gallop sounds like \200\234Tenne-ssee. \200\235 When S 3 and S 4 occur during tachycardia , they may appear together as a single loud sound, a summation gallop . An aortic ejection sound is heard early in systole with bicuspid aortic valves, aortic stenosis, or a dilated aortic root. The right heart equivalent lesions may also cause clicks (e.g., pulmonary ejec tion sound). Mid-systolic clicks occur in mitral valve prolapse. An opening snap precedes t he mid-diastolic murmur of mitral stenosis. A pericardial knock is a loud early diastolic s ound that can occur in constric- tive pericarditis (higher frequency than S 3 and heard ove r a wider area). Prosthetic sounds are caused by mechanical valves. Prosthetic mitral valve clicks occur in time with S 1 , and aortic valve clicks are timed with S 2 . s l l i k s l a c i n i l C 51 Figure 3.5 The cardiac cycle QRS P T ECG 4th 1st 2nd 3rd Heart sounds A P 110 ) g H m m Aortic pressure ( 50 e r u s s e r P Left atrial pressure Left ventricular pressure 0 End-diastolic volume Left ventricular volume 52 130 ) L m ( e m u o v l 65 r a l u c End-systolic volume Position of atrioventricular valves Position of aortic and pulmonary valves i r t n e v Open Open Open Systole 3 2 t f e L Diastole 1 Diastole 1 Phase of cardiac cycle 4 1 = Ventricular filling 2 = Isovolumetric ventricular contraction 3 = Ventricular ejection 4 = Isovolumetric ventricular relaxation After P . Paolini. Heart murmurs Always consider other symptoms and signs before auscultation and think: What do I expect to hear? However, don \200\231t let your expectations determine what you hear. Use the stethoscope correctly. Remember that the bell is used to detect low-pitched sounds (e.g., mitral stenosis) and should be applied gently to the skin (a bell applied tightly to the skin becomes a diaphragm). The dia- phragm is used to detect higher-pitched sounds (e. g., aortic regurgitation). Consider any murmur in terms of timing (systolic, diastolic, or continuous), intensity (see Table 3.8 and Figure 3.6), pitch , and location (where the mur- mur is loudest and where it radiates). An innocent systolic murmur (also called functional murmur ) is soft (grade 1 or 2), early in systole, and heard along the left sternal border . Anything beyond this description (including all diastolic murmurs) could indicate underlying structu ral heart disease and may need an echocardiogram to further evaluate. Timing and quality A systolic-ejection murmur ( SEM , crescendo \200\223decre- scendo) usually originates from a bnormal flow over an outflow tract and waxes and wanes with the intraventricular pressures. SEMs may be innocent and are common in children and high-output states (e.g., tachycardia, preg- nancy). Pathologic causes include aortic stenosis and sclerosis, pulmonary stenosis, and hypertrophic obstructive cardiomyopathy (HOCM). A holosystolic murmur ( HSM ) is of un iform intensity and obscures both S 1 and S 2 . It occurs due to regurgitation from a ventr icle into a low-pressure chamber (e.g., mitral or tricuspid regurgitation, VSD). Mitral val ve prolapse may produce a late systolic murmur and a midsystolic click. Early diastolic mur murs are high-pitched, blowing, and decrescendo. These occur in aortic and, although rare, pulmonary regurgitation. Mid-diastolic murmurs are low-pitched and rumbling. They occur in mitral stenosis (often accentuated presystolically also) and are easily missed: Listen for the \200\234absence of silence \200\235 in diastole. Also often seen in moderate or severe aortic regurgitation (Austin Flint murmur). Continuous murmurs begin in systole and contin ue into diastole and may occur with a patent ductus arteriosus, arteriovenous fistula, or c oarctation of the aorta. Intensity Intensity is generally a poor guide to the severity of a lesion (exceptions include aortic and mitral regurgitation, where murmurs of grade \211 3 indicate more severe disease). Many patients with right-sided val- vular lesions (such as tricuspid regurgitation), and many with mild mitral or aortic regurgitation, do not have a udible murmurs. To help distinguish the etiology of a systolic murmur, observe how its inte nsity changes with changing cardiac cycle lengths (as in atrial fibrillation): Mitral regur gitation does not change in intensity, but aortic stenosis becomes louder after a longer du ration diastole (HOCM responds unpredictably to changing cycle lengths). See Table 3.8. Are a where loudest The location (and timing) of a systolic murmur does not reliably distinguis h aortic stenosis from mitral regurgitation. However, highest intensity of murmur at second right intercostal space (among sys- tolic murmurs radiating to the right clavicle) can hel p determine likelihood of severe aortic stenosis. Radiation The SEM of aortic stenosis clas sically radiates to the right clavicle and carotids (if the murmur over the right clavicle is absent, then aortic stenosis is considerably less likely), in contrast to the HSM of mit ral regurgitation, which classically radiates to the axilla. Accentuating maneuvers Movemen ts that bring the relevant part of the heart closer to the stethoscope accentuate murmurs ( e.g., leaning forward for aortic regurgitation, left lateral decubitus position for mitral stenosis). Right-sided murmurs characteristically intensify during normal inspiration (insp iration increases venous return to the right side of the heart and decreases it to the left side of the heart). The Valsalva maneuver (forced expiration against a closed glottis) dec reases systemic venous return, accen- tuating the systolic murmur of HOCM. Squatting-to-sta nding also decreases venous return and may also intensify mitral valve prolapse. Increasing afterload (via isometric handgrip exercise or transient arterial occlusion) will intensify murmurs of mitral regurgitation and VSD. Nonvalvular murmurs A pericardial friction rub ma y be heard in pericardi- tis. It is a superficial scratching sound, not confined to systole or diastole. s l l i k s l a c i n i l C 53 Figure 3.6 Common heart murmurs \200\223Ejection-systolic e.g., aortic stenosis \200\223Early diastolic e.g., aortic regurgitation S1 S2 S1 S1 S2 S1 \200\223Pansystolic e.g., mitral regurgitation \200\223Mid-diastolic murmur e.g., mitral stenosis S1 S2 S1 S1 S2 S1 Opening snap Presystolic accentuation Table 3.8 Grading intensity of heart murmurs The intensity of murmurs is graded on a 1 \200\2236 scale: Grade 1/6: Grade 2/6: Grade 3/6: Grade 4/6: Grade 5/6: Grade 6/6: 54 Very soft, only heard after listening for a while Soft, but detectable immediately Clearly audible, but no thrill palpable Clearly audible, palpable thrill Audible with stethoscope p artially touching chest Can be heard without placing stethoscope on chest The respiratory system Presenting symptoms Duration (see Table 3.9)? Character (e.g., dry \212Cough vs. productive; bloody)? Nocturnal (asthma)? Exacerbating factors (cold air, dust, fumes, f ragrances)? Associated symptoms (including constitutional symptoms, wheezing, dyspnea, rhin orrhea, heartburn, hoarseness, etc.)? \212Dyspnea Duration? Steps climbed/distance walked before onset? Associated symptoms (cough, wheezing, chest pain, orthopnea, leg swelling, etc.)? \212Hoarseness Duration? Acute laryngitis is usually a viral infec- tion; chronic laryngitis is due to an irritant such as acid reflux or inhaled toxins. Risk factors for cancer (e.g., tobacco, alcohol use)? Differential diagnosis includes benign voc al fold lesions, malignancy, neurologic disease, and many others. \212Fever/ night sweats (p. 76) \212 Chest pain (p. 90) \212 Wheeze (p. 57) \212 Stridor (pp. 56,82) Past history Previous history with presenting symptoms? History of heart, lung, or neuromus cular disease? Immunocompromised (e.g., due to HIV infection, malignancy, chemotherapy or o ther immunosuppressive medi- cations)? Atopy (asthma/eczema/hay fever)? Previous chest x-ra y (CXR) abnormalities (e.g., lung nodule, or hilar adenopathy as in sarcoidosis)? Family hi story Atopy? chronic obstructive pulmonary disease (COPD)/ emphysema? Pulmonary embolism? T B? Other lung or neuromuscular disease? Social history Quantify smoking in terms of pack-ye ars (20 cigarettes/day for 1 yr = 1 pack-year). Occupational and other exposures (farming, min- ing, asbestos, secondhand smoke exposure)? Animals at home (e.g., birds)? Recent trave l/TB contacts? Illicit drugs? Medications Review all, with particular attention to inhaled or nebulized respiratory medications and those with respiratory side effects (e.g., ACE inh ibitors, cytotoxics, \222 -blockers, amiodarone)? Examining the chest See Figure 3.7 for r eview of anatomy. See next sec- tion for review of inspection, palpation, percussion, and a uscultation. Other relevant examination: Review vital signs including pulse oximetry. Exami ne the hands for clubbing (p. 72), peripheral cyanosis, nicotine staining, and wasting/weak ness of the intrinsic muscles (e.g., Pancoast \200\231s tumor; also accompanied by Horner \200\231s syndrome). Pain on palpation of the hands, wrists, ankles, or other joints may in dicate hypertrophic pulmonary osteoarthropathy (often associated with lung cancer). Inspect the face Check for the ptosis and miosis of Horner \200\231s syndrome (e.g., Pancoast \200 \231s tumor). Are the tongue and lips bluish (central cyanosis)? Examine the heart Includin g assessment of JVP (p. 47) and for signs of cor pulmonale (p. 198). s l l i k s l a c i n i l C 55 Table 3.9 Differential diagnosis of cough Cough is a relatively nonspecific symptom, resulting from mechanical or chemical irritation of cough receptors anywhere from the pharynx to the lungs (and also located in the pericar dium, esophagus, diaphragm, and stomach). Duration of cough helps inform the differential d iagnosis: Acute cough (<3 wks) is usually due to acute respiratory tract infection; also co nsider COPD exacerbation, pneumonia, pulmonary embolism. Subacute cough (3 \200\2238 wks) i s often postinfectious; also consider Pertussis infection. Chronic cough (>8 wks) is most c ommonly due to postnasal drip, asthma, gastroesophageal reflux disease (GERD), angiotensin- converting enzyme (ACE)-inhibitor therapy, and chronic bronchitis (also lung infections, br onchiectasis, pulmonary fibrosis, neoplasm, and many others). Do not ignore a change in cha racter of a chronic cough; it may signify a new problem, such as infection or malignancy. Figure 3.7 The respiratory segments supplied by the segmental bronchi POSTERIOR ANTERIOR This diagram reminds us that we must auscultate anteriorly in order to examine the right mi ddle lobe. Examining the chest Inspection Look for deformities of the spine (kyphoscoliosis) or chest wall (e.g., barrel chest, p. 71) or scars from surgery. Count respiratory rate (usu- ally d one while pretending to count the radial pulse, as the respiratory rate may change if atten tion is drawn to it), note breathing pattern (e.g., Is the expiratory phase prolonged? Lips pursed? Periods of apnea? Cheyne-Stokes breathing? p. 71) and note use of accessory muscle s of respiration (sterno- cleidomastoid and scalene muscles). Palpation Lymphadenopathy: Ch eck for cervical, supraclavicular, and axil- lary lymphadenopathy. Tracheal position: Is it central or displaced to one side (toward an area of collapse, away from a large pleural ef fusion or ten- sion pneumothorax; slight deviation to the right is normal). Expansion (or \200\234excursion \200\235): Stand behind the patient, touch the lateral thorax bilaterally , and assess for any visible difference in excursion between the two sides of the chest. Un ilaterally reduced chest expansion suggests pleural effusion or consolidation, and bilatera l reduction is seen in chronic airflow obstruc- tion. Classically, <5 cm change in chest ci rcumference between maximum inspiration and expiration (using a tape measure at the level o f the fourth ICS) is considered abnormal, although this overlaps with the lower limit seen in normal persons (2 \200\2233 cm). Test tactile fremitus (the palpation of low-frequency v ibrations transmitted by a patient \200\231s voice through the chest) by asking the patient to repeat \200\234ninety-nine \200\235 while firmly palpating the chest wall over symmetr ic respiratory segments bilaterally. Absence of tactile fremitus can be a normal finding; f ocus on asymmetry as being abnormal (asymmetrically diminished fremitus seen in unilateral pneumothorax, pleu- ral effusion, pleural thickening, or neoplasm; increased fremitus sugge sts consolidation, as in unilateral pneumonia). Percussion Percuss symmetrical areas of the anterior, posterior, and axillary regions of the chest wall. A normal chest should sound e qually resonant on both sides. However, patients with significant lung disease also often h ave normal percussion findings. It is important to know the upper border of liver dullness on the right side: In the fifth space in the 56 mid-clavicular line, the seventh space in the mid-axillary line, and the ninth space in the scapular line ( \200\234579 rule \200\235). Causes of a dull percussion note: P leural eff usion, consolidation, pleural thickening, atelectasis, or elevated hemidiaphragm. Causes of a hyperresonant percussion note: P neumothorax or hyperinflation (COPD). Auscultation Ask the patient to breathe normally in and out of the mouth. Listen with the diaphragm over sym metrical areas of the anterior, posterior, and axillary regions of the chest wall, focusing on quality and intensity of breath sounds, the transmission of spoken words , and the pres - ence of adventitious sounds . Quality and intensity Normal breath sounds (as heard over t he posterior chest) have a soft, rustling quality and are described as vesicular . Bronchia l breath sounds (normally heard over the trachea and right apex; abnormal elsewhere) have a prominent expiratory component and much harsher quality, as if air was blown forcibly thro ugh a hollow tube. Bronchial breath sounds occur when lung tissue that has become solid, co llapsed, or consoli- dated is contiguous with the chest wall (usually due to pneumonia or p leu- ral effusion). Diminished breath sounds occur with pleural effusions, pleural thickeni ng, pneumothorax, bronchial obstruction, asthma, or COPD. The silent chest occurs in life-t hreatening asthma and is due to severe broncho- spasm that prevents adequate air entry into the chest. Transmission of spoken words (to a stethoscope placed on the patient \200\231s chest) is called \200\234vocal resonance \200\235 and is usually muffled, weak, and uninte l- ligible. Abnormalities include bronchophony (patient \200\231s voice sounds much louder than normal), whispered pectoriloquy (patient \200\231s whispered words are intelligible), and egophony (patient \200\231s \200\234E \200\235 vocalization changes into a loud nasal \200\234A \200\235 or \200\234AH \200\235, also called \200\234E-to-A \200\235 change). Asymmetry of findings is again key in detecting abnormality. Abnormal vocal resonance has t he same significance as bronchial breath sounds. Adventitious sounds Wheezes are caused by air passing through nar- rowed airways. They are classically heard in COPD and asthma, alth ough decompensated left ventricular failure ( \200\234cardiac asthma \200\235) is always im por- tant to consider in the dyspneic patient (remember to examine the neck veins for eleva ted jugular venous pressure). Longer and high-pitched wheezes indicate worse obstruction th an shorter and low-pitched ones. Crackles (rales) are caused by the reopening, during inspi ration, of the small distal airways that collapsed during expiration. The sound resembles p ulling apart strips of Velcro. Coarse crackles are thought to originate in larger, more pro ximal airways than are fine crackles. The timing of crackles is impor- tant; early inspirat ory crackles suggest small airways disease (e.g., COPD), whereas late inspiratory fine crac kles are typical of interstitial fibrosis. The crackles of heart failure and pneumonia are either coarse or fine and can be pan inspiratory. Rhonchus is an ambiguous term that should be avoided. That said, rhonchi most often refers to coarse discontinuous sounds heard in p atients with airway secretions; we suggest simply labeling these \200\234coarse breath sou nds \200\235 (these often clear with cough). Stridor is a loud, high-pitched musical sound confined to inspiration that indicates upper airway obstruc- tion. Pleural rubs are caused by movement of the visceral pleura over the parietal pleura, when both surfaces are roughen ed (e.g., by an inflammatory exudate). Causes include adjacent pneumonia, pulmonary infarct ion. s l l i k s l a c i n i l C 57 GI history Presenting symptoms Abdominal pain Nausea and vomiting (p. 207) Dysphagia (p. 206) Upper GI bleeding (hematemesis, Past history Peptic ulcer Cancer Jaundice, hepatitis Blood transfusions Previous operations Last menstrual period, LMP melena p. 217) Indigestion (dyspepsia, GERD p. 208) Recent change in bowel habit Diarrhea (p. 210) or constipation (p. 213) Rectal bleeding (p. 82) Appetite, weight change Jaundice (p. 202) Pruritus; dark urine, pal e stools Medications GI drugs NSAIDs Antibiotics Metformin Steroids Oral contraceptives 58 Social history Smoking, alcohol Intranasal cocaine, injection drugs Family history Irritable bowel disease Inflammatory bowel disease Peptic ulcer Polyps, canc er (risk factors for hepatitis C [HCV] infection) High-risk sexual activity (risk for HBV infection) Overseas travel, tropical illnesses Contact with jaundiced persons Occupational exposures, dietary history, recent changes Examining the GI system Signs of chronic liver disease \212 Fetor hepaticus (sign of severe portosystemic shunting; breath is a mix of rotten eggs and garlic) Drowsiness, confusion \212 \212 \212 Parotid (and lacrimal) gland enlargement Spider telangiectasia (spider angiomas; also seen in pregnancy and malnutrition) \212 \212 \212 \212 Jaundice Diminished axillary hair Male gynecomastia Asterixis (an irregular hand and finger \200\234flap \200\235 seen when patient holds arms outstretched with wrists fully extended and fingers spread apart; not specific to liver di sease, but one of the earliest findings of encephalopathy) s l l i k s \212 Palmar erythema (pale hand with islands of redness over thenar and hypothenar eminence) \212 \212 \212 \212 \212 \212 Clubbing (rare; only in biliary cirrhosis) l a c i n Terry \200\231s nails ( p. 43) Scratch marks i l C Edema Testicular atrophy Dilated abdominal veins (e.g., caput medusae; in contrast, dilated abdominal veins due to S VC or IVC syndrome tend to appear on the lateral aspects of the abdominal wall) \212 Splenomegaly, ascites (see Table 3.10) Genitourinary history Presenting symptoms Fever, groin pain, dysuria, urinary Past history Urinary tract infection (UTI), frequency, hematuria, incontinence Sexually transmitted disease (STD) 59 Kidney disease, stones Prostate disease Urethral/vaginal discharge Sex: Any problems? Painful intercourse (dyspareunia) Diabetes mellitus (DM), hypertension (HTN), NSAID use Irregular menses, endometriosis Pregnancy Previous operations Medications Anticholinergics Diuretics Prostate drugs Social history Smoking Sexual history Contraception Menses: Menarche, menopause, length of periods, amount, pain? Irregular bleeding? Last period (LMP)? Lower urinary tract symptoms (e.g., from benign prostatic enlarge- ment causing bladder out let obstruction, or overactive bladder). Ask: \212 \212 \212 \212 \212 Any pain or burning on urination? ( On feeling an urge to urinate, do you have to go at onc e? ( Do you urinate often at night? ( Too often during the day? ( When you want to urinate, is it hard to get the stream started? ( Hesitancy ) Is your stream getting weaker? ( Does the flow stop and start? Do you go on dribbling when you think you \200\231ve stopped? ( Te rminal dribbling ) Do you ever leak urine? ( Do you feel the bladder is not empty after uri nating? ( emptying ) Dysuria ) Urgency ) Nocturia ) Frequency ) \212 \212 Weak stream ) \212 \212 Incontinence ) Sense of incomplete Important note on physical examination Remember to have a chaperone present when performing intimate examina- tions (breast, genitourinary, rectal). Table 3.10 Examining the abdomen Adjust the patient so that he or she is lying flat, with his or her head resting on only on e pillow and arms at the sides. The examiner is posi- tioned on the patient \200\231s right side. Ask permission to expose the patient \200\231s abdomen and open a drape (flat sheet) to first cover patient \200\231s legs and pelvic area prior to the patient raising his or her gown. Inspection Inspect abdomen for contour (distention, bulging flanks, hernia), scar s, ecchymoses (may indicate intraperitoneal or retroperi- toneal hemorrhage), dilated veins , striae, masses (e.g., Sister Mary Joseph \200\231s nodule; i.e., metastatic carcinoma of the umbilicus), pulsations, peristalsis. Auscultation Listen with the diaphragm of the stet hoscope for bowel sounds for 10 \200\22315 sec just below and to the right of the umbilicus . Do this before percussing or palpating (which may stimulate bowel sounds and alter the ex am findings). In patients with small bowel obstruction, about 40% have hyperactive bowel so unds (>34/min) and about 25% have hypoactive (<5/min) or absent (none heard for 2 min) bowe l sounds. Listen for abdominal bruits (may be general markers of vascular disease or indica te renovascular hypertension), although they occur in 4 \200\22320% of healthy persons. Per cussion and palpation Clinicians \200\231 hands should be warm and expected tender areas sh ould be examined last. If the abdominal wall is tense, it can be further relaxed by asking the patient to bend her knees. Observe the patient \200\231s face for signs of discomfort d uring the exam. Briefly percuss in all four quadrants, listening for tympany and dullness. Then systematically perform light palpation followed by deep palpation. Note tenderness and guarding (involuntary tensing of abdominal muscles because of pain or fear of it). If the patient has abdominal pain, test for rebound tenderness (a sign of peritoneal inflammation) by releasing your hand quickly from the abdomen. \212Examining the liver: A practical app roach involves starting with palpa- tion. Beginning deep in the right lower quadrant, place right hand on patient \200\231s abdomen just lateral to the rectus abdominis; ask patient to take a deep breath and try to feel the liver edge as it descends. Note liver texture (so ft, firm, nodular) as it passes under your fin- gers. If liver edge is not felt below the c ostal margin, do not proceed with percussion. If liver edge is palpated, then percuss for t he upper border (>15 cm = enlargement by percussion in mid-clavicular line). Percussed live r span correlates modestly with the actual span, but underestimates it. As percussed liver span is also dependent on tech- nique, you will develop your sense of \200\234normal \200 \235 vs. \200\234abnormal \200\235 based on using your individual technique to examine man y patients. Evidence does not support using the \200\234scratch test \200\235 to measure l iver span. Two important points in assessing for hepatomegaly: Palpating the liver edge bel ow the costal margin is an unreliable sign of hepatomegaly, as half of all palpable livers are not enlarged. About half of all livers that extend below the costal margin are not palp able (consistency seems to be important, and diseased/firm livers are much more likely to b e palpable). 60 \212 \212 (Continued) s l l i k s Table 3.10 (Continued) Examining the spleen: The physical exam is best used when ruling in a diagnosis of splenome galy in a patient for whom suspicion is moderately high (the exam is more specific than sen sitive). Start by percussing in the lower left rib spaces in the mid-axillary line. If dull (instead of tympanic), proceed with supine, one-handed palpation (many other methods of pa lpation are also acceptable). Start in the right lower quadrant with gentle pressure and fe el for a descending spleen as patient takes a long, deep breath. Reposition and repeat palp ation at 2 cm increments head- ing through the umbilical area to the left upper quadrant. T o confidently rule out splenomegaly, imaging (e.g., ultrasound) is required. Assessing for ascites: Fluid wave and edema are the most helpful findings in diagnosing ascites. To elici t a fluid wave , the examiner places one hand firmly against the lateral abdominal wall and uses the other hand to tap firmly on the opposite lateral wall (unless there is \200\234t ense \200\235 ascites, the patient or an assistant must also apply firm pressure against th e ante- rior abdominal wall during the exam to restrict waves from traveling through the su bcutaneous tissue). Shifting dullness (flank dullness whose position shifts as the patient rolls on to one side) also increases the probability of ascites. To confidently rule out as cites, imaging (e.g., ultra- sound) is required. l a c i n i l C 61 The neurological system History This should be taken from the patient and, if possible, fro m a close friend or relative as well. The patient \200\231s memory, perception, or speech m ay be affected by the disorder, making the history difficult to obtain. Note the progressio n of the symptoms and signs: Gradual deterioration (e.g., tumor) versus intermittent exacer bations (e.g., multiple sclerosis) versus rapid onset (e.g., stroke). Ask about age, occupa tion, right- or left-handed? See Table 3.11. Presenting symptoms \212Headache: (p. 345) Different from usual headaches? Acute/chronic? Speed of onset? Intensity (worst headache of your life?). Course (recurrent, pro- gressive) ? Unilateral or bilateral? Associated aura (migraine, p. 349)? Any meningismus? Other assoc iated symptoms (e.g., fever, visual disturbance, nausea, etc.)? \212Weakness: Speed of onset? Muscle groups affected (e.g., symmetric proxi- mal weakness is usually due to muscle disease)? Sensory loss? Pain? Varies during the day? Associated pt osis or dysphagia? \212Visual disturbance: E.g., blurring, double vision (diplopia), photophobia, visual loss , red eye, eye pain. Speed of onset? Any preceding or associated symptoms? Trauma? \212Special senses: Hearing, smell, taste. \212Dizziness: (p. 355) Clarify vertigo (illus ion of surroundings moving, spin- ning) versus light-headedness (feeling faint) versus dyse quilibrium? Hearing loss or tinnitus? Any loss of consciousness? New medications? \212Speech disturbance: Difficulty in expression, articulation, or comprehen- sion? Sudden onset or gradual? Other focal symptoms? \212Dysphagia: Solids and/or liquids? Intermittent or constant/progressive? Temporal progr ession of symptoms? Associated symptoms (e.g., weight loss, heartburn)? Painful (odynophagi a)? \212Seizures: (p. 378) Context/circumstances? Preceding aura? Describe ictal events. Loss of consciousness? Tongue biting? Incontinence? Any residual weakness/confusion? Family hist ory? Alcohol or benzodiazepine withdrawal? \212Sensory disturbance: E.g., numbness, \200\234pins and needles \200\235 (paresthesias) , pain, odd sensations? Distribution? Speed of onset? Associated weakness? \212Tremor: (p. 384) Am plitude? Appears with rest, posture, or activity? Taking \222 -agonists? Metoclopramide? N euroleptics? Suspicion for hyper- thyroidism? Any family history? Cognitive state If there is any doubt about the patient \200\231s cognition, an objective m easure is performance on a cognitive test such as the Mini-Mental State Examination (MMSE, p. 67). Past medical history Ask about cancer, HIV infection, mental illness; meningitis/en cephalitis, head/spine trauma, seizures, previous operations, risk factors for stroke (atri al fibrillation [AF], HTN, hyperlipidemia, DM, smoking). Is there any chance that the patie nt is pregnant (preeclampsia)? Medications Any anticonvulsant/antipsychotic/antidepressant medication? Any medication with neurological side effects (e.g., isoniazid)? Social and fam ily history Functional status (activities of daily living [ADLs], etc.) and limitations? To bacco, alcohol, illicit drugs? Caffeine intake, dietary history? Recent travel? Any neurolo gical or psychiatric disease in the family? 62 Table 3.11 Examining the neurological system Along with the history, the neurologic exam is performed to help pre- cisely localize the s ite of pathology within the nervous system (p. 329). The neurological system is usually the most daunting examination to learn, but the most satisfying once perfected. Learn at the b edside from a senior colleague, preferably a neurologist. There is no substitute for practi ce. Be aware that books present ideal situations: Often one or more signs are equivocal or even contrary to expectation. Don \200\231t be put off; consider the whole picture, and con sider retaking the history. Level of consciousness Can say awake, drowsy, stuporous, or com a- tose; but be sure to more precisely describe the patient \200\231s level of arousal (e.g ., \200\234Patient is very drowsy; falls asleep between questions \200\235). General inspe ction During history, note speech quality (assess for dysarthria, fluency, coherence). On l ooking at the patient, do you notice any asymmetry (facial, extremities, movements)? Reduce d muscle bulk or tone? Are movements and walking fluid and coordinated? Any tremor or muscl e twitching? Mental status examination See p. 69. Cranial nerves See p. 63. Motor exam Test muscles individually by asking the patient to contract the muscle strongly while you try t o resist any movement. Grade muscle strength (p. 332); note any asymmetry. Identify whether the pattern of motor weakness is consistent with lower or upper motor neuron dys- function (lower or upper motor neurons [LMN or UMN], p. 332). Pronator drift: Detects subtle weakne ss. Ask the patient to extend both arms straight out in front of himself with palms up, as if he is holding a tray, for 10 sec. Does one arm pronate and drift downward (positive pron ator drift)? (Continued) s l l i k s Table 3.11 (Continued) Tone: Look for hypotonia (flaccidity; a sign of LMN disease), spasticity (increased muscle tone with associated weakness, and flexor and exten- sor tone differ; a sign of UMN disease ), or rigidity (increased tone with no associated weakness, and flexor and extensor tone ar e the same; a sign of extrapyramidal disease, e.g., Parkinson \200\231s). Coordination: Loo k for ataxic movements that lack the speed, smooth- ness, and accuracy seen in normal perso ns (a sign of cerebellar disease). Tests include finger \200\223to-nose (must be done at fu ll arm \200\231s extension), heel-to-shin , and rapid alternating movements (if abnormal, t his is called dysdiadochokinesia). Gait: Observe patient walking normally, then on the toes , heels, and using tandem steps (heel-to-toe). Note whether any gait disturbance is sym- me tric or asymmetric. A positive Romberg \200\231s sign is inability to stand for 60 sec with feet together and eyes closed (signals a disturbance of pro- prioception, either from neur opathy or posterior column disease; not a sign of cerebellar disease). Reflexes Proper pati ent positioning and good technique are required to elicit muscle stretch reflexes. Grade as absent (0), 1+ (present with rein- forcement; e.g., when patient hooks fingers of both han ds and pulls them apart as strongly as possible), normal (2+), brisk (3+), or hyperactive ( 4+ including clonus ; i.e., rhythmic oscillations that continue as long as tension is appli ed to a hyperreflexic muscle). Enhanced reflexes are a sign of UMN disease, and reduced/abs ent reflexes are a sign of LMN disease (although these findings are nonspecific and may be seen in persons without neu- rologic disease). Associated nerve roots to memorize include C 6 (biceps and brachioradialis), C7 (triceps), L3 \200\2234 (patellar), and S1 (ankle). Also assess the Babinski reflex bilaterally (use a key or handle of reflex hammer to slowly scr atch a J-shaped stroke beginning at the lateral plantar surface up to the ball of the foot) . A normal response (i.e., Babinski is \200\234absent \200\235 or \200\234normal \200\235 ) is flexion of all toes, and a positive response is an upgoing (extension) of the great to e (with a fanning of the other four toes). Sensory exam Extent of testing depends on the cl inical setting but may include all four simple sensations: Light touch (cotton wool), pain (pin-prick), vibration (128 Hz tuning fork), and temperature (cold stem of tuning fork). Co mpare patient \200\231s perceptions to the contralateral side; note distribution and symmet ry of abnormality. Also assess proprioception (sensation of move- ment of great toe up or d own); proprioceptive loss is common in peripheral neuropathy, spinal cord disease, and seve re hemispheric disease. l a c i n i l C 63 Cranial nerve examination Approach to examining the cranial nerves In patients without neu- rologic complaints, a quick screening exam can include testing pupillary responses to ligh t, eye movements, visual field testing (in one eye), and facial strength. For clinical corr elations, see Table 3.12. I: Smell: Test ability of each nostril to differentiate familiar smells (rarely performed). II: Acuity: Test in each eye separately using a pocket Snellen card; have patients wear usu al corrective lenses. Visual fields: Compare during con- frontation with your own fields. P upils: (p. 81) Assess responses to the \200\234swinging flashlight test \200\235 (in relat ive afferent papillary defect, pupils con- strict with light into the normal eye and dilate with light into the abnor- mal eye). Funduscopic exam: Darken the room. Starting 12 \200 \22318 inches away from the patient \200\231s eye, look through the scope to find the red reflex. Slowly move in and bring a retinal vessel into focus; trace vessels medially toward the nose to find the optic disc, inspecting its shape, color, and clarity. III, IV, and VI: Assess for ptosis and test eye movements . III palsy: Ptosis, eye down and out, +/ \210\222 dilated pupil. May cause both vertical and hori- zontal diplopia. IV pals y: Vertical diplopia (often noticed on descending stairs). Tilting the head toward the affe cted side aggravates the diplopia; many patients compensate by tilting their head away from the side of the lesion. VI nerve palsy: Esotropia (inward deviation) and an inability to a bduct the affected eye. Patient complains of horizontal diplopia on look- ing out at a dist ance. Nystagmus is involuntary, often jerky, eye oscilla- tions. Nystagmus lasting two beat s or less is normal, as is brief nystagmus at the extremes of gaze. Horizontal nystagmus is often due to cerebellar disease or peripheral vestibular disease (but may be due to other central nervous system disorders). Vertical nystagmus is often from a central etiology. V: Motor palsy: \200\234 Open your mouth \200\235: Jaw deviates to side of lesion. Sensory : Corneal reflex lost first; check light touch in all three divisions on the face. VII: Facial nerve lesions cause facial asymmetry (droop) and weakness of ipsilateral facial movements (except for lid movements). As the forehead has bilateral representation in the brain, only the lower two-thirds is affected in UMN lesions, but all of one side of the fac e in LMN lesions. Ask patient to \200\234raise your eyebrows \200\235 and \200\234show me your teeth. \200\235 64 VIII: Hearing: Rub your fingers together softly while holding them a few inches away from t he patient \200\231s ear. An alternative is the \200\234whispered voice test \200\235 (whi sper a combination of three letters or numbers while standing 2 feet behind the patient; th e examiner must occlude and rub the external auditory canal of the untested ear). The Weber and Rinne tests are not recommended for routine screening. IX and X: Ipsilateral palate elevation: Ask the patient to say \200\234aaah \200\235 and o bserve whether the two sides of the palate move fully and symmetrically. Can also use a swa b to assess pharyngeal sensation and gag reflex, although the gag reflex is often absent in normal persons, especially the elderly. XI : Trapezius: \200\234 Shrug your shoulders \200\235 against resistance. Sternocleidomas toid: \200\234 Turn your head to the left/right \200\235 against resistance. XII: Tongue protrus ion: Deviates to the side of the lesion. Table 3.12 Causes of cranial nerve lesions Any cranial nerve may be affected by diabetes mellitus, stroke, multiple sclerosis (MS), tu mors, sarcoidosis, vasculitis (e.g., polyarteritis nodosa [p. 416]), lupus, syphilis. Chron ic meningitis (malignant, TB, or fungal) tends to pick off the lower cranial nerves one-by- one. I: Trauma, respiratory tract infection, frontal lobe tumor, meningitis II: Field defec ts may start as small areas of visual loss ( scotomas ; e.g., in glaucoma). Monocular blind ness: Lesions of one eye or optic nerve (e.g., MS, giant cell arteritis, trauma) Bilateral blindness: Diabetes, glaucoma, infection, methanol Field defects: Bitemporal hemianopsia: O ptic chiasm compression (e.g., pituitary adenoma, craniopharyngioma, internal carotid arter y aneurysm) Homonymous hemianopsia: Affects half the visual field contralateral to the lesi on in each eye. Lesions lie beyond the chiasm in the tracts, radiation, or occipital cortex (e.g., stroke, abscess, tumor). (Continued) s l l i k s Table 3.12 (Continued) Papilledema (swollen disks): (1) \206\221 Intracranial pressure (ICP) (tumor, abscess, enc ephalitis, hydrocephalus, benign intracranial hypertension); (2) retro-orbital lesion (e.g. , cavernous sinus thrombosis, p. 368) Optic atrophy (pale optic disks and reduced acuity): MS, frontal tumors, Friedreich \200\231s ataxia, retinitis pigmentosa, syphilis, glaucoma,