Chapter 1 - General physical examination
In this chapter, we consider some aspects of the general physical examination that are especially pertinent to neurologic evaluation. Not all elements of examination can (or should) be conducted on every patient. An efficient diagnostic approach utilizes historical data and information gathered from a basic screening physical examination in a problem-oriented fashion to guide further examination. Of course, this puts a high premium on the ability to extract a cogent history, on the quality of initial observations and the ability to perform an efficient screening exam.
Vital signs may reflect abnormalities in the nervous system.
Respiration: Evaluation of the respiratory rate and pattern is particularly important in the evaluation of patients with depressed consciousness. This topic will be elaborated on in the section on the evaluation of coma in Chapter 17. There are characteristic, and therefore localizing patterns of respiration at each level of bilateral damage to the nervous system from the diencephalon through the medulla. Unilateral damage usually does not produce respiratory abnormalities. These abnormal breathing patterns represent loss of higher control of the primary medullary respiratory centers. Suppression of these medullary centers by metabolic or direct damage results in hypoventilation and, ultimately, apnea. Figure 1-1 is a schematic diagram of the kind of respiratory pattern that would be expected with bilateral lesions at various rostro-caudal levels in the brain stem.
Blood pressure: Increased intracranial pressure usually is associated with increased systemic blood pressure and the blood pressure then drops when intracranial pressure is lowered. Blood pressure is also frequently elevated during an ischemic stroke, possibly as a compensatory response to loss of part of the cerebral blood supply. Typically, the blood pressure will revert to baseline level over hours to days after the stroke without need of therapeutic intervention. Attempts to lower the blood pressure, unless it is at an extreme high level, can be counterproductive (by producing hypotension that can result in further ischemia). Medullary or upper spinal cord lesions often drop blood pressure to very low levels. However, for therapeutic purposes, patients with severely depressed blood pressure should be assumed to be due to hemodynamic rather than neural causes since severe hypotension due to brain stem or upper spinal cord injury is much less likely to be due to reversible causes.
Orthostatic hypotension is often the most prominent symptom of autonomic (particularly sympathetic) failure. Sympathetic nerves must increase the vasomotor tone in the lower portion of the body when going from lying to sitting or standing. If this does not happen, hypotension ensues. The assessment of orthostatic hypotension requires testing blood pressure and pulse in the recumbent and upright position, looking for a drop of at least 20 mm Hg of systolic pressure, or a diastolic blood pressure decrease of at least 10 mm Hg within three minutes of standing. Symptoms of light-headedness or faintness would indicate that this was symptomatic orthostasis. If the pulse rate increases as the blood pressure drops, the orthostasis is most likely due to hypovolemia. Exercise prior to orthostatic testing (which causes a reactive peripheral vasodilation, lowering peripheral resistance) may exaggerate any orthostasis. When orthostasis is found, it may be due to damage (or blockade) of peripheral elements of the sympathetic system or to failure of normal central control mechanisms. Peripheral failure most often occurs due to conditions that produce generalized peripheral neuropathy, such as diabetes, alcoholism, or malnutrition (see Chapter 21). Many medications are also capable of blocking normal sympathetic nervous system responses. Certain degenerative conditions, including Parkinson disease, can cause central failure of autonomic responses (including decrease in urinary bladder tone, erectile dysfunction, etc).
Pulse: Increased intracranial pressure may slow (bradycardia) or accelerated (tachycardia) the pulse. Arrhythmias, particularly sinus arrhythmias, and nonspecific ST-T wave changes, are frequently seen on electrocardiograms of persons who have had subarachnoid hemorrhage or either hemorrhagic or ischemic strokes. Atrial fibrillation, which produces an irregularly irregular pulse, is a risk factor of systemic embolization of thrombus that tends to form in the non-pulsatile left atrium. This may result in a stroke.
Changes in the shape and size of the cranium may reflect changes in the intracranial contents.
In young children, before the age of closure of skull sutures, increased intracranial pressure is reflected in widened suture lines that may be palpable and quite visible in radiographs. If the pressure is prolonged, a mottled decalcification or beaten silver appearance of the skull, along with demineralization of the dorsum sellae may be seen on x-rays. Bulging of the anterior fontanelle in the seated or upright infant is a reliable sign of increased intracranial pressure. Progressively enlarging ventricles (hydrocephalus), causes enlargement of the skull. Early diagnosis of hydrocephalus is possible by measuring the cranial circumference during well-baby check-ups (comparing it with standard charts). Subdural fluid effusions, usually associated with meningitis and subdural or epidural hematomas, also cause excessive skull enlargement in infants and toddlers who have nonfused suture lines. A small head circumference may be a sign of failure of normal brain development and is an important sign requiring evaluation of neurologic development.
In addition to recognizing overall abnormalities in head circumference, it is also necessary to recognize premature closure of sutures. This causes characteristic distortions of the head that may restrict brain expansion. This can result in neuronal damage and mental retardation if untreated (Figure 1-2).
In adults, the shape and size of the cranium are less revealing. Meningioma may result in bone proliferation that can produce an asymmetric bony prominence of the skull. This should be suspected if it appears contralateral to sensory motor deficits or in a person with focal seizures suggests. Certain metabolic conditions result in characteristic skull abnormalities. An example includes the presence of prominent supraorbital ridges and "frontal bossing" in patients with acromegaly.
In both adults and children who have a history of head trauma or in persons who are stuporous or comatose for unknown reason, the skull should be gingerly palpated for soft-tissue swelling, which may indicate underlying trauma skull damage, possibly fracture. Ecchymoses at the base of the occiput (Battle sign) or around the eyes but contained by the orbital rim ("raccoon eyes") suggest basal skull fractures.
Distortion or inflammation of sensitive intracranial structures (such as blood vessels, meningies and cranial nerves) may result in pain. In such cases, gentle rotation of the head may result in pain that the patient can localize. This happens because the brain is essentially floating in the subarachnoid cerebrospinal fluid and is tethered to the dura and contiguous skull by cranial nerves, blood vessels, and arachnoid membranes. "Sloshing" of the brain can stretch these sensitive structures, but is normally painless unless there is some pathology. This may be something benign, such as migraine that results in sensitization of cranial blood vessels, or may be a reflection of more serious conditions distorting or inflaming intracranial structures.
Vascular bruits are most often sought over major blood vessels, where they may indicate the presence of turbulent blood flow, possibly due to atherosclerosis (see Chapter 27). Bruits may also be detected by auscultation over the cranium (with the bell of a stethoscope) in areas such as the mastoid region, temporal region, forehead, closed eyes, or (in bald individuals) anywhere lacking hair. Although this is not part of the routine exam, it may indicate the presence of an arteriovenous malformation near the brain surface. The bruit is caused by the increased, turbulent flow in the arteriovenous short-circuit that makes up the malformation.
In whom should auscultation of the head be considered? The person with a history suggesting an arteriovenous malformation is one candidate. This would include patients with headaches that are always on one side of the head (most patients with migraine, for example, have at least occasional headaches on the other side) or patients with focal seizures. Of course, in both these cases, cranial imaging is the most important and sensitive test. On occasion the person with arteriovenous malformation may be aware of their own bruit, particularly at night when distractions are at a minimum. Although this is usually just due to some benign turbulence in the carotid artery as it passes through the temporal bone (immediately adjacent to the inner ear), careful auscultation of the head may help to localize the sound and further investigation may be warranted.
Prominent bruits, heard over the entire head, may occur in the small child or infant with a congenital arteriovenous malformation in the area of the internal cerebral veins and the vein of Galen. In this case, there may even be congestive heart failure due to the high flow demands of the shunt. There may also be an enlarging head, the result of a communicating hydrocephalus (due to elevated pressure in the venous dural sinuses). This increased venous pressure decreases absorption of cerebrospinal fluid through the arachnoid granulations. Compression of the aqueduct of Sylvius by the swollen vein of Galen may also result in internal hydrocephalus.
Diffuse cranial bruits in infants may also result from high blood flow through the cerebral or diploic vasculature. This may occur in the infant with meningitis or the infant or child with severe anemia. In the older children or adults (with thicker skulls) these bruits are usually inaudible.
There are several features of the examination of the eyes that should be considered as part of the neurologic exam. The conjunctiva and sclera can show signs of icterus or of inflammatory, vasculitic processes. A prominent corneal arcus can suggest dyslipidemia, which, in turn, suggests the potential for atherosclerosis. Funduscopic examination can be very revealing. First of all, it may show whether visual abnormalities are due to refractive problems, including poor visual correction or opacities (of the lens or cornea). It is also the only place in the body where blood vessels can be directly visualized. The health of these blood vessels is a reflection of the health of small blood vessels in the nervous system (including signs of atherosclerosis or of diabetic vascular disease that can effect the brain and peripheral nerves).
We will specifically discuss two phenomena of neurologic import, papilledema and subhyaloid hemorrhage. Papilledema results from increased intracranial pressure, which occurs when the contents of the cranium exceed the capacity of the intracranial physiologic mechanisms to accommodate. The major accommodating factors include: the cerebrospinal fluid space (ventricular and subarachnoid) and its ability to be drained by the venous sinuses; the venous space and its collapsibility; the ability of sutures to spread in infants and toddlers; the ability of brain tissue to be compressed and lose substance; the ability of the foramen magnum (and to a lesser degree other foramina) to transmit pressure to the extracranial spaces; and finally, the possibility of decreased production of cerebrospinal fluid from the choroid plexi when intracranial pressure rises to high levels. The major causes of increased intracranial pressure are cerebral edema, acute hydrocephalus (blockage of cerebrospinal fluid flow or deficiencies of absorption), mass lesions (e.g., neoplasm, abscess, hemorrhage), and venous occlusion (e.g., sagittal or transverse sinus thrombosis).
Papilledema or edema of the optic disk usually indicates increased intracranial pressure. When it is fully developed, recognition is not difficult; swollen, blurred and elevated disk edges, engorged and pulseless veins, and increased vascularity of the disk margins are the obvious signs. This is usually bilateral. At these stages, vision is usually unaffected (outside of possible slight increase in the physiologic blind spot *). With further development, hemorrhage (both superficial and deep) and exudates appear. If the process is chronic, filmy white strands of glia proliferate in and around the disk. It is at this late stage that the patient may complain of episodic obscured vision. This precedes final occlusion of the retinal arterial supply and infarction of the retina with permanent blindness. Early recognition is important in order to diagnose the underlying cause and also in order to prevent vision loss.
It is usually possible to detect early, subtle signs of intracranial hypertension by examination of the fundus of the eye. Prior to well-established and easily recognizable papilledema, the normal pulsations in the veins of the optic disk disappear with elevated pressures. These pulsations are best seen in the normal fundus where the veins disappear into the substance of the disk. They reflect the arterial pulse pressure superimposed on a baseline intraocular pressure; the veins partially collapse during systole and expand during diastole. If the pulsations are not spontaneously present (as they are in about 75% of normal individuals), a minimal amount of pressure on the globe brings them out in almost all persons who do not have increased intracranial pressure (i.e., less than 200 mm of CSF). The minimal compression partially collapses the veins and allows them to expand during diastole. The higher the intracranial pressure is, the less likely there are to be spontaneous pulsations, and they are not usually present when intracranial pressure is 200 mm of CSF or greater. **
Papillitis or inflammatory edema of the disk looks very similar to papilledema. Indeed, in most cases, they are identical. Papillitis is most often caused by demyelinating processes in young and middle-aged persons (such as multiple sclerosis) and by optic nerve arterial occlusion in older individuals. It is not associated with increased intracranial pressure. As opposed to papilledema, however, it is almost always unilateral. The visual field loss associated with papillitis is usually greatest near the center of vision, because the macular (cone vision) fibers are primarily affected. This leads to early loss of color, particularly red, vision. A central scotoma (blind area) is typically present and thus visual acuity is severely limited and the loss of acuity can not be corrected by refraction (see Chapter 3). This is distinct from papilledema which usually only produces slight enlargement of the blind spot until quite late when the arterial supply may be compromised by compression. Even then, the vision loss of papilledema is usually distinct because it starts at the periphery, with central vision preserved until late.
Subhyaloid hemorrhage is another finding that can be seen with the ophthalmoscope. This is a collection of extravasated blood just beneath the inner limiting membrane of the retina (Figure 1-3). This is different from most retinal hemorrhages, which occur deep to the nerve fiber layer.*** Subhyaloid hemorrhages may occur spontaneously in patients with diabetic retinopathy, usually unilaterally. However, from the perspective of the neurologist, they are frequently observed close to the disk margins with an acute, catastrophic rise in intracranial pressure. This is most likely due to intracranial arterial hemorrhage (subarachnoid or intracerebral) or to head trauma with hemorrhage and brain contusion or laceration. They are often seen in "battered infant" syndrome, for example. When they result from intracranial causes, they appear almost immediately and most often on the background of a relatively normal-appearing retina. This is as opposed to diabetic subhyaloid hemorrhage, which has the background of diabetic retinopathy. The intracranial causes are presumably due to a rapid and excessive rise in the central retinal venous pressure, which leads to rupture of the small venular radicals near the disk. Therefore they may be bilateral and papilledema may follow within several hours. Subhyaloid hemorrhages that appear in front of an otherwise normal retina are diagnostic. This observation should allow the physician to avoid lumbar puncture, which, in the presence of cerebral hemorrhage or cerebral contusion or laceration, could further predispose the patient to brain herniation (see Chapter 17).
A finding of middle ear infection, acute or chronic, during otoscopic examination may provide clues as to the origin of bacterial meningitis. Indeed, particularly in children, this is one of the most frequent portals of entry for the infectious agent. The presence of otitis media is readily visible on otoscopic examination as an opaque, bulging, erythematous tympanic membrane. Successful care of the meningitis may depend on eradication of the otitis, which may necessitate puncturing the eardrum (myringotomy) for drainage in addition to administering appropriate antibiotics. Chronic otitis media or mastoiditis may also provide a portal for direct extension of infection to the adjacent temporal lobe, resulting in cerebritis and an abscess.
It is important to perform an otoscopic exam on the patient who is unconscious without apparent cause. This is part of the examination for possible head trauma (along with observation and palpation of the head and scalp) because a bulging, blue-red tympanic membrane may indicate hemorrhage into the middle ear, likely the result of severe head trauma. Basilar skull fracture with dissection through the middle ear is the probable cause; however, severe shearing of the ossicles may be enough to cause tears in blood vessels and hemorrhage.
In the person with hearing loss, especially if the deficit is of the conduction type, obstructions of the external ear canal or abnormality of the tympanic membrane or middle ear cavity should be considered (see Chapter 6).
The spinal cord, meninges and cervical roots and even lumbar nerve roots are stretched slightly when the head is flexed onto the chest. This ordinarily can be done without any discomfort. However, this is not so when the meninges and/or nerve roots are inflamed and flexion causes reflex stiffening of the neck muscles. This is particularly powerful when the meninges are inflamed and it has been called "nuchal rigidity" or meningismus. Because the spinal cord is pulled upward slightly in the spinal canal by neck flexion, the lower lumbosacral nerve roots are also stretched and pain may be experienced in the low back and legs as well as the neck. Occasionally, spontaneous flexion of the legs and hips occurs on neck flexion (termed Brudzinski sign). This reflex movement of the lower limbs induces a bit of slack in the lumbosacral nerve roots, diminishing the tension produced by the neck flexion. Although this movement is usually not able to lessen the pain significantly, it is a strong indication of meningitis and other causes of root irritation.
A majority of the population by age 65 to 70 has some degenerative disease of the cervical spine. This osteoarthritic change, frequently referred to as cervical spondylosis, appears to be a product of the constant trauma of the weight of the oversized human head on the neck when in the erect position. Despite the appearance of severe cervical osteoarthritis on x-rays, disabling symptoms do not occur in the majority of people with cervical spondylosis. Spondylosis does correlate with gradually increasing limitations in neck mobility (mostly in rotation and lateral bending). Flexion is usually not very limited and there is usually not much (or any) pain directly attributable to the spondylosis.
The most important symptoms and signs that may result from spondylosis are due to irritation or destruction of the cervical roots and/or the spinal cord by the hypertrophic degenerative disks and joints. Nerve root involvement due to osteophytic spurs of bone, or bulging intervertebral disks may produce signs of nerve root irritation (radiculitis) or damage (radiculopathy). There may be positive symptoms of pain and paresthesias. There also may be negative signs and symptoms (e.g., loss of sensation, reflexes and power). Damage to the spinal cord (myelopathy) by spondylosis can result in motor and sensory symptoms below the neck due to interruption of the long tracts of the spinal cord by impingement. This may present as ataxia (difficulty walking) or overactivity of urinary bladder function in older individuals.
Lhermitte symptom (or Lhermitte sign) includes a sensation of "electric shocks" radiating from the posterior neck region into the arms, trunk, and legs separately or in combination produced by forcible, passive neck extension or flexion. This can result from cervical spinal cord damage from any cause and is probably due to rapid distortion of the cervical cord. This distortion causes depolarization of overly sensitive, injured axons in sensory tracts within the cord. This may result from neck flexion because this movement directly stretches the cervical cord. Neck extension produces this symptom because of narrowing of the cervical spinal canal during this movement. This narrowing can directly impact the cervical spinal cord if the canal dimensions are excessively small (due to any combination of congenital narrowing, disk bulging, osteophytic bone spurs and/or buckling of the ligamentum flavum, see Figure 11-3). Cervical osteoarthritis is the most common cause of this "cervical stenosis" because degenerative changes are associated with thickening of the ligamentum flavum as well as posterior bulging of the intervertebral disks and bone proliferation (osteophytes) at the margins of the disks. The vertebral canal is further narrowed upon extension of the neck. This may cause pressure on the ventral or dorsal surface of the cord with some traumatic depolarization of axons in the sensory tracts. Lhermitte initially described this symptom in patients with multiple sclerosis involving the cervical spinal cord although it could just as easily result from other lesion (e.g., neoplasm or syrinx). In general, a physician should suspect an extramedullary lesion (i.e., pressure on the outside of the cord) if Lhermitte symptom is elicited by extension of the neck and an intramedullary lesion if elicited by flexion.
Posterolateral protrusion of an intervertebral disk and narrowing of an intervertebral foramen due to encroachment by degenerative osteophytes are the two most common reasons for nerve root damage or irritation (radiculopathy). A useful maneuver for corroborating that upper extremity symptoms are due to radiculopathy incorporates the combined motion of extending the patient's neck and then pressing down on the head. This narrows the spinal foramina and may reproduce the patient's symptoms, thus corroborates their cervical origin. More marked foraminal narrowing can be elicited by extending the head and then laterally flexing and rotating the head to one side while pressing down on the top of the head (Spurling's maneuver). This results in further foraminal occlusion on the side to which the head is flexed and rotated (Figure 1-4). Direct pressure on the posterior lateral part of the neck with the thumb or index finger may also produce discomfort over the involved roots, although pain with this maneuver is more likely to detect painful muscles. Of course, any forced movement of the neck should be done cautiously in patients with possible spinal cord injury or injury to the cervical spinal column. Only enough force should be used to elicit the sign or symptoms and, in the case of acute injury it may be necessary to perform x-rays before any such maneuver.
Movements of the lower extremity beyond a certain point will stretch the lumbosacral plexus and associated nerve roots. Straight leg-raising (i.e., passive flexion of the straightened leg on the hip), or the reverse, extension of the leg on the hip, is used in an attempt to reproduce lower extremity radicular symptoms in patients who are thought to have irritation or damage to the lumbosacral plexus and roots. When the leg is flexed on the hip, the nerve roots of the posterior-lying sciatic nerve, which originates in the lower lumbar and upper sacral roots (L4-S2), begin to be stretched once the limb has reached about 30 degrees of flexion (Figure 1-5A). Extension of the leg on the hip (with the patient lying on their side or prone) stretches the anterior-lying femoral nerve, which originates from the middle lumbar roots (L2-4) (Figure 1-5B).
Any mass or inflammatory process impinging on the nerve, plexus, or nerve roots is capable of binding or irritating these structures, causing pain in the peripheral distribution of the nerve. This pain is often in the muscle and bone distribution of the nerves as opposed to the skin or dermatomal distribution. Buttock, posterior thigh, calf, as well as heel discomforts are characteristic of sciatic system involvement, whereas groin and anterior thigh pains are characteristic of femoral system involvement. If there is skin involvement, loss of sensation occurs in appropriate dermatomes or peripheral nerve distribution. However, loss of sensation or weakness will only occur if the lesion is destructive. It is more common to have paresthesias (pins-and-needles sensations) than actual loss of sensation when a nerve root is damaged. A symptomatic irritative lesion may not cause any actual loss of nerve function despite causing significant pain.
Herniated disk is the most common cause of lumbosacral radiculopathy. The great majority of symptomatic intervertebral disks are between the L4-5 or L5-S1 vertebral bodies. Because the L5 and S1 roots exist at these spaces, straight leg-raising with the patient supine, causing sciatic stretch, is the maneuver of choice. A relatively small percentage of lower spine disk problems occur at L3-4 or L2-3, and a tiny number are found at L1-2 or thoracic levels (although these have been recognized more frequently in the era of magnetic resonance imaging). With the higher lumbar protrusions, femoral stretching is the maneuver that is most likely to reproduce symptoms. It must be noted that an increase of back pain, alone, is not considered an indication of nerve root involvement and is considered a negative straight leg-raising test. Such a "negative test" may still cause pain, but this is probably due to stretching irritated tendons, joints and muscles in the back. Also, a true positive test must be distinguished from tightness of the hamstring muscles, which can produce discomfort during straight leg-raising.
Flexion of the head on the chest (chin to chest) pulls the spinal cord upward and stretches the lumbosacral roots somewhat. Therefore, lower extremity symptoms may be exacerbated in the patient with lumbosacral root irritation.
Meningitis can inflame the meninges and nerve roots at all spinal levels. Therefore straight leg-raising is often positive with meningitis. In fact, there may be involuntary flexion of the knees during attempted straight leg-raise (Kernig sign).
Acute or chronic arthritis of the hip, on occasion, causes referred pain in the knee and, less commonly, in the foot. Straight leg-raising may irritate a damaged hip joint and may give a misleading impression of sciatic root irritation. However, hip joint pathology is easily detected by rotating the femur on the hip while the knee and hip are flexed. This flexion of the knee puts slack on the sciatic and femoral nerves and should not put significant stretch on the sciatic nerve roots (Figure 1-6). Pain and limitations of motion in internal and external rotation of the flexed hip (Patrick maneuver) suggests hip disease, and appropriate x-rays can confirm this suspicion.
Back pain is a common, nearly ubiquitous symptom. Pathologic processes (degenerative, neoplastic, or inflammatory) in or near the spinal column frequently give rise to local muscle spasm and pain. This may lead to postural abnormality and/or palpable firmness and tenderness of muscles. When the paraspinal muscles contract unilaterally, they bow the spine laterally; the concave side of the bow appears on the side of increased muscle tension (Figure 1-7B). This lateral bowing is called scoliosis and can be observed most easily when the patient is erect. Observation is further facilitated by making a mark with a pen on the palpable top of the dorsal spinous processes of the vertebrae. The only exception to the rule of contralateral bowing occurs at the lumbosacral junction where the paraspinal muscles are broadly attached to the sacrum and the ilium. The bowing occurs toward the side of the spasm in this instance (Figure 1-7A).
Many neurologic conditions result in abnormal muscle tone. When these begin early in life there may be associated skeletal abnormalities, including severe scoliosis. Although many scolioses are "idiopathic," probably related to problems of skeletal maturation, severe scoliosis, particularly when accompanied by other signs such as pes cavus (high arched feet) should prompt some neurologic examination. Progressive scoliosis, even when it does not result from neurologic abnormality, can cause neurologic dysfunction if not arrested.
Most back pain is benign. Rarely, it can result from localized serious pathology (infectious, neoplastic, hemorrhagic, etc). In many such cases, percussion of the spine to elicit point tenderness often produces localized pain. This percussion is carried out with the hypothenar portion of the fist. Because a large area is covered with each blow to the spine and there is diffusion to several vertebral segments, use of a percussion hammer to tap each spinous process may more accurately localize the involved segments, prompting some consideration of imaging.
Every general medical evaluation should include examination of the abdomen, pelvis and rectum. However, in the focused evaluation of the neurologic patient, these components of the examination are not called for unless the patient cues them by certain complaints. The most common cue is the complaint of low-back pain with or without radiation into the legs. Even though disk and spine or paraspinous disorders are the usual cause of this complaint, several common abdominal and pelvic conditions may give rise to this symptom. For example, neoplastic disorders may involve the spine and can directly invade lumbosacral nerve roots. This is a potential cause of a positive straight leg-raising sign. Carcinoma of the cervix is the most common form of female pelvic neoplasm while prostate cancer is the most common in this region in the male. These tumors may metastasize (often to the spine) but they also tend to spread by local extension. Therefore, they may first become symptomatic as low-back and/or leg pain. Rectal carcinoma occasionally gives rise to low-back pain because of spread to and enlargement of local lymph nodes. Rectal and pelvic examinations are mandatory with new or recent onset of low back pain, or a significant change in character of back pain, especially in middle-aged and older adults and particularly in the patient with a history of cancer. Breast cancer is another important consideration in any woman with new back pain or, for that matter, bone pain involving any level of the spinal axis. Screening tests are appropriate in such cases.
Acute, new back pain should give rise to consideration of possible abdominal aortic aneurysm (often palpable or visible on lumbar x-rays and measurable by ultrasound). Renal disease should be considered in patients with flank pain, particularly if the pain is colicky.
Rectal examination is indicated in patients with urinary or fecal incontinence in order to evaluate both reflex and voluntary anal sphincter function.
Define the following terms:Battle sign, raccoon eyes, bruit, papilledema, myelopathy, radiculopathy, radiculitis, Lhermitte symptom, meningissmus, Brudzinski sign, Kernig sign, Patrick test.
1-1. What happens to blood pressure and pulse with increased intracranial pressure?
1-2. What part of the brain contains the primary respiratory centers?
1-3. What is the most common finding that differentiates orthostatic hypotension due to hypovolemia from that due to sympathetic failure?
1-4. Can the brain cause EKG changes that appear as ischemia?
1-5. What is the most reliable finding of increased intracranial pressure in an infant?
1-6. Why is it important to measure cranial circumference in young children?
1-7. What are some causes of cranial bruits?
1-8. What are the major causes of increased intracranial pressure?
1-9. What is the most sensitive finding in increased intracranial pressure?
1-10. What is the difference in appearance between papillitis (inflammation of the optic nerve head at the optic disc) and papilledema?
1-11. What is the difference between Lhermitte symptom produced by intrameduallary disease as opposed to that caused by extramedullary compression?
1-12. What is Spurling maneuver and what does it show?
1-13. What is the function of the straight leg-raising test?
*The retina is very sensitive to mechanical pressure. You may demonstrate this by pressing very lightly on the lateral side of one of your eyes. The depolarization block caused by minimal compression of the retina creates a blind spot (scotoma) in the contralateral field (i.e., next to your nose). In like manner, early and poorly visible swelling of the disk margin depolarizes and blocks the proximate retina and enlarges the physiologic blind spot. The blind spot represents the retina-deficient optic disk and is routinely plotted and of fairly uniform size when formal visual fields are studied with a tangent screen or perimeter (see Chapter 3).
**The mechanism for loss of venous pulsations is presumed to be an increase in venous backpressure subsequent to intracranial hypertension. It is presumed that papilledema is a function of the ratio of intracranial (and, therefore, intravenous) pressure to intraocular pressure; elevation of the former or depression of the latter is adequate to abolish pulsations and elicit edema of the disk. For practical purposes, papilledema is almost always the result of increased intracranial pressure. Increased intraocular pressure (glaucoma) should delay the appearance of papilledema; it can be the source of some diagnostic confusion.
***In persons with long-standing diabetes mellitus or systemic hypertension, the blot-like hemorrhages may be present but are usually associated with other abnormalities of the retina, including hemorrhages of the nerve fiber layer (flame-shaped or striated), narrowing and atherosclerotic distortion of the arteries, exudates, capillary aneurysms, and vascular proliferation (neovascularization).