seen under CN 3 for specifics of testing.

For more information about CN 2, see the following links:

Yale University Cranial Nerve Review Site

Uniform Services School of Medicine Cranial Nerve Review Site

CN 3 (Occulomotor): This nerve is responsible for most of the eyeball's mobility, referred to as extra-occular movement. CN 3 function is assessed in concert with CNs 4 and 6, the other nerves responsible for controlling eyeball movement. CN 4 controls the Superior Oblique muscle, which allows each eye to look down and medially. CN 6 controls the Lateral Rectus muscle, which allows each eye to move laterally. CN 3 controls the muscles which allow motion in all other directions. The pneumonic "S O 4 � L R 6 � All The Rest 3" may help remind you which CN does what (Superior Oblique CN 4 � LateralRectus CN 6 � All The Rest of the muscles innervated by CN 3). Testing is done as follows:

1. Ask the patient to keep their head in one place. Then direct them to follow your finger while moving only their eyes.
2. Move your finger out laterally, then up and down.
3. Then move your finger across the patient's face to the other side of their head. When it is out laterally, move it again up and down. You will roughly trace out the letter "H", which takes both eyeballs through the complete range of movements. At the end, bring your finger directly in towards the patient's nose. This will cause the patient to look cross-eyed and the pupils should constrict, a response referred to as accommodation.

CN 3 also innervates the muscle which raises the upper eye lid. This can first be assessed by simply looking at the patient. If there is CN 3 dysfuntion, the eyelid on that side will cover more of the iris and pupil compared with the other eye. This is referred to as ptosis.

Right CN3 Lesion: Note patient's right eye is deviated laterally and there is ptosis of the lid (picture on left),
and the right pupil (middle picture) is more dilated than the left pupil (picture on far right).

CN6 Palsy: This patient is unable to move left eye lateral of midline due to left CN6 lesion.

It's also worth noting that disorders of the extra ocular muscles themselves (and not the CN which innervate them) can also lead to impaired eye movement. For example, pictured below is a patient who has suffered a traumatic left orbital injury. The inferior rectus muscle has become entrapped within the resulting fracture, preventing the left eye from being able to look downward.

Entrapment of Left Inferior Rectus Muscle

The response of pupils to light is controlled by afferent (sensory) nerves that travel with CN 2 and efferent (motor) nerves that travel with CN 3. These innervate the ciliary muscle, which controls the size of the pupil. Testing is performed as follows:

1. It helps if the room is a bit dim, as this will cause the pupil to become more dilated.
2. Using any light source (flashlight, oto-ophtahlmoscope, etc), shine the light into one eye. This will cause that pupil to constrict, referred to as the direct response.
3. Remove the light and then re-expose it to the same eye, though this time observe the other pupil. It should also constrict, referred to as the consensual response. This occurs because afferent impulses from one eye generate an efferent response (i.e. signal to constrict) that is sent to both pupils.
4. If the patient's pupils are small at baseline or you are otherwise having difficulty seeing the changes, take your free hand and place it above the eyes so as to provide some shade. This should cause the pupils to dilate additionally, making the change when they are exposed to light more dramatic. If you are still unable to appreciate a response, ask the patient to close their eye, generating maximum darkness and thus dilatation. Then ask the patient to open the eye and immediately expose it to the light. This will (hopefully) make the change from dilated to constricted very apparent.

Interpretation:

1. Under normal conditions, both pupils will appear symmetric. Direct and consensual response should be equal for both.
2. Asymmetry of the pupils is referred to as aniosocoria. Some people with anisocoria have no underlying neuropathology. In this setting, the asymmetry will have been present for a long time without change and the patient will have no other neurological signs or symptoms. The direct and consensual responses should be preserved.
3. A number of conditions can also affect the size of the pupils. Medications/intoxications which cause generalized sympathetic activation will result in dilatation of both pupils. Other drugs(e.g. narcotics) cause symmetric constrictionof the pupils. These findings can provide important clues when dealing with an agitated or comatose patient suffering from medication overdose. Eye drops known as mydriatic agents are used to paralyze the muscles, resulting marked dilatation of the pupils. They are used during a detailed eye examination, allowing a clear view of the retina. Addiitonally, any process which causes increased intracranial pressure can result in a dilated pupil that does not respond to light.
4. If the afferent nerve is not working, neither pupil will respond when light is shined in the affected eye. Light shined in the normal eye, however, will cause the affected pupil to constrict. That's because the efferent (signal to constrict) response in this case is generated by the afferent impulse received by the normally functioning eye. This is referred to as an afferent pupil defect.
5. If the efferent nerve is not working, the pupil will appear dilated at baseline and will have neither direct nor consensual pupillary responses.

For more information about pupillary response and CN 3, see the following links:

Yale University Cranial Nerve Review Site
UC Davis Extra-Occular Movement and Pupilary Response Simulator

CN 4 (Trochlear): Seen under CN 3.

CN 5 (Trigeminal): This nerve has both motor and sensory components.

Assessment of CN 5 Sensory Function: The sensory limb has 3 major branches, each covering roughly 1/3 of the face. They are: the Ophthlamic, Maxillary, and Mandibular. Assessment is performed as follows:

1. Use a sharp implement (e.g. broken wooden handle of a cotton tipped applicator).
2. Ask the patient to close their eyes so that they receive no visual cues.
3. Touch the sharp tip of the stick to the right and left side of the forehead, assessing the Ophthalmic branch.
4. Touch the tip to the right and left side of the cheek area, assessing the Maxillary branch.
5. Touch the tip to the right and left side of the jaw area, assessing the Mandibular branch.

The patient should be able to clearly identify when the sharp end touches their face. Of course, make sure that you do not push too hard as the face is normally quite sensitive. The Ophthalmic branch of CN 5 also receives sensory input from the surface of the eye. To assess this component:

1. Pull out a wisp of cotton.
2. While the patient is looking straight ahead, gently brush the wisp against the lateral aspect of the sclera (outer white area of the eye ball).
3. This should cause the patient to blink. Blinking also requires that CN 7 function normally, as it controls eye lid closure.

Assessment of CN 5 Motor Function: The motor limb of CN 5 innervates the Temporalis and Masseter muscles, both important for closing the jaw. Assessment is performed as follows:

1. Place your hand on both Temporalis muscles, located on the lateral aspects of the forehead.
2. Ask the patient to tightly close their jaw, causing the muscles beneath your fingers to become taught.
3. Then place your hands on both Masseter muscles, located just in from of the Tempero-Mandibular joints (point where lower jaw articulates with skull).
4. Ask the patient to tightly close their jaw, which should again cause the muscles beneath your fingers to become taught. Then ask them to move their jaw from side to side, another function of the Massester.

For more information about CN 5 motor function, see the following links:

Yale University Cranial Nerve Review Site

Uniform Services School of Medicine Cranial Nerve Review Site

CN6 (Abducens): See under CN 3.

CN7 (Facial): This nerve innervates many of the muscles of facial expression. Assessment is performed as follows:

1. First look at the patient's face. It should appear symmetric. That is:
   1. There should be the same amount of wrinkles apparent on either side of the forehead� barring asymmetric Bo-Tox injection!
   2. The nasolabial folds (lines coming down from either side of the nose towards the corners of the mouth) should be equal
   3. The corners of the mouth should be at the same height

   If there is any question as to whether an apparent asymmetry if new or old, ask the patient for a picture (often found on a driver's license) for comparison.

2. Ask the patient to wrinkle their eyebrows and then close their eyes tightly. CN 7 controls the muscles that close the eye lids (as opposed to CN 3, which controls the muscles which open the lid). You should not be able to open the patient's eyelids with the application of gentle upwards pressure.
3. Ask the patient to smile. The corners of the mouth should rise to the same height and equal amounts of teeth should be visible on either side.
4. Ask the patient to puff out their cheeks. Both sides should puff equally and air should not leak from the mouth.

Interpretation: CN 7 has a precise pattern of inervation, which has important clinical implications. The right and left upper motor neurons (UMNs) each innervate both the right and left lower motor neurons (LMNs) that allow the forehead to move up and down. However, the LMNs that control the muscles of the lower face are only innervated by the UMN from the opposite side of the face.

CN7 - Facial Nerve
Precise Pattern of Innervation

Thus, in the setting of CN 7 dysfunction, the pattern of weakness or paralysis observed will differ depending on whether the UMN or LMN is affected. Specifically:

1. UMN dysfunction: This might occur with a central nervous system event, such as a stroke. In the setting of R UMN CN 7 dysfunction, the patient would be able to wrinkle their forehead on both sides of their face, as the left CN 7 UMN cross innervates the R CN 7 LMN that controls this movement. However, the patient would be unable to effectively close their left eye or raise the left corner of their mouth.



Right central CN7 dysfunction: Note preserved abiltiy to wrinkle forehead. Left corner of mouth, however, is slightly lower than right. Left naso-labial fold is slightly less pronounced compared with right.

2. LMN dysfunction: This occurs most commonly in the setting of Bell's Palsy, an idiopathic, acute CN 7 peripheral nerve palsy. In the setting of R CN 7 peripheral (i.e. LMN) dysfunction, the patient would not be able to wrinkle their forehead, close their eye or raise the corner of their mouth on the right side. Left sided function would be normal.

Left peripheral CN7 dysfunction: Note loss of forehead wrinkle, ability to close eye, ability to raise corner of mouth, and decreased naso-labial fold prominence on left.

This clinical distinction is very important, as central vs peripheral dysfunction carry different prognostic and treatment implications. Bell's Palsy (peripheral CN 7 dysfunction)tends to happen in patient's over 50 and often responds to treatment with Acyclovir (an anti-viral agent) and Prednisone (a corticosteroid). Over the course of weeks or months there is usually improvement and often complete resolution of symptoms. Assessment of acute central (UMN) CN 7 dysfunction would require quite a different approach (e.g. neuroimaging to determine etiology).

CN 7 is also responsible for carrying taste sensations from the anterior 2/3 of the tongue. However as this is rarely of clinical import, further discussion is not included.

For more information about CN 7, see the following links:

Yale University Cranial Nerve Review Site

Uniform Services School of Medicine Cranial Nerve Review Site

CN8 (Acoustic): CN 8 carries sound impulses from the cochlea to the brain. Prior to reaching the cochlea, the sound must first traverse the external canal and middle ear. Auditory acuity can be assessed very crudely on physical exam as follows:

1. Stand behind the patient and ask them to close their eyes.
2. Whisper a few words from just behind one ear. The patient should be able to repeat these back accurately. Then perform the same test for the other ear.
3. Alternatively, place your fingers approximately 5 cm from one ear and rub them together. The patient should be able to hear the sound generated. Repeat for the other ear.

For more information about ear anatomy, see the following link:

Washington University Inner Ear Anatomy

These tests are rather crude. Precise quantification, generally necessary whenever there is a subjective decline in acuity, requires special equipment and training.

The cause of subjective hearing loss can be assessed with bedside testing. Hearing is broken into 2 phases: conductive and sensorineural. The conductive phase refers to the passage of sound from the outside to the level of CN 8. This includes the transmission of sound through the external canal and middle ear. Sensorineural refers to the transmission of sound via CN 8 to the brain. Identification of conductive (a much more common problem in the general population) defects is determined as follows:

Weber Test:

1. Grasp the 512 Hz tuning fork by the stem and strike it against the bony edge of your palm, generating a continuous tone. Alternatively you can get the fork to vibrate by "snapping" the ends between your thumb and index finger.
512 Hz Tuning Fork



2. Hold the stem against the patient's skull, along an imaginary line that is equidistant from either ear.
3. The bones of the skull will carry the sound equally to both the right and left CN 8. Both CN 8s, in turn, will transmit the impulse to the brain.
4. The patient should report whether the sound was heard equally in both ears or better on one side then the other (referred to as lateralizing to a side).

Weber Test

Rinne Test:

1. Grasp the 512 Hz tuning fork by the stem and strike it against the bony edge of your palm, generating a continuous tone.
2. Place the stem of the tuning fork on the mastoid bone, the bony prominence located immediately behind the lower part of the ear.
3. The vibrations travel via the bones of the skull to CN 8, allowing the patient to hear the sound.
4. Ask the patient to inform you when they can no longer appreciate the sound. When this occurs, move the tuning fork such that the tines are placed right next to (but not touching) the opening of the ear. At this point, the patient should be able to again hear the sound. This is because air is a better conducting medium then bone.
Rinne Test

Interpretation:

1. The above testing is reserved for those instances when a patient complains of a deficit in hearing. Thus, on the basis of history, there should be a complaint of hearing decline in one or both ears.
2. In the setting of a conductive hearing loss (e.g. wax in the external canal), the Webber test will lateralize (i.e. sound will be heard better)in the ear that has the subjective decline in hearing. This is because when there is a problem with conduction, competing sounds from the outside cannot reach CN 8 via the external canal. Thus, sound generated by the vibrating tuning fork and traveling to CN 8 by means of bony conduction is better heard as it has no outside "competition." You can transiently create a conductive hearing loss by putting the tip of your index finger in the external canal of one ear. If you do this while performing the Webber test, the sound will be heard on that side.
3. In the setting of a sensorineural hearing loss (e.g. a tumor of CN 8), the Webber test will lateralize to the ear which does not have the subjective decline in hearing. This is because CN 8 is the final pathway through which sound is carried to the brain. Thus, even though the bones of the skull will successfully transmit the sound to CN 8, it cannot then be carried to the brain due to the underlying nerve dysfunction.
4. In the setting of conductive hearing loss, bone conduction (BC) will be better then air conduction (AC) when assessed by the Rinne Test. If there is a blockage in the passageway (e.g. wax) that carries sound from the outside to CN 8, then sound will be better heard when it travels via the bones of the skull. Thus, the patient will note BC to be better then or equal to AC in the ear with the subjective decline in hearing.
5. In the setting of a sensorineural hearing loss, air conduction will still be better then bone conduction (i.e. the normal pattern will be retained). This is because the problem is at the level of CN 8. Thus, regardless of the means (bone or air) by which the impulse gets to CN 8, there will still be a marked hearing decrement in the affected ear. As AC is normally better then BC, this will still be the case.

Summary:

Identifying conductive v sensorineural hearing deficits requires historical information as well as the results of Webber and Rinne testing. In summary, this data is interpreted as follows:

1. First determine by history and crude acuity testing which ear has the hearing problem.
2. Perform the Webber test. If there is a conductive hearing deficit, the Webber will lateralize to the affected ear. If there is a sensorineural deficit, the Webber will lateralize to the normal ear.
3. Perform the Rinne test. If there is a conductive hearing deficit, BC will be greater then or equal to AC in the affected ear. If there is a sensorineural hearing deficit, AC will be greater then BC in the affected ear.

For more information about CN 8, see the following links:

Yale University Cranial Nerve Review Site

Uniform Services School of Medicine Cranial Nerve Review Site

CN9 (Glosopharyngeal) and CN 10 (Vagus): These nerves are responsible for raising the soft palate of the mouth and the gag reflex, a protective mechanism which prevents food or liquid from traveling into the lungs As both CNs contribute to these functions, they are tested together.

Testing Elevation of the soft palate:

1. Ask the patient to open their mouth and say, "ahhhh," causing the soft palate to rise upward.
2. Look at the uvula, a midline structure hanging down from the palate. If the tongue obscures your view, take a tongue depressor and gently push it down and out of the way.
3. The Uvula should rise up straight and in the midline.


Normal Oropharynx

Interpretation:

If CN 9 on the right is not functioning (e.g. in the setting of a stroke), the uvula will be pulled to the left. The opposite occurs in the setting of left CN 9 dysfunction.

Left CN9 Dysfunction: Patient status post stroke affecting left CN9. Uvula therefore pulled over towards right.

Be aware that other processes can cause deviation of the uvula.A peritonsilar abscess, for example, will push the uvula towards the opposite (i.e. normal) tonsil.

Left peritonsillar abscess: infection within left tonsil has pushed uvula towards the right.

Testing the Gag Reflex:

1. Ask the patient to widely open their mouth. If you are unable to see the posterior pharynx (i.e. the back of their throat), gently push down with a tongue depressor.
2. In some patients, the tongue depressor alone will elicit a gag. In most others, additional stimulation is required. Take a cotton tipped applicator and gently brush it against the posterior pharynx or uvula. This should generate a gag in most patients.
3. A small but measurable percent of the normal population has either a minimal or non-existent gag reflex. Presumably, they make use of other mechanisms to prevent aspiration.

Gag testing is rather noxious. Some people are particularly sensitive to even minimal stimulation. As such, I would suggest that you only perform this test when there is reasonable suspicion that pathology exists. This would include two major clinical situations:

1. If you suspect that the patient has suffered acute dysfunction, most commonly in the setting of a stroke. These patients may complain of/be noted to cough when they swallow. Or, they may suffer from recurrent pneumonia. Both of these events are signs of aspiration of food contents into the passageways of the lungs. These patients may also have other cranial nerve abnormalities as lesions affecting CN 9 and 10 often affect CNs 11 and 12, which are anatomically nearby.
2. Patient's suffering from sudden decreased level of consciousness. In this setting, the absence of a gag might indicate that the patient is no longer able to reflexively protect their airway from aspiration. Strong consideration should be given to intubating the patient, providing them with a secure mechanical airway until their general condition improves.

CN 9 is also responsible for taste originating on the posterior 1/3 of the tongue. As this is rarely a clinically important problem, further discussion is not included.

CN 10 also provides parasympathetic innervation to the heart, though this cannot be easily tested on physical examination.

For more information about CN 9 and 10, see the following links:

Yale University Cranial Nerve Review Site

Uniform Services School of Medicine Cranial Nerve Review Site

CN11 (Spinal Accessory): CN 11 innervates the muscles which permit shrugging of the shoulders (Trapezius) and turning the head laterally (Sternocleidomastoid).

1. Place your hands on top of either shoulder and ask the patient to shrug while you provide resistance. Dysfunction will cause weakness/absence of movement on the affected side.
   
   
   
   
2. Place your open left hand against the patient's right cheek and ask them to turn into your hand while you provide resistance. Then repeat on the other side. The right Sternocleidomasoid muscle (and thus right CN 11) causes the head to turn to the left, and vice versa.
   
   
   

CN12 (Hypoglossal): CN 12 is responsible for tongue movement. Each CN 12 innervates one-half of the tongue.

Testing:

1. Ask the patient to stick their tongue straight out of their mouth.
2. If there is any suggestion of deviation to one side/weakness, direct them to push the tip of their tongue into either cheek while you provide counter pressure from the outside.
   
   
   

Interpretation:

If the right CN 12 is dysfunctional, the tongue will deviate to the right. This is because the normally functioning left half will dominate as it no longer has opposition from the right. Similarly, the tongue would have limited or absent ability to resist against pressure applied from outside the left cheek.

Left CN 12 Dysfunction: Stroke has resulted in L CN 12 Palsy.
Tongue therefore deviates to the left.

For more information about CN12, see the following links:

Yale University Cranial Nerve Review Site

Uniform Services School of Medicine Cranial Nerve Review Site

Sensory and Motor Examinations - A Brief Review of Anatomy and Physiology:

Sensory Testing

Motor Testing

Testing of motor and sensory function requires a basic understanding of normal anatomy and physiology. In brief:

1. Voluntary movement begins with an impulse generated by cell bodies located in the brain.
2. Signals travel from these cells down their respective axons, forming the Cortiospinal (a.k.a. Pyramidal) tract. At the level of the brain stem, this motor pathway crosses over to the opposite side of the body and continue downward on that side of the spinal cord. The nerves which comprise this motor pathway are collectively referred to as Upper Motor Neurons (UMNs). It's important to note that there are other motor pathways that carry impulses from the brain to the periphery and help modulate movement. A discussion of these tracts can be found in other Neurology reference texts.

For more information about motor pathways, see the following link:

University of Washington Review of Motor Pathways

3. At a specific point in the spinal cord the axon synapses with a 2^nd nerve, referred to as a Lower Motor Neuron (LMN). The precise location of the synapse depends upon where the lower motor neuron is destined to travel. If, for example, the LMN terminates in the hand, the synapse occurs in the cervical spine (i.e. neck area). However, if it's headed for the foot, the synapse occurs in the lumbar spine (i.e. lower back).
4. The UMNs are part of the Central Nervous System (CNS), which is composed of neurons whose cell bodies are located in the brain or spinal cord. The LMNs are part of the Peripheral Nervous System (PNS), made up of motor and sensory neurons with cell bodies located outside of the brain and spinal cord. The axons of the PNS travel to and from the periphery, connecting the organs of action (e.g. muscles, sensory receptors) with the CNS.
5. Nerves which carry impulses away from the CNS are referred to Efferents (i.e. motor) while those that bring signals back are called Afferents (i.e. sensory).
6. Axons that exit and enter the spine at any given level generally connect to the same distal anatomic area. These bundles of axons, referred to as spinal nerve roots, contain both afferent and efferent nerves. The roots exit/enter the spinal cord through neruoforamina in the spine, paired openings that allow for their passage out of the bony protection provided by the vertebral column.

For more information about spinal cord anatomy, see the following link:

Review of Spinal Anatomy

7. As the efferent neurons travels peripherally, components from different roots commingle and branch, following a highly programmed pattern. Ultimately, contributions from several roots may combine to form a named peripheral nerve, which then follows a precise anatomic route on its way to innervating a specific muscle. The Radial Nerve, for example, travels around the Humerus (bone of the upper arm), contains contributions from Cervical Nerve Roots 6, 7 and 8 and innervates muscles that extend the wrist and supinate the forearm.
It may help to think of a nerve root as an electrical cable composed of many different colored wires, each wire representing an axon. As the cable moves away from the spinal cord, wires split off and head to different destinations. Prior to reaching their targets, they combine with wires originating from other cables. The group of wires that ultimately ends at a target muscle group may therefore have contributions from several different roots.

For more information about radial nerve anatomy and function, see below.

8. Afferents carry impulses in the opposite direction of the motor nerves. That is, they bring information from the periphery to the spinal cord and brain.
9. Sensory nerves begin in the periphery, receiving input from specialized receptor organs. The axons then move proximally, joining in a precise fashion with other axons to form the afferent component of a named peripheral nerve. The Radial Nerve, for example, not only has a motor function (described previously) but also carries sensory information from discrete parts of the hand and forearm.
10. As the sensory neurons approach the spinal cord, they join specific spinal nerve roots. Each root carries sensory information from a discrete area of the body. The area of skin innervated by a particular nerve root is referred to as a dermatome. Dermatome maps describe the precise areas of the body innervated by each nerve root. These distributions are more or less the same for all people, which is clinically important. In the setting of nerve root dysfunction, the specific area supplied by that root will be affected. This can be mapped out during a careful exam (see below), identifying which root(s) is dysfunctional.

To view a dermatomal map, see the following link:

Dermatome Map University of Scranton

11. Sensory input travels up through the spinal cord along specific paths, with the precise route defined by the type of sensation being transmitted. Nerves carrying pain impulses, for example, cross to the opposite side of the spinal cord soon after entering, and travel up to the brain on that side of the cord. Vibratory sensations, on the other hand, enter the cord and travel up the same side, crossing over only when they reach the brain stem (see following sections for detailed descriptions).

For more information about sensory pathways, see the following link:

University of Washington Review of Sensory Pathways

12. Ultimately, the sensory nerves terminate in the brain, where the impulses are integrated and perception occurs.

Understanding the above neruo-anatomic relationships and patterns of innervation has important clinical implications when trying to determine the precise site of neurological dysfunction. Injury at the spinal nerve root level, for example, will produce a characteristic loss of sensory and motor function. This will differ from that caused by a problem at the level of the peripheral nerve. An approach to localizing lesions on the basis of motor and sensory findings is described in the sections which follow. Realize that there is a fair amount of inter-individual variation with regards to the specifics of innervation. Also, recognize that often only parts of nerves may become dysfunctional, leading to partial motor or sensory deficits. As such, the patterns of loss are rarely as "pure" as might be suggested by the precise descriptions of nerves and their innervations.

Sensory Testing

Sensory testing of the face is discussed in the section on Cranial Nerves. Testing of the extremities focuses on the two main afferent pathways: Spinothalamics and Dorsal Columns.

1. Spinothalamics: These nerves detect pain, temperature and crude touch. They travel from the periphery, enter the spinal cord and then cross to the other side of the cord within one or two vertebral levels of their entry point They then continue up that side to the brain, terminating in the cerebral hemisphere on the opposite side of the body from where they began.
2. Dorsal Columns: These nerves detect position (a.k.a. proprioception), vibratory sensation and light touch. They travel from the periphery, entering the spinal cord and then moving up to the base of the brain on the same side of the cord as where they started. Upon reaching the brain stem they cross to the opposite side, terminating in the cerebral hemisphere on the opposite side of the body from where they began.

A screening evaluation of these pathways can be performed as follows:

Spinothalamics

1. The patient's ability to perceive the touch of a sharp object is used to assess the pain pathway of the Spinothalamics. To do this, break a Q-tip or tongue depressor in half, such that you create a sharp, pointy end. Alternatively, you can use a disposable needle as the sharp-ended probe. I would discourage the use of the pointy, metal spikes that accompany some reflex hammers. If, for example, you used this and caused bleeding, it's possible (if the tip were not well cleaned) to transmit blood borne infections from one patient to another. Better to use a disposable implement.
2. Ask the patient to close their eyes so that they are not able to get visual clues.
3. Start at the top of the foot. Orient the patient by informing them that you are going to first touch them with the sharp implement. Then do the same with a non-sharp object (e.g. the soft end of a q-tip). This clarifies for the patient what you are defining as sharp and dull.
   
   
   
   
4. Now, touch the lateral aspect of the foot with either the sharp or dull tool, asking them to report their response. Move medially across the top of the foot, noting their response to each touch.
5. If they give accurate responses, do the same on the other foot. The same test can be repeated for the upper extremities (i.e. on the hand), though this would only be of utility if the patient complained of numbness/impaired sensation in that area.

Dorsal Columns

Proprioception: This refers to the body's ability to know where it is in space. As such, it contributes to balance. Similar to the Spinothalamic tracts, disorders which affect this system tend to first occur at the most distal aspects of the body. Thus, proprioception is checked first in the feet and then, if abnormal, more proximally (e.g. the hands).

Technique:

1. Ask the patient to close their eyes so that they do not receive any visual cues.
2. Grasp either side of the great toe. Orient the patient as to up and down. Flex the toe (pull it upwards) while telling the patient what you are doing. Then extend the toe (pull it downwards) while again informing them of which direction you are moving it.
   

   Testing Proprioception

3. Alternately deflect the toe up or down without telling the patient in which direction you are moving it. They should be able to correctly identify the movement and direction.
4. Both great toes should be checked in the same fashion. If normal, no further testing need be done in the screening exam.
5. If the patient is unable to correctly identify the movement/direction, move more proximally (e.g. to the ankle joint) and repeat (e.g. test whether they can determine whether the foot is moved up or down at the ankle).

Similar testing can be done on the fingers. This is usually reserved for those settings when patients have distal findings and/or symptoms in the upper extremities.

Vibratory Sensation: Vibratory sensation travels to the brain via the dorsal columns. Thus, the findings generated from testing this system should corroborate those of proprioception (see above).

Technique:

1. Start at the toes with the patient seated. You will need a 128 hz tuning fork.


128 Hz tuning fork

2. Ask the patient to close their eyes so that they do not receive any visual cues.
3. Grasp the tuning fork by the stem and strike the forked ends against the heel of your hand, causing it to vibrate.
4. Place the stem on top of the interphalangeal joint of the great toe. Put a few fingers of your other hand on the bottom-side of this joint.


Testing vibratory sensation

5. Ask the patient if they can feel the vibration. You should be able to feel the same sensation with your fingers on the bottom side of the joint.
6. The patient should be able to determine when the vibration stops, which will correlate with when you are no longer able to feel it transmitted through the joint. It sometimes takes a while before the fork stops vibrating. If you want to move things along, rub the index finger of the hand holding the fork along the tines, rapidly dampening the vibration.

Repeat testing on the other foot.

Additional/Special Testing for Dorsal Column Dysfunction

Testing Two Point Discrimination: Patients should normally be able to distinguish simultaneous touch with 2 objects which are separated by at least 5mm. These stimuli are carried via the Dorsal Columns. While not checked routinely, it is useful test if a discrete peripheral neruropathy is suspected (e.g. injury to the radial nerve).

Technique:

1. Testing can be done with a paperclip, opened such that the ends are 5mm apart.
2. The patient should be able to correctly identify whether you are touching them with one or both ends simultaneously, along the entire distribution of the specific nerve which is being assessed.

Special Testing for Early Diabetic Neuropathy: A careful foot examination should be performed on all patients with symptoms suggestive of sensory neuropathy or at particular risk for this disorder (e.g. anyone with Diabetes). Loss of sensation in this area can be particularly problematic as the feet are a difficult area for the patient to evaluate on their own. Small wounds can become large and infected, unbeknownst to the insensate patient. Sensory testing as described above can detect this type of problem. Disposable monofilaments (known as the Semmes-Weinstein Aethesiometer) are specially designed for a screening evaluation. These small nylon fibers are designed such that the normal patient should be able to feel the ends when they are gently pressed against the soles of their feet.

Monofiliment

Technique:

1. Have the patient close their eyes so that they do not receive any visual cues.
2. Touch the monofilament to 5-7 areas on the bottom of the patient's foot. Pick locations so that all of the major areas of the sole are assessed. Avoid calluses, which are relatively insensate.
3. The patient should be able to detect the filament when the tip is lightly applied to the skin.


Monofiliment testing: Patients with normal sensation should be able to detect the monofiliment when it is lightly applied (picture on left). If the force required to provoke a sensory response is strong enough to bend the monofiliment
(picture on right), then sensation is impaired.

Interpretation: If the examiner has to supply enough pressure such that the filament bends prior to the patient being able to detect it, they likely suffer from sensory neuropathy. Testing should be done in multiple spots to verify the results. Patient's with distal sensory neuropathy should carefully examine their feet and wear good fitting shoes to assure that skin breakdown and infections don't develop. Efforts should also be made to closely control their diabetes so that the neuropathy does not progress.

Neuropathic Ulcer: Large ulcer has developed in this patient with severe diabetic neuropathy.

Interpreting Results of Sensory Testing

Patterns of Impairment for the Spinothalamic Tracts:

1. Patients should be able to correctly distinguish sharp sensation, indicating normal function of the spinothalamic pathway.
2. Mapping out regions of impaired sensation: The examination described above is a screening evaluation for evidence of sensory loss. This is perfectly adequate in most clinical settings. Occasionally, the history or screening examination will suggest a discrete anatomic region that has sensory impairment. When this occurs, it is important to try and map out the territory involved, using careful pin testing to define the medial/lateral and proximal/distal boundaries of the affected region. You may even make pen marks on the skin to clearly identify where the changes occur. As most clinicians have not memorized the distributions of all peripheral nerves or spinal nerve roots, you can simultaneously consult a reference book to see if the mapped territory matches a specific nerve distribution. This type of mapping is somewhat tedious and should only be done in appropriate situations.
3. Diffuse Distal Sensory Loss: A number of chronic systemic diseases affect nerve function. The most commonly occurring of these, at least in Western countries, is Diabetes. When control has been poor over many years, the sensory nerves become dysfunctional. This first affects the most distal aspects of the nerves and then moves proximally. Thus, the feet are the first area to be affected. As it is a systemic disease, it occurs simultaneously in both limbs. Exam reveals loss of ability to detect the sharp stimulus across the entire foot. Thus, the sensory loss does not follow a dermatomal (i.e. spinal nerve root) or peripheral nerve distribution. As the examiner tests more proximally, he/she will ultimately reach a point where sensation is again normal. The more advanced the disease, the higher up the leg this will occur. Hands can be affected, though much less commonly then feet as the nerves traveling to the legs are longer and thus at much greater risk. This pattern of loss is referred to as a Stocking or Glove distribution impairment, as the area involved covers an entire distal region, much as a sock or glove would cover a foot or hand. Such deficits may be associated with neuropathic pain, a continuous burning sensation affecting the distal extremity.
4. Peripheral Nerve Distribution: A specific peripheral nerve can become dysfunctional. This might, for example, occur as the result of trauma or infarction (another complication of diabetes). In this setting, there will be a pattern of sensory impairment that follows the distribution of the nerve. Radial nerve palsy, for example, can occur if an intoxicated person falls asleep in a position that puts pressure on the nerve as it travels around the Humerus (bone of the upper arm). Intoxication induced loss of consciousness then prevents the patient from reflexively changing position, the normal means by which we prevent nerves from being exposed to constant direct pressure. The resultant sensory loss would involve the back of the hand and forearm. Motor function would also be affected (see under motor exam). Pinning down the culprit nerve requires knowledge of nerve anatomy and innervation. On a practical level, most clinicians don't commit this to memory. Rather, they gather a history suggestive of a discrete nerve deficit, verify the territory of loss on exam, and then look it up in a reference book.

For more information about peripheral nerve injuries, see the following links:

Peripheral nerves and their territories of innervation

University of Washington Case Study #6, Radial Nerve Injury.

5. Nerve Root Impairment: A nerve root (or roots) can be damaged as it leaves the cord. This will result in a sensory deficit along its specific distribution, which can in turn be identified on examination. The S1 nerve root, for example, can be compressed by herniated disc material in the lumbar spine. This would cause sensory loss along the lateral aspect of the lower leg and the bottom of the foot. Only the leg on the affected side would have this deficit. As mentioned under peripheral nerve dysfunction, most clinicians do not memorize the dermatomes related to each nerve root. Rather, they gather a history suggestive of a discrete nerve deficit, verify a dermatomal distribution of loss on exam, and then look it up in a reference book.

For more information about nerve root compression, see the following links:

University of Wisconsin, Anatomy and pathophysiology of nerve root compression

Image of Herniated Disk

University of WashingtonLower Case Study #6, Lumbar Disc Herniation

6. The Spinothalamics are also responsible for temperature discrimination. For practical reasons (i.e. it's often hard to find test tubes, fill them with the requisite temperature water, etc) this is omitted in the screening exam. The information from sharp stimulus testing as described above should suffice. Temperature discrimination could be assessed as a means of verifying any abnormality detected on sharp/dull testing.
7. Testing of the sacral nerve roots, serving the anus and rectum, is important if patients complain of incontinence, inability to defecate/urinate, or there is otherwise reason to suspect that these roots may be compromised. In the setting of Cauda Equina syndrome, for example, multiple sacral and lumbar roots become compressed bilaterally (e.g. by posteriorly herniated disc material or a tumor). When this occurs, the patient is unable to urinate, as the lower motor neurons carried in these sacral nerve roots no longer function. Thus there is no way to send an impulse to the bladder instructing it to contract. Nor will they be aware that there bladders are full. There will also be loss of anal spincter tone, which can be appreciated on rectal exam. Ability to detect pin pricks in the perineal area (a.k.a. saddle distribution) is also diminished.

For more information about peripheral nerves and their territories of innervation, see the following link:

Peripheral nerves and their territories of innervation

Patterns of Impairment for Dorsal Column Dysfunction:

Proprioception:

Patients should be able to correctly identify the motion and direction of the toe. In the setting of Dorsal Column dysfunction (a common complication of diabetes, for example), distal testing will be abnormal. This is similar to the pattern of injury which affects the Spinothalamic tracts described above.

Vibratory Sensation:

1. Patients should be able to detect the initial vibration and accurately determine when it has stopped.
2. As described under testing of proprioception, dorsal column dysfunction tends to first affect the most distal aspects of the system. When this occurs, the patient is either unable to detect the vibration or they perceive that the sensation extinguishes too early (i.e. they stop feeling it even though you can still appreciate the sensation with your fingers on the underside of the joint).
3. The findings on vibratory testing should parallel those obtained when assessing proprioception, as both sensations travel via the same pathway.

Motor Testing

The muscle is the unit of action that causes movement. Normal motor function depends on intact upper and lower motor neurons, sensory pathways and input from a number of other neurological systems. Disorders of movement can be caused by problems at any point within this interconnected system.

Muscle Bulk and Appearance:

This assessment is somewhat subjective and quite dependent on the age, sex and the activity/fitness level of the individual. A frail elderly person, for example, will have less muscle bulk then a 25 year old body builder. With experience, you will get a sense of the normal range for given age groups, factoring in their particular activity levels and overall states of health.

Things to look for:

1. Using your eyes and hands, carefully examine the major muscle groups of the upper and lower extremities. Palpation of the muscles will give you a sense of underlying mass. The largest and most powerful groups are those of the quadriceps and hamstrings of the upper leg (i.e. front and back of the thighs). The patient should be in a gown so that the areas of interest are exposed.
2. Muscle groups should appear symmetrically developed when compared with their counterparts on the other side of the body. They should also be appropriately developed, after making allowances for the patient's age, sex, and activity level.

Muscle Assymetry
While both legs have well developed musculature, the left has greater bulk.

There should be no muscle movement when the limb is at rest. Rare disorders (e.g. Amyotrophic Lateral Sclerosis) result in death of the lower motor neuron and subsequent denervation of the muscle. This causes twitching of the fibers known as fasciculations,which can be seen on gross inspection of affected muscles.

For more information about ALS, see the following link:

NIH Sponsored Site About ALS

3. Tremors are a specific type of continuous, involuntary muscle activity that results in limb movement. Parkinson's Disease (PD), for example, can cause a very characteristic resting tremor of the hand (the head and other body parts can also be affected) that diminishes when the patient voluntarily moves the affected limb. Benign Essential Tremor, on the other hand, persists throughout movement and is not associated with any other neurological findings, easily distinguishing it from PD.

	To see a video demonstrating features of benign essential tremor, click on the movie icon.
	To see a video demonstrating features of Parkinson's Disease, click on the movie icon.

For more information about Parkinson's Disease, see the following link:

NIH Sponsored Site About Parkinson's Disease

4. The major muscle groups to be palpated include: biceps, triceps, deltoids, quadriceps and hamstrings. Palpation should not elicit pain. Interestingly, myositis (a rare condition characterized by idiopathic muscle inflammation) causes the patient to experience weakness but not pain.
5. If there is asymmetry, note if it follows a particular pattern. Remember that some allowance must be made for handedness (i.e. right v left hand dominance). Does the asymmetry follow a particular nerve distribution, suggesting a peripheral motor neuron injury? For example, muscles which lose their LMN inervation become very atrophic. Is the bulk in the upper and lower extremities similar? Spinal cord transection at the Thoracic level will cause upper extremity muscle bulk to be normal or even increased due to increased dependence on arms for activity, mobility, etc. However, the muscles of the lower extremity will atrophy due to loss of innervation and subsequent disuse. Is there another process (suggested by history or other aspects of the exam) that has resulted in limited movement of a particular limb? For example, a broken leg that has recently been liberated from a cast will appear markedly atrophic.



Diffuse Muscle Wasting: Note loss muscle bulk in left hand due to peripheral denervation.
In particular, compare left and right thenar eminences.

Tone: When a muscle group is relaxed, the examiner should be able to easily manipulate the joint through its normal range of motion. This movement should feel fluid. A number of disease states may alter this sensation. For the screening examination, it is reasonable to limit this assessment to only the major joints, including: wrist, elbow, shoulder, hips and knees.

Technique:

1. Ask the patient to relax the joint that is to be tested.
2. Carefully move the limb through its normal range of motion, being careful not to maneuver it in any way that is uncomfortable or generates pain.
3. Be aware that many patients, particularly the elderly, often have other medical conditions that limit joint movement. Degenerative joint disease of the knee, for example, might cause limited range of motion, though tone should still be normal. If the patient has recently injured the area or are in pain, do not perform this aspect of the exam.

Things to look for:

1. Normal muscle generates some resistance to movement when a limb is moved passively by an examiner. After performing this exam on a number of patients,you'll develop an appreciation for the range of normal tone.
2. Increased tone (hypertonicity) results from muscle contraction. At the extreme end is spasticity, which occurs when the upper motor neuron no longer functions. In this setting, the affected limb is held in a flexed position and the examiner may be unable to move the joint. This is seen most commonly following a stroke, which results in the death of the upper motor neuron cell body in the brain.
3. Flaccidness is the complete absence of tone. This occurs when the lower motor neuron is cut off from the muscles that it normally innervates.
4. Disorders that do not directly affect the muscles, upper or lower motor neurons can still alter tone. Perhaps the most common of these is Parkinson's Disease (PD). This is a disorder of the Extra Pyramidal System (EPS). The EPS normally contributes to initiation and smoothness of movement. PD causes increased tone, generating a ratchet-like sensation (known as cog wheeling) when the affected limbs are passively moved by the examiner.

Strength: As with muscle bulk (described above), strength testing must take into account the age, sex and fitness level of the patient. For example, a frail, elderly, bed bound patient may have muscle weakness due to severe deconditioning and not to intrinsic neurological disease. Interpretation must also consider the expected strength of the muscle group being tested. The quadriceps group, for example, should be much more powerful then the Biceps.

There is a 0 to 5 rating scale for muscle strength:

0/5	No movement
1/5	Barest flicker of movement of the muscle, though not enough to move the structure to which it's attached.
2/5	Voluntary movement which is not sufficient to overcome the force of gravity. For example, the patient would be able to slide their hand across a table but not lift it from the surface.
3/5	Voluntary movement capable of overcoming gravity, but not any applied resistance. For example, the patient could raise their hand off a table, but not if any additional resistance were applied.
4/5	Voluntary movement capable of overcoming "some" resistance
5/5	Normal strength

'+' and '-' can be added to these values, providing further gradations of strength. Thus, a patient who can overcome "moderate but not full resistance" might be graded 4+ or 5- . This is quite subjective, with a fair amount of variability amongst clinicians. Ultimately, it's most important that you develop your own sense of what these gradations mean, allowing for internal consistency and interpretability of serial measurements.

Specifics of Strength Testing - Major Muscle Groups: In the screening examination, it is reasonable to check only the major muscles/muscle groups. More detailed testing can be performed in the setting of discrete/unexplained weakness. The names of the major muscles/muscle groups along with the spinal roots and peripheral nerves that provide their innervation are provided below. Nerve roots providing the greatest contribution are printed in bold. More extensive descriptions of individual muscles and their functions, along with their precise innervations can be found in a Neurology reference text.

1. Intrinsic muscles of the hand (C 8, T 1): Ask the patient to spread their fingers apart against resistance (abduction). Then squeeze them together, with your fingers placed in between each of their digits (adduction). Test each hand separately. The muscles which control adduction and abduction of the fingers are called the Interossei, innervated by the Ulnar Nerve.
   
   

   

   For more information about finger abductors and adductors, see the following links:

   University of Washington, Anatomy of finger abductors and adductors

2. Flexors of the fingers (C 7, 8, T1): Ask the patient to make a fist, squeezing their hand around two of your fingers. If the grip is normal, you will not be able to pull your fingers out. Test each hand separately. The Flexor Digitorum Profundus controls finger flexion and is innervated by the Median (radial �) and Ulnar (medial �) Nerves.
   
   
   

   For more information about finger flexors, see the following links:

   University of Washington, Anatomy of finger flexors 1
   University of Washington, Anatomy of finger flexors 2

3. Wrist flexion (C 7, 8, T 1): Have the patient try to flex their wrist as you provide resistance. Test each hand separately. The muscle groups which control flexion are innervated by the Median and Ulnar Nerves.
   
   
   

   For more information about wrist flexors, see the following links:

   University of Washington, Anatomy of wrist flexors 1
   University of Washington, Anatomy of wrist flexors 2

4. Wrist extension (C 6, 7, 8): Have the patient try to extend their wrist as you provide resistance. Test each hand separately. The Extensor Radialis muscles control extension and are innervated by the Radial Nerve. Clinical Correlate: Damage to the radial nerve results in wrist drop (loss of ability to extend the hand at the wrist). This can occur via any one of a number of mechanisms. For example, the nerve can be compressed against the humerus for a prolonged period of time when an intoxicated person loses consciousness with the inside aspect of the upper arm resting against a solid object (known as a "Saturday Night Palsy").
   
   
   

   For more information about wrist extensors, see the following links:

   University of Washington, Anatomy of wrist extensors 1
   University of Washington, Anatomy of wrist extensors 2

5. Elbow Flexion (C 5, 6): The main flexor (and supinator) of the forearm is the Brachialis Muscle (along with the Biceps Muscle). Have the patient bend their elbow to ninety degrees while keeping their palm directed upwards. Then direct them to flex their forearm while you provide resistance. Test each arm separately. These muscles are innervated by the Musculocutaneous Nerve.
   
   
   

   For more information about elbow flexors, see the following links:

   University of Washington, Anatomy of elbow flexors 1
   University of Washington, Anatomy of elbow flexors 2

6. Elbow Extension (C 7, 8): The main extensor of the forearm is the triceps muscle. Have the patient extend their elbow against resistance while the arm is held out (abducted at the shoulder) from the body at ninety degrees. Test each arm separately. The Triceps is innervated by the Radial Nerve.
   
   
   

   For more information about elbow extensors, see the following link:

   University of Washington, Anatomy of elbow extensors

7. Shoulder Adduction (C 5 thru T1): The main muscle of adduction is the Pectoralis Major, though the Latissiumus and others contribute as well. Have the patient flex at the elbow while the arm is held out from the body at forty-five degrees. Then provide resistance as they try to further adduct at the shoulder. Test each shoulder separately.
   
   
   

   For more information about shoulder adductors, see the following links:

   University of Washington, Anatomy of shoulder adductors 1
   University of Washington, Anatomy of shoulder adductors 2

8. Shoulder Abduction (C 5, 6): The deltoid muscle, innervated by the axillary nerve, is the main muscle of abduction. Have the patient flex at the elbow while the arms is held out from the body at forty-five degress. Then provide resistance as they try to further abduct at the shoulder. Test each shoulder separately.
   
   
   

   For more information about shoulder abductors, see the following link:

   University of Washington, Anatomy of shoulder abductors

9. Hip Flexion (L 2, 3, 4): With the patient seated, place your hand on top of one thigh and instruct the patient to lift the leg up from the table. The main hip flexor is the Iliopsoas muscle, innervated by the femoral nerve.
   
   
   

   For more information about hip flexors, see the following links:

   University of Washington, Anatomy of hip flexors 1
   University of Washington, Anatomy of hip flexors 2

10. Hip Extension (L5, S1): With the patient lying prone, direct the patient to lift their leg off the table against resistance. Test each leg separately. The main hip extensor is the gluteus maximus, innervated by inferior gluteal nerve.
    
    
    

    For more information about hip extensors, see the following link:

    University of Washington, Anatomy of hip extensors

11. Hip Abduction (L 4, 5, S1): Place your hands on the outside of either thigh and direct the patient to separate their legs against resistance. This movement is mediated by a number of muscles.
    
    
    

    For more information about hip abductors, see the following links:

    University of Washington, Anatomy of hip abductors 1
    University of Washington, Anatomy of hip abductors 2
    University of Washington, Anatomy of hip abductors 3

12. Hip Adduction (L 2, 3, 4): Place your hands on the inner aspects of the thighs and repeat the maneuver. A number of muscles are responsible for adduction. They are innervated by the obturator nerve.
    
    
    

    For more information about hip adductors, see the following links:

    University of Washington, Anatomy of hip adductors 1
    University of Washington, Anatomy of hip adductors 2
    University of Washington, Anatomy of hip adductors 3
    University of Washington, Anatomy of hip adductors 4

13. Knee Extension (L 2, 3, 4): Have the seated patient steadily press their lower extremity into your hand against resistance. Test each leg separately. Extension is mediated by the quadriceps muscle group, which is innervated by the femoral nerve.
    
    
    

    For more information about knee extensors, see the following links:

    Univervsity of Washington, Anatomy of knee extensors 1
    Univervsity of Washington, Anatomy of knee extensors 2
    University of Washington, Anatomy of knee extensors 3
    University of Washington, Anatomy of knee extensors 4

14. Knee flexion (L 5; S 1, 2): Have the patient rest prone. Then have them pull their heel up and off the table against resistance. Each leg is tested separately. Flexion is mediated by the hamstring muscle group, via branches of the sciatic nerve.
    
    
    

    For more information about knee flexors, see the following links:

    University of Washington, Anatomy of knee flexors 1
    University of Washington, Anatomy of knee flexors 2
    University of Washington, Anatomy of knee flexors 3
    University of Washington, Anatomy of knee flexors 4
    University of Washington, Anatomy of knee flexors 5

15. Ankle Dorsiflexion (L 4, 5): Direct the patient to pull their toes upwards while you provide resistance with your hand. Each foot is tested separately. The muscles which mediate dorsiflexion are innervated by the deep peroneal nerve. Clinical Correlate: The peroneal nerve is susceptible to injury at the point where it crosses the head of the fibula (laterally, below the knee). If injured, the patient develops "Foot Drop," an inability to dorsiflex the foot.
    
    
    

    For more information about ankle dorsiflexors, see the following link:

    University of Washington, Anatomy of ankle dorsiflexors

16. Ankle Plantar Flexion (S 1, S 2). Have the patient "step on the gas" while providing resistance with your hand. Test each foot separately. The gastrocnemius and soleus, the muscles which mediate this movement, are innervated by a branch of the sciatic nerve. Plantar flexion and dorsiflexion can also be assessed by asking the patient to walk on their toes (plantar flexion) and heels (dorsiflexion).
    
    
    

    For more information about ankle plantar flexors, see the following links:

    University of Washington, Anatomy of ankle plantar flexors 1
    University of Washington, Anatomy of ankle plantar flexors 2
    University of Washington, Anatomy of ankle plantar flexors 3

It is generally quite helpful to directly compare right v left sided strength, as they should more or less be equivalent (taking into account the handedness of the patient). If there is weakness, try to identify a pattern, which might provide a clue as to the etiology of the observed decrease in strength. In particular, make note of differences between:

1. Right v Left
2. Proximal muscles v distal
3. Upper extremities v lower
4. Or is the weakness generalized, suggestive of a systemic neurological disorder or global deconditioning

Special Testing for subtle weakness: Subtle weakness can be hard to detect. Pay attention to how the patient walks, uses and holds their arms and hands as they enter the room, get up and down from a seated position, move onto the examination table, etc. Pronator drift is a test for slight weakness of the upper extremities. The patient should sit with both arms extended, palms directed upward. Subtle weakness in either arm will cause slight downward drift and pronation of that limb (i.e. the arm will rotate slightly inward and down).

Common peripheral nerves, territories of innervation, and clinical correlates.

Common Peripheral Nerves and Their Anatomy

Peripheral Nerve	Sensory Innervation	Motor Innervation	Contributing Spinal Nerve Roots	Clinical
Radial Nerve	Back of thumb, index, middle, and 1/2 ring finger; back of forearm University of Washington, Case Study # 6, Radial Nerve Injury. University of Washington, radial nerve anatomy	Wrist extension and abduction of thumb in palmer plane	C6, 7, 8	At risk for compression at humerus, known as "Saturday Night Palsy" Radial Nerve Palsy Image Radial Nerve Palsy Video
Ulnar Nerve	Palmar and dorsal aspects of pinky and 1/2 of ring finger University of Washington,Ulnar nerve anatomy	Abduction of fingers (intrinsic muscles of hand)	C7, 8 and T1	At risk for injury with elbow fracture. Can get transient symptoms when inside of elbow is struck ("funny bone" distribution)
Median Nerve	Palmar aspect of the thumb, index, middle and 1/2 ring finger; palm below these fingers. University of Washington case study #3, carpal tunnel syndrome.	Abduction of thumb perpendicular to palm (thenar muscles).	C8, T1	Compression at carpal tunnel causes carpal tunnel syndrome
Lateral Cutaneous Nerve of Thigh	Lateral aspect thigh University of Washington, Lateral cutaneous nerve anatomy		L1, 2	Can become compressed in obese patients, causing numbness over its distribution
Peroneal	Lateral leg, top of foot University of Washington, Peroneal nerve anatomy	Dorsiflexion of foot (tibialis anterior muscle)	L4, 5; S1	Can be injured with proximal fibula fracture, leading to foot drop (inability to dorsiflex foot) Foot Drop video

This table provides information about usual patterns of innervations. There is occasionally interindividual variation. In the setting of peripheral nerve dysfunction, the level of the lesion will determine the extent of the deficit. That is, proximal insults will cause the entire nerve distribution to be affected while more distal lesions will only impact function beyond the site of the injury.

More on carpal tunnel syndrome...

Video of findings in advanced carpal tunnel syndrome.

Carpal Tunnel Induced Atrophy: Chronic, severe compression of the median nerve within the carpal tunnel has led to atrophy of the Thenar muscles (hand on right). A normal appearing Thenar Eminence is demonstrated on left.

Cranial Nerves

Sensory and Motor Examinations

Reflex Testing

Cerebellar Testing

Gait Testing

Making Sense of Neurological Findings