THE NEUROLOGIC EXAMINATION

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THE NEUROLOGIC EXAMINATION

  1. 1. THE NEUROLOGIC EXAMINATION Raymond A. Martin, MD Houston Neurology Associates Houston, TX Eun-Kyu Lee, MD Associate Professor, Department of Neurology University of California, Davis Sacramento, CA Edward L. Langston, MD, RPh. American Health Network Board of Directors, ACGME Council on Medical Education, AMA Lafayette, IN 1
  2. 2. Section One The Neurologic History As family practitioners you will see patients with complaints that cover the full spectrum of medical practice. Many of these patients, present with symptoms of pain, dizziness, forgetfulness, numbness, weakness and difficulty speaking or comprehending as their primary complaint, or as a portion of their history. In addition to a full medical evaluation, accurate assessment of these neurological complaints will be of increasing importance in our current health care environment. Since up to 10 to 15% of a family practitioner's workload consists of neurological problems, it is the goal of this program to provide an effective and efficient means of gaining this knowledge. As a first step in evaluating the patient with a neurological problem the practitioner must obtain an accurate history. A good history alone will often suggest the correct diagnosis and the examination can be tailored to specifically search for corroborating physical signs. Patients with neurological disease may have impairments that make it difficult to elicit accurate information and the diligent examiner may need to spend extra time questioning the patient or obtaining information from family or friends. While this may seem tedious, time spent obtaining an accurate history often brings a rapid, correct diagnosis, thereby saving time and reducing health care costs. An important consideration in history taking is to not only record the patient’s complaint, eg, dizziness, but to question exactly what the patient means by that complaint. The symptom “dizziness” often has different meanings to the lay public and the term could be used to connote lightheadedness, vertigo, tiredness, or malaise. If the examiner assumes it means vertigo then needless time and resources may be wasted in pursuing a non-existent complaint. Another example is “weakness” which to many patients may mean fatigability or lack of energy rather than loss of strength in specific muscle groups. The history should be recorded in chronological order and in a systematic manner, noting the date of onset of symptoms and developing the story in sequence. Symptoms should be characterized and described in terms of severity, location, temporal profile, as well as aggravating and ameliorating factors. Any relation to the past history should be established and noted. Certain questions may be specific to certain disease processes; in other diseases, symptoms will be similar but the diagnosis may be established by a difference in temporal profile, ie, whether it is acute, subacute or chronic. For example, numbness and weakness of an extremity that is abrupt in onset suggests transient cerebral ischemia or stroke while the same symptoms, if they develop over minutes, may be associated with the aura of migraine. Progression of the same symptoms over days may be due to a brain abscess and over weeks to months, a brain tumor. How the history is obtained affects reliability. It is important to have the patient describe symptoms in his or her own words and for this to be reflected in the record as such. Be careful not to interpret the complaints and record them in a fashion that biases the history to suggest a diagnosis that you may suspect, but is not borne out by the patient’s story. Poor historians may 2
  3. 3. have to be questioned in a number of different ways and afforded much patience. Additional information may need to be obtained on subsequent interviews. Information that is suspected to be false or inaccurate may have to be corroborated by family members or other more reliable witnesses. Chronological and accurate recording of historical events gives perspective to the tempo of a disease process and serves as a valuable record that may be referred back to in the event of future illness. It may also serve as a medico-legal document in compensation and liability cases. The time afforded to obtaining an accurate history is often half the time devoted to the entire patient encounter. The customary sequence of information collection in the neurological interview is outlined below: • Chief Complaint • History of Present Illness • Past Medical History • Review of Systems or Functional Inquiry • Family History • Social History As in any medical history the interview should be initiated by obtaining and recording the chief complaint. This is recorded in the beginning of the history and is noted in the patient’s own words. This is followed by the history of present illness. The patient should be allowed to tell his story without interruption for a certain period; as the interview progresses important details can be added by more pointed questioning. Important information includes date of onset, symptom description, temporal profile, other complicating complaints, aggravating and ameliorating factors, effects of treatment and progress of the symptoms over time. It is helpful to record dates as a heading in historical sections or in a parallel location in the margins of the document. Obtain information about how the symptoms affect the daily life of the patient and whether or not they impair daily activities and the ability to engage in gainful employment. With increasing experience and knowledge of neurological disease processes the history will become more meaningful and more readily suggest a possible diagnosis. As the concept of what disorder may be afflicting the patient begins to materialize, cogent questions can be asked to support or refute the putative diagnosis; eg, if a patient develops position dependent intermittent numbness of the thumb, index and middle finger, affirmative responses to questions about job related excessive wrist activity or hypothyroidism will support the diagnosis of carpal tunnel syndrome. Once the information related to the present illness is fully elicited and recorded it is useful to obtain information about past medical history that may have direct relevance to the current illness. In patients whose present illness suggests transient ischemic attack or stroke, relevant information would concern history suggestive of coronary artery disease such as angina, 3
  4. 4. and of peripheral vascular disease such as claudication. Other diseases, associated with and contributing to morbidity and mortality in stroke are hypertension and diabetes. Habits which adversely affect incidence and outcome are smoking and excessive use of alcohol. Obtaining this historical information enables the practitioner to: 1. Better understand the pathological process afflicting the patient. 2. More effectively plan an appropriate treatment regimen. 3. Provide counseling that will hopefully bring about behavior changes leading to a healthier lifestyle. In such a manner further history relating to past relevant illnesses should be obtained and recorded in a section following that of the present illness and stated in a way that makes any relationship to the present illness apparent. Having completed this portion of the history one should proceed to the neurological review of systems or functional inquiry. This portion of the history may turn up more information that relates to the present illness as well as provide an over all historical portrait of the patient’s health status. It may also be the most time consuming portion of the history, however, the way it is reported by the patient may also give insight into the patient’s personality and thought processes. Many patients with psychosomatic illness will give long descriptions about symptoms such as dizziness, memory disturbance or pain. Increasing experience and patience will enable the practitioner to develop a unique set of skills and techniques, enable him/her to both control and get maximum information from the interview. At the same time the patient will feel that he/she has had adequate opportunity to convey personal symptoms and fears. One can develop a pattern of questioning for this portion of the history, which is facilitated by a predetermined outline. A partial, but useful, list should include questions about the following symptoms: • Smell • Involuntary movement • Pain • Visual defect • Weakness • Numbness • Diplopia • Gait disturbance • Paresthesia/anesthesia • Ptosis • Incoordination • Headache • Hearing disturbance • Muscle atrophy • Seizure/syncope • Vertigo, Lightheadedness • Tremor • Memory • Swallowing difficulty • Muscle Cramps • Thinking (confusion) • Speech disturbance • Bladder/bowel control • Behavior/Mood change • Sleep disturbance • Weight change • Aphasia The family history will occasionally identify a patient with a specifically inherited disorder such as a muscular dystrophy, cerebellar degeneration or perhaps Huntington’s chorea. This is usually not the case, but an inquiry should always be made. Certain diseases may not be directly inheritable but having an affected family member may put the subject at a higher risk 4
  5. 5. than the general population. Such is the case in multiple sclerosis and some autoimmune diseases. Care must be taken not to frighten patients about disease prospects if there is a hereditary disease in their family. Proper education, genetic evaluation and counseling should be made available to all interested family members. If patients are not aware of their family medical history an attempt should be made to have either the examiner or an interested family member speak with a more knowledgeable family member. The family practitioner is in a unique position to evaluate familial diseases since many family members may already be patients and have medical records with longitudinal histories. If a hereditary condition is suspected, or confirmed, longitudinal follow-up for a variety of physical complaints in all family members will enable the family practitioner to exercise the best therapeutic and preventative strategies for his patients’ well being. The social history often sheds light on acquired illness since many social behaviors have adverse outcomes on a person’s health status, eg, excessive smoking and drinking. The rising use of illegal drugs and higher incidence of sexually transmitted diseases may also have a negative impact on your patient. Obtaining history about these and other social behaviors is a necessary and important part of the interview; in this way the practitioner can devise a treatment plan and structure advice that will benefit his/her patients. Information should be obtained about habits such as alcohol, tobacco, recreational drug use and sexual habits of patients, especially if there are multiple partners. Certain job situations may expose patients to toxins such as volatile agents or heavy metals that may cause peripheral neuropathy. Carbon monoxide exposure at non-lethal levels may produce headache and confused thinking and may be seen in individuals working on gasoline combustion engines or home heating systems in the absence of adequate ventilation. The history of present illness will help direct the questioning about social history. Presentation with stroke and hypertension might reveal an individual without insurance or adequate funds for appropriate medications. This in turn enables planning for the patient's discharge and subsequent supply of medication. Other information to be gathered during the interview concerns prior neurological testing such as magnetic resonance imaging (MRI), computed tomography (CT) or neurophysiologic testing (EEG, EMG, evoked responses), especially those related to the present illness. These studies may make similar testing unnecessary, thereby saving time and reducing health care costs. Finally a list of the patient’s current medications and dosage schedule should be obtained and analyzed. Sometimes a patient’s symptoms may be due to the side effects of a particular medication or due to drug interactions. Always question whether a symptom developed shortly after a new drug was started or its dosage adjusted; for example, metoclopramide may induce a movement disorder or Parkinson-like symptoms and signs. 5
  6. 6. Recognition of such interactions provides a quick and inexpensive cure, and is gratifying to both physician and patient. The Neurological Examination The neurological examination should always be included as part of the general physical examination; unfortunately it is often done superficially and without thought to how the findings may fit into the general pathological state of the patient. Although there are some esoteric neurological diseases, the majority presenting in primary care settings are just another part of the pathological state produced by a particular disease. If one carefully examines the insulin dependent diabetic there may be evidence of sensory or motor peripheral neuropathy characterized by stocking sensory loss, toe weakness and hyporeflexia. There may be focal cortical signs suggesting partial ischemic stroke and postural hypotension indicative of autonomic peripheral neuropathy. Abnormalities such as these warrant the institution of symptomatic, as well as preventative, therapy and may also prompt further investigation, ie, carotid Doppler and duplex scanning. An adequate neurological examination requires a few simple tools: a reflex hammer, disposable pin, cotton, tuning fork, tape measure, visual acuity card, aromatic substance to test smell, and printed copies of the Mini-Mental State Examination to include on the patients chart. These are small enough to carry in laboratory coat pockets or in a small travel case. The following overview emphasizes points that a family practitioner should keep in mind; Examples will be used to point out the significance of each portion of the examination and how the findings relate to the patient's medical picture as a whole. Basic neuroanatomy will be reviewed but it will be done in a way that is clinically useful and easy to remember. Note that the descriptions may differ slightly from precise anatomical pathways and neurophysiological relationships but will serve adequately for clinical localization and treatment application. In this fashion we hope to provide an educational tool that has utility and is user friendly. In addition to the CD, a video is included that will demonstrate how to correctly perform and interpret the neurological exam. It is to be used in conjunction with the text. Individual performance of the examination can be refined by repeated performance and evaluation by your clinical neurology faculty person. Inspection and Observation From the time the physician greets the patient he gets to observe him speaking, sitting, walking, making facial expressions and socially interacting. The trained neurological examiner can often discern abnormalities during this part of the encounter that will aid in diagnosis. Examples are the hemiparetic or parkinsonian gait, facial asymmetry due to facial muscle weakness, presence of tremor, dysphasic or dysarthric speech and a whole host of other clinical signs. Patients may have pronounced muscle atrophy, the distribution of which can help provide important diagnostic clues. These signs are often missed solely because they are not looked for 6
  7. 7. and, once pointed out, are obvious. Obtaining and utilizing information such as this is what makes a good clinician. The psychological state of the patient should also be noted. Patients may be depressed, hostile, apprehensive, preoccupied and even uncooperative. Recognizing such moods will help the examiner choose the approach best suited to maximize the information he obtains from the encounter. Reassurance and patience on the part of the examiner go a long way in gaining a patient’s trust and cooperation. The presence of pain may affect a patient’s countenance, gait, and even ability to cooperate during the examination. It takes experience, gained by doing many of these examinations, to be able to recognize when patients are truly impaired or when symptoms and signs are exaggerated for secondary or other gain. Vital Signs and Neurovascular Examination If it is to be performed in isolation, the neurological examination should always begin with recording of vital signs. The physician then proceeds to the neurovascular examination, which includes examining the neck for carotid bruits and checking for postural hypotension (if the patient complains of being lightheaded on going from the supine to erect position). Peripheral pulses are palpated if signs of peripheral vascular disease are being sought. Palpation of the carotid arteries is often performed in examining for carotid occlusive disease but a common or external carotid artery pulse is often felt even if the internal carotid artery is occluded. Rarely a thrombus in the carotid artery may break loose and embolize due to vigorous palpation; considering this, be extremely careful. Auscultation over the orbit with the stethoscope bell may disclose a bruit secondary to stenosis of the carotid siphon. In such cases reliance on carotid Doppler studies alone may not give enough information to make a decision for medical versus surgical therapy. If there is significant intracranial carotid stenosis, an endarterectomy in the cervical region will not fully re- establish intracranial circulation and the patient may incur a surgical risk with only partial benefit. Such patients need to be studied further with magnetic resonance or conventional angiography. Recent evidence supports the benefit of carotid endarterectomy in some cases where there is co-existent siphon stenosis. When the carotid arteries are auscultated, localize the bruit by determining whether it is loudest over the common (lower neck) or internal (external) carotid regions (below angle of the mandible) or if it is being radiated from a separate area such as the subclavian artery or heart. Such bruits are usually loudest over their point of origin and this point source should be sought and documented. High-pitched bruits may sometimes be indicative of tight carotid stenosis; but overall, the loudness of a bruit does not correlate with the severity of the stenosis. If subclavian bruits are present one should measure the blood pressure in each arm to rule out significant subclavian stenosis, which may sometimes be associated with subclavian steal syndrome. 7
  8. 8. System Integration When neurology is learned in the classic sense, the student studies individual functional neurological systems such as the motor, sensory, and cerebellar systems. This enables a greater depth of understanding, but in a one-month clinical rotation, time does not permit this luxury. If one is to gain clinically useful information in a limited time frame, it is best to provide understanding of broader functional concepts. These concepts must easily lend themselves to clinical application in patient care settings. In the spirit of this approach the following description will illustrate how the body moves, by discussing the interactions of the extrapyramidal, pyramidal, sensory and cerebellar functional systems. A useful concept is to imagine the human body as a marionette, all of whose controlling strings have no tension, and the puppet lies crumpled on the floor (Figure 1-1). For the puppeteer to create life-like movements he must first stand the puppet up. To do this he puts tension on the strings that cause the trunk to become erect and the legs to extend (Figure 1-2). This provides the basic framework to initiate motion of the extremities. By analogy, a similar but lengthier process occurs in human infants as their nervous systems mature. The infant first lies supine on its trunk, with arms and legs flexed. Gradually, extensor tone straightens the legs and truncal erector tone enables it to sit up. Finally the baby is able to stand although it is wobbly and must grasp for support. Figure 1-1: Initial state: Atonic The portion of the nervous system responsible for this function is the extrapyramidal system. It consists of a number of reverberating circuits in the basal ganglia and brain stem that ultimately send impulses through spinal cord pathways that tonically innervate spinal interneurons controlling the tone of muscles, which support the spine and keep the body erect. This is all done on an unconscious level. When something goes wrong with this system, as in Parkinson’s disease, the normal erect posture of the body becomes flexed, and more rigid. As the extrapyramidal system matures, fluid control of body posture provides the framework for initiation of individual extremity movements. Figure 1-2: Extensor tone established. Extrapyramidal System. 8
  9. 9. Voluntary movements, (Figure1-3), are largely initiated by the pyramidal system. Impulses go from premotor integrating areas in the frontal lobe to the upper motor neuron, which sends a crossed axon to the anterior horn cell in the spinal cord. Pyramidal tract initiated movements are crude and lack finesse. They are smoothed out and made more agile by the influence of other systems, such as the cerebellar, and via practice effect. There is also an inherent ability of the system to mature to certain degrees explaining the phenomenon of the “natural born athlete." Lesions of the pyramidal tract produce weakness, increased clumsiness, and alteration of motor tone. This will be discussed in greater detail later. The development of erector tone, which has provided the supporting framework, and the initiation of voluntary movements are, however, still rudimentary and uncoordinated. Figure 1-3: Voluntary What is needed is a system, which monitors the motor activity movement. Pyramidal and then smoothes out any irregularities in the desired action. System. The cerebellum occupies a large portion of the posterior fossa, and is in a unique position to monitor impulses entering and leaving the brain. It's foreboding anatomical structure, with its many lobes and folia, often discourages students from getting a better understanding of how this elegant structure works. A most useful concept is to think of the cerebellum as a servomechanism. A good example of such a device is the automatic piloting system on an airplane. The pilot will set the autopilot to control speed at “x” knots, the course at a certain latitude-longitude, and the altitude at so many thousand feet. The servomechanism is basically a computer which compares the actual airplane speed, read from the speedometer; the altitude, read from the altimeter; and course (direction), read from a compass, to the settings that the pilot has entered as desired. Any discrepancy between the desired and actual readings will be corrected by output from the computer. Altitude and position can be adjusted by moving the wing flaps, direction changed in similar manner, and speed by increasing or decreasing engine revs. The cerebellum works in a manner similar to a servomechanism. It receives input from the sensory system and information about output from the pyramidal and extrapyramidal systems. When a person swings a tennis racquet, impulses travel down the pyramidal pathway to specific anterior horn cells in the spinal cord, which initiate movement. These same impulses are sent to the cerebellum, which receives them before the anterior horn cells, so that the cerebellum knows what movement is intended. As the arm begins to move sensory proprioreceptors send information back to the thalamus and sensory cortex so that the person is aware of his achieved arm movement. The cerebellum “knows” what was intended and what is actually being achieved. If there is any discrepancy, the cerebellum corrects this via inhibitory outflow pathways, which alter muscle tone and action. One can thus visualize a dynamic and fluid interaction between these three systems, which enable the body to move in the most efficient manner. It is derangement of one or more of 9
  10. 10. these systems that produce the pathological states seen in symptomatic neurological disease. Understanding how these systems work will enable the clinician to recognize and localize nervous system disorders. An example from the preceding concept is illustrated by the clinical finding of ataxia. Ataxia is defined as motor incoordination but may be produced by lesions involving motor, sensory or cerebellar pathways. If a patient is noted to have arm clumsiness on finger to nose testing, this could be secondary to weakness of arm and hand muscles, to loss of proprioception in the upper extremity or due to a cerebellar lesion. If weakness is present, the clumsiness is defined as motor ataxia. If strength is normal, and there is a marked proprioceptive deficit, such that the patient can determine the arm’s position only by looking at it, then we have sensory ataxia as the cause of arm clumsiness. Sensory ataxia of lower extremity and truncal muscles produces Romberg’s sign whereby the patient can only maintain balance while standing if his eyes are open. This is because he has absent proprioceptive cues and must rely on vision to keep his balance. Finally, if motor strength and sensation are normal, and incoordination is still present, it is most likely of cerebellar origin. Localizing lesions to specific portions of the cerebellum will be covered later in this chapter. Section Two System Review In the following section the systems will be reviewed in greater detail. ►Cranial Nerves ► Mental Status Examination ► Sensory System ► Extrapyramidal System ► Pyramidal System ► Cerebellum ► Peripheral Nervous System ► Individual Muscle Testing ► Evaluation of Speech and Language Cranial Nerves There are 12 cranial nerves, which are numbered along the rostrocaudal axis with all but the first two cranial nerves located between the uppermost part of the midbrain and the caudal medulla. Their names refer to their function. Knowledge of the location and course of the cranial nerves is important in localizing lesions, particularly those within the brainstem from which the majority of cranial nerves originate and emerge. 10
  11. 11. III. Oculomotor nucleus IV. Trochlear nucleus V. Trigeminal Figure 2-1: Dorsal view of cranial nerve motor nucleus VII. Facial V. Sensory nuclei in the brainstem and upper cervical nucleus nucleus of V cord. Cranial nerve motor nuclei are on the left and sensory nuclei on the right. VII. Abducens nucleus VIII. Vestibular IX. X. Nucleus nucleus ambiguus X. Dorsal motor VIII. Cochlear nucleus of vagus nucleus XII. Hypoglossal nucleus ucleus solitarius Anatomically, the nuclei of the somatic, VII. IX. X (homologous to spinal nerves), cranial XI. Spinal Accessory nucleus nerves (III, IV, VI, and XII) are located just off the midline of the brainstem (Figure 2-1). In comparison, the nuclei of the branchial, (derive from gill arches), cranial nerves (V, VII, IX, X, and XI) are located more laterally. The special sensory (I, II, VIII) cranial nerves are derived from outpouchings, or diverticulae, of the brain and have projections within the brain, which are relatively complex. Each of the cranial nerves will be reviewed individually for anatomy, tests of function and potential pathology. Cranial Nerve I - Olfactory Nerve Cranial nerve I consists of first order neurons, which are bipolar sensory cells within the nasal mucosa whose distal axons group to form the olfactory nerve. The olfactory nerve passes through the cribiform plate of the ethmoid bone and synapses onto the olfactory bulb. The olfactory bulb, in turn, is composed of second order neurons, which traverse posteriorly and terminate in the ipsilateral hippocampal gyrus, with complex connections with multiple nuclei of the limbic system. To examine the olfactory nerve, the patient is asked to close his/her eyes while compressing each nostril separately. A test tube containing a common substance with a strong odor, such as coffee, cinnamon or peppermint, is then placed below the nostril. The patient is asked if he can smell the substance and, if so, recognize it. The patient's ability to simply smell the substance eliminates anosmia (absence of smell). The most common causes of anosmia are the common cold and allergic rhinitis. Tumors of the frontal lobe, such as meningioma, may compress the olfactory nerve or bulb and produce anosmia. Smell, like other sensations, may diminish with age. In the setting of head trauma, the 11
  12. 12. olfactory nerve is the most commonly injured cranial nerve due to shearing injuries, which may or may not be associated with fractures of the cribiform plate. If rhinorrhea occurs after head trauma, nasal drip should be checked for the presence of glucose with a Dextrostix or urine test strip. A positive test for glucose suggests cribiform plate fracture with cerebrospinal fluid leak, as discharge from nasal mucosa does not contain glucose. Cranial Nerve II - Optic nerve (see Chapter on the Visual System for a separate discussion) Cranial nerve II, the optic nerve, is composed of axons, which originate in the ganglion cell layer of the retina. The optic disk of the fundus corresponds to the attachment of the optic nerve to the retina. The absence of rods and cones, the fundamental organs of sight, at the optic disk accounts for the blind spot in one's visual field. The optic nerve traverses posteriorly from the orbit through the optic foramen (which also contains the ophthalmic artery) and merges with the contralateral optic nerve to form the optic chiasm. A partial decussation of the optic nerves at the optic chiasm results in the formation of the optic tracts. Each tract contains axons from both retina and project around the cerebral peduncles to synapse at the lateral geniculate body. Some fibers from the lateral geniculate body project to the midbrain to participate in the pupillary light reflex. From the lateral geniculate body arise the optic radiations, which hug the lateral ventricles as they traverse posteriorly and then medially to the primary visual cortex in the occipital lobe. The optic nerve is a special sensory nerve, which can be assessed by testing for visual acuity, visual fields and fundoscopic examination of the retina. Visual acuity reflects central vision or vision subserved by the macula where cones are in highest concentration. Monocular vision is tested by having the patient cover one eye, hold a pocket-sized Snellen chart at arm's length, and read the smallest numbers on the chart that can be read. Visual acuity is graded from 20/20 to 20/800. Corrective lens, if available, should be worn during testing. In the event that visual acuity is so severely impaired that a miniature Snellen chart is not useful, ask the patient to count fingers placed about 14 inches in front. Failing this check for perception of movement, then light. Poor visual acuity may be associated with lesions involving the lens (cataracts), anterior optic chamber (glaucoma), retina (macular degeneration) or optic nerve (optic neuritis). Evaluation of the size of the patient's blind spot is a quick method to assess optic nerve dysfunction. The patient is asked to face the examiner as if testing visual fields by confrontation, with one eye closed and the other fixated on the examiner's contralateral eye. A red-tipped ball or matchstick is then brought laterally into the patient's visual field until it disappears into the blind spot, after which it reappears as the red object is moved more medially. The perimeter of the patient's blind spot is mapped by asking the patient when the red ball reappears as it is moved laterally and vertically from the center of the identified blind spot. The examiner is the control to determine whether the patient's blind spot is enlarged. Patients with multiple sclerosis who present with retrobulbar neuritis, (inflammation of the optic nerve behind the disc so swelling or papillitis is not appreciated on fundoscopic examination), have demonstrable enlargement of their blind spot in addition to marked diminution in monocular visual acuity and sometimes retrobulbar pain. 12
  13. 13. Visual field testing assesses the integrity of the optic pathways as it comes from the retina, optic nerves, optic chiasm, optic tracts, and optic radiations to the primary visual cortex. It is most commonly performed by confrontation (Figure 2-2). The patient faces the examiner while covering one eye so that he fixates on the opposite eye of the examiner, directly in front of him. The examiner, using himself as a control, then wiggles a finger at the outer boundaries of the four quadrants of vision, the upper and lower nasal and temporal fields, while the patient points to the quadrant in which movement is perceived. The patient and examiner should perceive movement at the same points. Object Optic Nerve Figure 2-2: Examination of the patient's left Optic chiasm eye visual fields by confrontation. The Optic tract Lateral geniarte patient is asked to identify the number of body fingers, which the examiner raises in each Optic radiations quadrant while centering his gaze on the (geniculoccal- carine tract) examiner's right eye. Temporal lobe Calcarine cortex Figure 2-3: Lesions of the optic nerve, optic (occipital lobe) chiasm, optic tract, optic radiations and primary visual cortex produce characteristic visual field deficits. Testing is also performed by covering one of the patient’s eyes and having the patient fixate on the examiner's nose. One to three fingers are then shown to the patient in each of the four visual quadrants of each uncovered eye and the patient asked to state the number of fingers seen. Lack of vision in quadrants can then be detected and mapped out to various types of field defect. If the patient is uncooperative, visual field examination may be grossly tested by asserting a threatening hand to half of a visual field (while cautiously avoiding movement of air that can result in a corneal blink reflex) and observing for a blink to threat. 13
  14. 14. Monocular visual field deficits are often due to lesions anterior to the optic chiasm, ipsilateral to the field cut as may be seen with lens dislocation or retinal infarction from occlusion of the ophthalmic artery. Homonymous visual field deficits (toward the same side, eg, left temporal, right nasal = left homonymous hemianopsia) imply a lesion posterior to the optic chiasm (Figure 2-3). The more congruous (looks the same for each eye) the homonymous field cut, the more posterior the lesion is along the optic radiations. If macular sparing, or sparing of the center of vision, is detected with a homonymous hemianopsia, the lesion is most likely in the occipital lobe, as the macular area of the visual cortex is kept viable after a posterior cerebral artery infarct by terminal branches of the middle cerebral artery. Fundoscopy is performed with an ophthalmoscope. The patient is asked to fixate on an object in the distance while the examiner uses his right eye to examine the patient's right eye and the left eye for examination of the patient's left eye. Once the fundus is visualized, systematic examination of the optic disk, with attention to color and definition of disk margins, arterial supply, venous pulsations, and surrounding retina is conducted. Swelling of the optic disk may be due to inflammation of the optic nerve, optic neuritis, or papilledema. These conditions may be difficult to differentiate based on fundoscopy alone. Typically, optic neuritis is associated with decreased visual acuity and an enlarged blind spot. Optic pallor implies optic atrophy from retrobulbar neuritis, as seen in multiple sclerosis, or ischemic optic neuropathy from small vessel infarction of the optic nerve secondary to long- standing hypertension. Papilledema implies increased intracranial pressure. Visual acuity is not affected unless there is secondary atrophy of the optic nerve from chronic pressure on the optic nerve. With papilledema, venous pulsations may be lost. Pallor of a segment of the fundus, associated with complaints of a "pie in the sky" loss of monocular vision, suggests branch central retinal artery occlusion secondary to embolic or thrombotic occlusion of either the ciliary or ophthalmic arteries, both of which supply the optic nerve. Cranial Nerves III, IV, and VI - Oculomotor, Trochlear and Abducens Nerves (see Chapter on the Visual System) The oculomotor (III), trochlear (IV), and abducens (VI), nerves together innervate the Superior Rectus Inferior Oblique Superior Rectus III III III extraocular muscles (Figure 2-4). The primary action of the medial rectus is adduction and that of the lateral rectus is Lateral Lateral abduction. The superior rectus and inferior Rectus Rectus VI VI oblique primarily elevate the eye while the inferior rectus and superior oblique primarily depress the eye. Inferior Rectus Superior Oblique Inferior Rectus III IV III Figure 2-4: The action and nerve supply of the extraocular muscles. 14
  15. 15. The oculomotor nerve (cranial nerve III) Periaquaductal Gray Aqueduct of Sylivius also innervates the levator Matter palpebrae muscle, which Oculomotor elevates the eyelid, the Red Nucleus ucleus III pupillo-constrictor muscle, which constricts Posterior Cerebral Artery the pupil, and the ciliary muscle, which controls the thickness of the lens, Superior Basilar artery allowing for Cerebellar Artery accommodation. The Petrous ridge nuclear complex of the Cranial nerve III oculomotor nerve lies (Oculomotor) Cavernous sinus medially within the Sella turcica midbrain, ventral to the Superior orbital Spheroid ridge Fissure aqueduct of Sylvius Optic nerve (Figure 2-5). It consists of the oculomotor nucleus, Eye which innervates the skeletal muscles of the eye and dorsally abuts the Edinger-Westphal nucleus, which carries Figure 2-5: The oculomotor nucleus sits adjacent to the periaqueductal gray of the midbrain and courses parasympathetic innervation to the pupil anteriorly between the posterior and superior and ciliary muscle. The oculomotor nerve cerebellar arteries, across the petrous ridge of the courses medially within the midbrain, temporal bone, through the cavernous sinus, and out exiting through the cerebral peduncles. the superior orbital fissure to innervate the Then it traverses anteriorly through the extraocular muscles. posterior fossa between the posterior cerebral and superior cerebellar arteries, across the petrous ridge of the sphenoid wing, under the optic tract, along the lateral wall of the cavernous sinus, where it divides into a superior and inferior branch, and through the superior orbital fissure. The superior branch of the oculomotor nerve supplies the superior rectus and levator of the upper lid while the inferior division innervates the medial rectus, inferior rectus, inferior oblique, pupilloconstrictor muscle and ciliary body. 15
  16. 16. A complete oculomotor Command R palsy will manifest as ptosis, dilated and fixed pupil, and L outward and slightly downward deviation of the eye, Look Ahead due to unopposed action of cranial nerves IV and VI, with inability to move the eye medially, superiorly or inferiorly Look to left (Figure 2-6). Pupil-sparing, isolated oculomotor nerve paresis is often due to ischemia from hypertension, diabetes, tertiary syphilis, or vasculitis, as the Look ahead pupillomotor fibers travel along the periphery (outside) of the oculomotor nerve, closer to the Examiner lifts Left eyelid. Note blood supply of the nerve and are the down and out less susceptible to end-arteriole position of globe ischemia that tends to affect the center of the nerve. On the other hand, acquired third nerve Look Ahead palsies, which involve the pupil, may be due to compressive lesions such aneurysm of the posterior communicating artery, Look to right head trauma, and tumors of the and down cerebral hemispheres compressing the oculomotor nerve and the parasympathetic fibers, which run peripherally within it. Figure 2-6: A complete left III nerve palsy is illustrated along with clinical presentations of left VI and IV nerve palsies. 16
  17. 17. Figure 2-7: The course of the trochlear nerve IV nerve nucleus in the pons, across the posterior and Medial longitudinal superior cerebellar arteries, across the fasciculus petrous ridge of the temporal bone, through the cavernous sinus, and out the superior Cranial nerve IV orbital fissure is illustrated. (Trochlear) Posterior cerebral artery The trochlear nerve (cranial Superior cerebellar verve IV) nucleus lies in the medial artery midbrain, at the level of the inferior colliculi, and wraps around the Petrous ridge midbrain dorsally, alongside the Sella turcica cerebral peduncles, and courses Cavernous sinus between the posterior cerebral and Superior orbital superior cerebellar arteries (Figure 2- fissure 7). Then, it crosses the petrous ridge of the sphenoid wing, through the lateral walls of the cavernous sinus, and innervates the contralateral superior oblique after emerging from the superior orbital fissure. As the trochlear nerve has the longest intracranial distance of the cranial nerves, head trauma is the most common cause of nerve injury. A large proportion of fourth nerve palsies, however, are congenital and associated with a superior oblique that is shortened and tethered. The abducens nerve (cranial 4th Ventricle nerve VI) nucleus lies near the floor of the fourth ventricle, close to the midline, in the caudal VI nucleus portion of the pons. The axons Spinal tract course ventrally through the pons of V and exit to run anteriorly along the petrous ridge of the temporal VII nucleus bone. Then, the abducens nerve travels in the middle of the cavernous sinus, through the superior orbital fissure and into Cranial Pyramidal nerve VII the lateral rectus muscle. As the Tract facial nerve loops around the abducens nerve nucleus within Paramedian Pontine Cranial nerve VI the pons, a pontine glioma or Reticular Formation fourth ventricular ependymoma (PRPF) will produce ipsilateral paralysis of the lateral rectus and lower motor neuron facial nerve palsy (Figure 2-8). Figure 2-8: Note how the facial nerve wraps around the nucleus of cranial nerve VI within the pons. 17
  18. 18. Inflammation or an abscess involving the petrous portion of the temporal bone, following a complicated otitis media, may result in diplopia, from extension of inflammation to the ipsilateral abducens nerve as it travels along the petrous ridge, ipsilateral facial pain from contiguous inflammation of the trigeminal nerve, and ipsilateral Bell's palsy from involvement of the peripheral facial nerve (Gradenigo's syndrome). Examination of the extraocular muscles is first conducted by examining 6 3 the alignment of the patient's eyes in the primary position (patient looking straight ahead). Shine a light into the patient's eyes and examine the corneal light reflection. If the light falls off center to a pupil, there is evidence of 5 2 ocular malalignment, termed 1 heterotropia of which there are four types: exotropia if the eye is laterally deviated, esotropia if the eye is medially deviated, hypertropia if the 7 4 eye is deviated upwards and hypotropia if the eye is deviated downwards. Figure 2-9: The arrows and numbers indicate the sequence of eye movements tested in the six cardinal fields of gaze. Next, examine ocular motility by asking the patient to follow the examiner's finger as it is moved through the six cardinal fields of gaze (Figure 2-9). During conjugate eye movements the yoke muscles are equally stimulated so a lag in eye movement is a subtle sign of extraocular muscle weakness. Complaints of double vision by the patient will not always manifest as visible extraocular muscle weakness. In those particular instances, the false (weak muscle) and true images (normal muscle) will be separated by the greatest distance in the direction of gaze, which tests the weak extraocular muscle. For example, if diplopia is greatest on right lateral gaze the weakness involves either the right lateral rectus (right eye) or left medial rectus (left eye). The false image, from the weaker muscle, is always farther away from the patient in the direction of gaze being tested and may be identified by asking the patient which image, the one closest or farthest from him, disappears upon covering one eye. The extraocular muscle contracting in the eye, which when covered results in the disappearance of the image farthest away from the patient, is the weak one. For example, if a patient has a weak right lateral rectus muscle when he looks to the right he will see two images laterally displaced. The image farthest to the right is due to the weak lateral rectus muscle. On covering the right eye he will say the images farther away disappeared thereby identifying the side of the weak muscle. Conversely when looking up and down the false image will be highest or lowest respectively. If using a pencil as a test object hold it in a position to maximize split of images, eg, vertical when testing horizontal movement, and horizontal when testing vertical eye movement. 18
  19. 19. Voluntary conjugate eye movements are controlled by Middle rectus muscle neurons in the frontal cortex, which descend into the anterior limb of the internal capsule and Posterior cross over to the contralateral frontal lobe. Lateral rectus Cortical muscle pons (Figure 2-10). In the center for pons, the axons synapse onto conjugate lateral gaze the parapontine reticular formation (PPRF) or lateral gaze center which, when Cranial erve IV activated, pull the eyes Cranial nerve III ipsilaterally. Thus, a stroke involving the left frontal lobe III nerve nucleus may manifest as right Medial longitudinal hemiparesis and eye deviation fasciculus away from the hemiparesis (MLF) (left). Alternately, a right pontine infarct may result in a Pontine center for left hemiparesis and eye conjugate deviation toward the side of lateral gaze paralysis (left). VI nerve nucleus Cranial Nerve V - Trigeminal Nerve The trigeminal nerve provides sensation to the face and mucous membranes of the nose, mouth, tongue and sinuses as well as motor innervation to the muscles of mastication, namely the Figure 2-10: The frontal gaze center innervates the contralateral parapontine reticular formation masseters, temporalis and medial and (PPRF). The PPRF, in turn, activates the lateral pterygoids. There are three nuclei ipsilateral VI nerve nucleus, which then of the trigeminal nerve, which span from communicates with the contralateral III nerve via the midbrain to the upper cervical cord. the medial longitudinal fasciculus (MLF). This The mesencephalic nucleus of V lies in sequence of innervations demonstrates how conjugate gaze laterally occurs. the midbrain and provides proprioceptive input from the muscles of mastication and periodontal membranes. The main sensory nucleus of V, which is located in the pons, mediates light touch over the face. Lastly, the spinal tract of V, which extends from the pons to the upper cervical cord, receives input on pain and temperature from the face and gives off branches to the spinal nucleus of V, second order neurons that cross the midline and ascend the brainstem to the contralateral ventral posteromedial nucleus of the thalamus. Thus, a thalamic infarct will result in contralateral hemianesthesia of the face and body. 19
  20. 20. The cell bodies of most sensory neurons innervating the face lie in the Gasserian ganglion and the rest are in the mesencephalic nucleus. There are three V1 sensory divisions of the trigeminal nerve, all with their origin in the Gasserian ganglion: the ophthalmic (V1), V2 maxillary (V2) and mandibular branches (V3). The ophthalmic division V3 travels along the upper part of the orbit, through the superior orbital fissure, to innervate the conjunctiva, cornea, upper lid, forehead, bridge of the nose and upper scalp to the vertex (Figure 2-11). V1 The maxillary branch leaves the skull through the foramen ovale, carrying sensory and motor neurons to the lower V2 jaw, pinna of the ear, anterior portion of the external auditory meatus, ipsilateral V3 tongue, lower teeth, and mucosal surface of the cheeks and floor of the mouth. The motor fibers innervate the temporalis, masseters and medial and Figure 2-11: The subdivisions of cranial nerve V lateral pterygoids. The mandibular innervation to the face are illustrated. branch exits the skull through the foramen rotundum, traverses the sphenomaxillary fossa, and passes through the inferior orbital fissure along the floor of the orbit and out the inferior orbital foramen. It innervates the cheek, lateral surface of the nose, upper teeth, jaw, and mucosal membranes of the nose and upper portion of the oropharynx. Pain, touch and temperature functions may be tested but the proprioceptive function of the muscles of mastication cannot be tested clinically. Light touch is assessed by using a cotton wisp and gently touching the areas innervated by the three divisions of the trigeminal nerve while the patient's eyes are closed. The patient is asked to say, "touch" whenever he feels the cotton. To test pain sensation, repeat the above maneuver with the sharp and round end of a safety pin, asking the patient to discriminate between "sharp" and "dull." Temperature sensation can be tested by filling two test tubes individually with cold and warm water, applying the test tubes to the three divisions of the trigeminal nerve and asking the patient to differentiate cold from warm. The corneal blink reflex tests the integrity of the ophthalmic division of V, which innervates the cornea and constitutes the sensory component of the reflex, and the facial nerve, which constitutes the motor arc of the reflex by innervating the orbicularis oculi and allowing closure of the eyelid. The sensory fibers of the cornea project to the ispilateral sensory nucleus of V and cross the midline in the pons to innervate the contralateral sensory nucleus of V, thereby allowing conjugate blinking reflexes in response to unilateral corneal stimulation. To 20
  21. 21. test the reflex, the end of a cotton Q-tip is twisted into a point. The patient is asked to look laterally and the cotton point applied gently onto the cornea from the direction contralateral to the gaze so as to avoid reflex defensive blinking. In patients who are comatose, the presence of a corneal blink reflex implies that the sensory nucleus of V and the facial nerve nucleus, both in the pons, are intact. In a patient complaining of hemianesthesia secondary to a thalamic infarct, the corneal blink reflex may be absent bilaterally with stimulation of the cornea contralateral to the lesion due to loss of sensation of the cornea (and resultant dysfunction of the sensory arc of the reflex). With Bell's palsy, the motor arc of the corneal blink reflex is unilaterally paralyzed. Thus, the corneal blink reflex, when tested ipsilaterally to the Bell's palsy, will be suppressed because of paralysis of the orbicularis oculi. However, the contralateral corneal blink reflex will be elicited as stimulation of the intact ophthalmic division of V ipsilateral to the Bell's palsy results in stimulation of the contralateral main sensory nucleus and resultant activation of the contralateral orbicularis oculi. The temporalis and masseter muscles are examined after asking the patient to clench down on his jaws. These muscles are palpated and attempts to open the mouth by pulling down on the lower mandible are made. The pterygoids are tested by asking the patient to open his mouth and then try to close it. Weakness of the pterygoids on mouth opening is indicated by deviation of the jaw towards the side of weakness as the pterygoids push the jaw in the contralateral direction. Cranial Nerve VII - Facial Nerve The facial nerve, cranial nerve VII, innervates all the muscles of facial expression, ie, the muscles around the eyes, mouth, nose, ears and neck. It also innervates the stapedius muscle in the ear, which dampens excessive movement of the ossicles when subject to loud sounds. The facial nerve subserves taste to the anterior two thirds of the tongue and sensation to the outer ear. The motor nucleus of VII sits in the pons while its axons loop around the nucleus of the abducens nerve and emerges from the pontomedullary junction. The facial nerve then courses through the internal auditory meatus where it is joined by the auditory nerve, and enters the facial canal of the temporal bone wherein lies the geniculate ganglion. Distal to the geniculate ganglion, the facial nerve gives off the chorda tympani, which supplies taste to the anterior two thirds of the tongue via the lingual nerve. The facial nerve exits the facial canal through the stylomastoid foramen, passing through the parotid gland, before innervating the muscles of the face, the posterior belly of the digastric, the stylohyoid, the buccinator, and the platysma. A branch of the facial nerve runs in the facial canal to innervate the stapedius muscle. The sensory component of the facial nerve consists of the lingual nerve, which innervates the anterior two thirds of the tongue and sensory branches, which in turn innervate the external auditory meatus. 21
  22. 22. The facial nerve also mediates parasympathetic innervation to the lacrimal, sublingual and submaxillary glands as well as the vessels of the mucous membranes of the palate, nasopharynx and nasal cavity. To test the facial nerve, first observe the patient's face for symmetry by paying close attention to the nasolabial folds, forehead Motor areas for face wrinkles, spontaneous smiling and blinking. Upper motor Then, ask the patient to show his teeth, raise his neuron lesion eyebrows, squeeze his eyes shut tightly and hold air in his cheeks. Facial weakness may be due to upper motor neuron or lower motor neuron facial palsy. Upper motor neuron palsy implies that there is a lesion contralateral to the side of facial Facial nerve nucleus weakness which is disrupting the face motor Corticobulbar fibers somewhere in its course from the primary tract motor cortex to the facial nucleus within the pons (ie, upper motor neuron to the facial nerve nucleus, Figure 2-12). A typical presentation of Facial nerve an upper motor neuron palsy is a patient with a right subcortical lacunar infarct resulting in flattened left nasolabial fold, decreased up Shaded area = Facial paralysis turning of the left corner of the mouth on smiling, and symmetric wrinkling of forehead bilaterally, in addition to a left hemiparesis. Figure 2-12: A right upper motor neuron VII Lower motor neuron palsy implies a lesion lesion due to a left subcortical stroke is involving the facial nerve at the nucleus in the illustrated. Motor area for face pons or along the course of the facial nerve ipsilateral to the side of facial weakness (Figure 2-13). Bell's palsy is a lower motor neuron facial palsy whereby the patient has unilateral Corticobulbar tract flattening of the nasolabial fold with inability to upturn the corner of the mouth upon smiling, inability to wrinkle his forehead, delayed or Facial nerve absent blinking due to weakness of the eyelid, nucleus and inability to hold air in the cheeks due to Facial nerve escape of air through the corner of the mouth which is weak. In addition, patients with Bell's palsy may complain of dry eye from disruption Lower motor neuron lesion of parasympathetic innervation of the lacrimal gland, hyperacusis or augmented hearing in the ear ipsilateral to the lesion from paralysis of the Shaded area=facial paralysis stapedius muscle and diminished taste from a lesion proximal to the lingual nerve, which Figure 2-13: A lower motor neuron VII lesion inhibits afferent signals concerning taste from due to a left peripheral facial nerve palsy is illustrated. 22
  23. 23. reaching the brainstem. Taste should be evaluated in any patient suspected of a lower motor neuron facial palsy by applying a wet cotton applicator dipped in sugar or salt on the patient's protruded tongue and asking the patient to identify the substance. (Do not allow the patient to stick his tongue back into his mouth, as unilateral taste can then not be accurately tested.) Be sure to look at the external auditory meatus where vesicles from herpes zoster may erupt from infection of the sensory branches of the peripheral facial nerve. In summary upper motor neuron facial weakness spares the frontalis (forehead muscle) so the patient can wrinkle his brow. Lower motor neuron facial weakness involves the forehead muscle and the patient can’t wrinkle the brow and in addition has unilateral hyperacusis and loss of taste. Facial diplegia, or bilateral lower motor neuron facial weakness, is seen in such conditions as Guillain-Barré syndrome or sarcoidosis. Cranial Nerve VIII - Acoustic Nerve The auditory nerve, cranial nerve VIII, is composed of two divisions, the cochlear nerve, which subserves hearing, and the vestibular nerve, which provides sense of balance. The cochlear nerve carries fibers from the spiral ganglion of the cochlea in the petrous portion of the temporal bone, through the internal auditory meatus, and to the cochlear nucleus, which sits in the lower pons, near the cerebellopontine angle. Each cochlear nucleus has connections to bilateral primary auditory cortices in the temporal lobes. Lesions of the cochlear nerve commonly present with ipsilateral decreased hearing and sometimes tinnitus. The vestibular nerve is composed of nerve fibers from the labyrinth of the inner ear, which converge on the vestibular ganglion within the internal auditory meatus and travel alongside the cochlear nerve to terminate on the vestibular nuclei within the lower pons. The vestibular nuclei have connections to: • the vestibulospinal tract of the spinal cord which allows reflex movements of the limbs in response to stimulation of the inner ear vestibular fibers • the medial longitudinal fasciculus which courses between the pons and midbrain and allows conjugate eye movements in relationship to head movements • the cerebellum that regulates muscle tone in relation to changes in posture. Acute vestibular nerve disease commonly presents with vertigo, nausea and ataxia. To test the auditory nerve, first check gross hearing in each ear by rubbing your fingers about 30 inches from the patient's ear, with the contralateral ear covered. If hearing in one ear is impaired, perform Rinne and Weber tests. Both tests employ the use of a 256 Hz tuning fork. In the Rinne test, the vibrating tuning fork is place over the mastoid process, behind the ear to test bone conduction (BC). Ask the patient to tell you when he no longer hears the vibrating fork, after which the tuning fork is placed in front of the ear and the patient asked if he can hear it (air conduction = AC). Next perform the Weber test by placing a vibrating tuning fork over the middle of the forehead and ask the patient if the sound is louder in one ear compared to the other. With conductive hearing loss, from middle ear disease or obstruction of the external auditory meatus with wax, BC will be greater than AC and Weber test will lateralize to the deaf ear. 23
  24. 24. However, with sensorineural hearing loss AC is better than BC and Weber test will lateralize to the good ear. Sensorineural hearing loss may result from lesions of: • the cochlea secondary to otosclerosis, Meniere's disease and noise- or drug-induced hearing loss • the auditory nerve from cerebellopontine angle tumors such as acoustic neuroma or trauma • the cochlear nerve in the pons from stroke or demyelinating disease. Vestibular nerve function can be tested with calorics or postural maneuvers. In patients suspected of vestibular nerve damage such as vestibular neuronitis or lesions of the inner ear, as seen with Meniere's disease, about 250 cc of cold water is injected into one ear with the patient lying down in a bed angled at 30 degrees at the head. The patient is asked to look straight ahead and the eyes observed for nystagmus. In the normal patient, nausea, nystagmus with the fast phase away from the stimulated ear, past pointing to the contralateral side, and falling to the injected side will ensue. With complete peripheral vestibular nerve lesions, no symptoms will be elicited. With partial peripheral vestibular nerve lesions, nystagmus will appear but at reduced amplitudes and velocity. In patients suspected of benign positional vertigo, presenting with vertigo or dizziness associated with changes in head position, the Hallpike maneuver should be attempted when not contraindicated due to severe cervical spine disease. To perform the Hallpike maneuver, the patient sits up in bed and then quickly lies back on command so that his head hangs over the edge of the bed. The head is tilted backward below the plane of his body and turned to one side by the examiner who holds the patient's head in his Figure 2-14: The Hallpike maneuver is hands. The patient is asked to look in the illustrated. The patient initially is seated direction that his head is turned (Figure 2-14). upright and asked to fall backwards, so that his Watch for nystagmus in the direction of gaze head is below the plane of his trunk. The and ask the patient if he feels vertigo. If no examiner then turns his head to one side and nystagmus is observed after 15 seconds, have asks the patient to look in the direction to which his head is turned. the patient sit up and repeat the maneuver turning the patients head and directing his gaze in the contralateral direction. The absence of nystagmus suggests normal vestibular nerve function. However, with peripheral vestibular nerve dysfunction, such as benign positional vertigo, the patient will complain of vertigo and rotary nystagmus will appear after a 1-5 second latency toward the direction in which the eyes are deviated. With repeated maneuvers, the nystagmus and sensation of vertigo will fatigue, and disappear, a sign of peripheral vestibular disease, in contrast to central vestibular disease from stroke or other intrinsic brainstem lesions, which manifests as nonfatigable nystagmus without delay in onset. 24
  25. 25. Cranial Nerves IX and X - The Glossopharyngeal and Vagus Nerves The glossopharyngeal nerve (cranial nerve IX) contains sensory and motor fibers as well as autonomic innervation to the parotid glands. It mediates taste to the posterior one third of the tongue and sensation to the pharynx and middle ear. These sensory fibers end in the nucleus solitarius of the medulla and connect with the superior salivary nucleus to allow the reflex of salivation. Nerves to the parotid gland originate in the inferior salivary nucleus, from which fibers travel through the middle ear to the lesser petrosal nerve and then on to the otic ganglion, which sends parasympathetic nerves to the parotid gland. The motor nucleus of the glossopharyngeal nerve originates in the medulla and innervates the stylopharyngeus muscle. Like the glossopharyngeal nerve, the vagus nerve (cranial nerve X) contains sensory, motor and autonomic fibers. It mediates sensation in the tympanic membrane, external auditory canal, and external ear (as do cranial nerves V, VII and IX) via the jugular ganglion and travels centrally into the spinal tract of the fifth nerve. Visceral sensations from the pharynx, larynx, bronchi, esophagus and the abdomen are carried by the vagus nerve to the tractus solitarius of the medulla. Motor innervation to the muscles of the soft palate, pharynx and larynx originates in the nucleus ambiguus of the medulla. Autonomic fibers arise from the dorsal motor nucleus of vagus and synapse at peripheral ganglia to provide parasympathetic innervation to the trachea, esophagus, heart, stomach, and small intestine. To test glossopharyngeal and vagus nerve function, examine the position of the uvula and its movement by asking the patient to say "Ah." the soft palate should elevate symmetrically and the uvula should remain in the midline. The gag reflex can be tested by touching the pharyngeal wall on each side with a cotton tip applicator. Normal Palsy of right palate This reflex relies on an intact sensory arc, as mediated by sensory fibers of the glossopharyngeal nerve to the soft palate, and an intact motor arc, as mediated by the motor fibers of the vagus nerve to the soft palate and pharynx. Figure 2-15: A normal soft palate is illustrated Deviation of the uvula to one side implies a lower on the left. On the right, a right palatal palsy from a lower motor neuron X nerve lesion hasmotor lesion of the vagus nerve contralateral to the side the uvula is deviating to (Figure 2-15). resulted in deviation of the uvula to the left. An upper motor neuron vagus nerve lesion will present with the uvula deviating toward the side of the lesion. The presence of a gag reflex does not necessarily imply that the patient can swallow without aspiration after a stroke. Impairment of swallowing is usually due to bilateral vagus nerve lesions. On the other hand, the absence of a gag reflex does not imply inability to swallow. Dysarthria and dysphagia, when associated with emotional lability, is suggestive of pseudobulbar palsy, a condition characterized by weakness of muscles innervated by the medulla (palate, pharynx, and larynx) because of interruption of corticobulbar fibers, as may be seen with multiple bilateral strokes. Hoarseness may be seen with tumors encroaching on the recurrent laryngeal nerve, a branch of the vagus nerve. This results in unilateral vocal cord paralysis. 25
  26. 26. Cranial Nerve XI - The Accessory Nerve The spinal accessory nerve, cranial nerve XI, innervates the sternocleidomastoid and trapezius muscles. It is composed of spinal fibers originating in the anterior horn cells of the first five cervical cord segments and an accessory component, which travels briefly alongside the vagus nerve. The dorsal and ventral roots from the first five cervical cord segments unite to enter the skull through the foramen magnum and exit through the jugular foramen. To test the strength of the sternocleidomastoids ask the patient to turn his head against your hand, which is placed over the mandible. Repeat this maneuver with your hand on the contralateral mandible. Observe the sternocleidomastoid, which is contralateral to the side to which the patient is turning his head. Weakness detected when the patient turns his head to the left implies that the right sternocleidomastoid is weak. To test the trapezius, ask the patient to shrug his shoulders and press down on the shoulders. Trapezius weakness is manifest as difficulty in elevating the shoulders. When the sternocleidomastoid and trapezius are weak on the same side, an ipsilateral peripheral accessory palsy, involving cranial nerves X and XI, is implied as may be seen with a jugular foramen tumor, ie, glomus tumor or neurofibroma. Because the cerebral hemisphere innervates the contralateral trapezius and ipsilateral sternocleidomastoid, a large right hemisphere stroke will result in weakness of the left trapezius and right sternocleidomastoid. Bilateral wasting of the sternocleidomastoid may be seen with myopathic conditions such as myotonic dystrophy and polymyositis or motor neuron disease, the latter usually associated with fasciculations. Cranial Nerve XII - Hypoglossal Nerve The hypoglossal nerve, cranial nerve XII, is a pure motor nerve, innervating the muscles of the tongue. It obtains supranuclear innervation from the contralateral motor cortex. The nucleus of the hypoglossal nerve sits in the medial aspect of the medulla, near the floor of the fourth ventricle and exits the skull through the hypoglossal canal. To test the function of the hypoglossal nerve, ask the patient to protrude his tongue and wiggle it from side to side. Look for deviation and atrophy. To check for subtle weakness, ask the patient to push his tongue against the wall of his cheek while you push against it through the outer cheek. Like the forehead, each side of the tongue receives upper motor neuron innervation from bilateral motor cortices. Each half of the tongue pushes the tongue in the contralateral direction, ie, left half of tongue pushes to the right (Figure 2-16). Thus, if the tongue deviates to one side, it is pointing to the side that is weak. Tongue deviation, combined with wasting on the side to which it is deviated, implies a unilateral, lower motor neuron, hypoglossal nucleus or nerve lesion as may be seen with syringobulbia (a degenerative cavity within the brainstem), with basilar meningitis, or foramen magnum tumor. If the tongue deviates and is of normal bulk, one should consider an upper motor neuron lesion, such as stroke or tumor in the hemisphere contralateral to the side of deviation, and look for associated hemiparesis on the side of tongue deviation. 26
  27. 27. Motor Cortex Hypoglossal nucleus Medulla Oblongata Hypoglossal nerve Mandible Genioglossus muscles Tongue Figure 2-16: The opposing action of the two halves of the tongue is illustrated. Note that the tongue, like most muscles in the body derives The Mental Status Examination As previously noted, the neurologic exam begins with an assessment of the patient's mental status. In most cases, a large part of the mental status exam may be ascertained from observation of the patient as history is provided. A more detailed mental status exam can be divided into the following components: • Level of consciousness • Intellectual performance • Thought processes • Psychomotor function or Praxis • Psychosensory function or Gnosia • Language Level of Consciousness Level of consciousness implies awareness of surroundings. If one is examining a patient who is somnolent or comatose, it is important to determine the degree of stimulation that is required to alert the patient, ie, voice, light touch, sternal rub. Consciousness is dependent on the normal functioning of the reticular activating system, which originates in the pons and projects to the cortex of bilateral hemispheres via the thalamus. The reticular activating system activates 27
  28. 28. the cortex when one awakens and inhibits the cortex when in sleep. The hypothalamus is also important in maintaining level of alertness. Structural damage to the reticular activating system, thalamus or hypothalamus from stroke or hemorrhage may impair consciousness to the same degree as large destructive lesions of bilateral cerebral hemispheres. During brain herniation, compression of the reticular activating system may produce profound coma. Similarly, metabolic abnormalities such as hyperglycemia or drugs may produce coma by impairing neuronal function diffusely within the brain. Evaluation of a comatose patient requires examination of four systems: the motor system, pupils and fundi, ocular movements, and respiratory pattern. The main task is to determine whether the etiology of coma is due to metabolic-toxic causes or structural damage. Metabolic-toxic causes should have nonfocal exams while structural injury to the cerebral hemispheres or brainstem will result in focal neurologic signs. Bilateral cortical dysfunction or disease of the reticular activating system in the brainstem is necessary to produce coma. Motor system. Look for lateralizing signs such as asymmetry of movement either spontaneously or to painful stimulation and asymmetric reflexes. Describe any spontan- eous posturing. Decorticate posturing is characterized by tonic flexion of the arms and extension of the legs and implies a lesion at the level of the midbrain (Figure 2-17). Decerebrate posturing is manifest as tonic adduction and extension of the arms and legs and suggests a lesion at the level of the pons. In general, metabolic disturbances do not result in posturing, although anoxia and hypoglycemia can produce posturing. A mass lesion, which previously produced lateralized signs, may result in decorticate or decerebrate Figure 2-17: Decorticate posturing is posturing when it expands and compresses the illustrated on the left. Decerebrate posturing brainstem. is on the right. Pupils and fundi. Papilledema suggests increased intracranial pressure from a mass lesion or cerebral edema. Check the pupils for size and reactivity to direct light. With metabolic disease the pupils tend to be small and sluggishly reactive. Asymmetry of pupil size and reactivity, particularly the unilateral dilated pupil, suggests mass effect with herniation. Figure 2-18: The Doll's eye maneuver is Thalamic lesions usually produce 2 mm illustrated. With an intact brainstem, the eyes non-reactive pupils, 4-5 mm fixed pupils conjugately deviate in the opposite direction of suggest a midbrain lesion, and pinpoint head turning. 28

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