|
THE NEUROLOGIC EXAMINATION Raymond A. Martin, MD Section One The Neurologic HistoryAs 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 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 often will 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 not only to 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 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 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:
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 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, 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:
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 overall 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, enabling 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:
The family history occasionally will 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 than the general population. Such is the case in multiple sclerosis and some autoimmune diseases. Care must taken to not 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. Recognition of such interactions provides a quick and inexpensive cure, and is gratifying to both physician and patient. The Neurologic ExaminationThe neurologic 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 neurologic 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 patient's 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. The CD includes video segments that demonstrate how to correctly perform and interpret the neurologic exam. Individual performance of the examination can be refined by repeated performance and evaluation by your clinical neurology faculty person. Inspection and ObservationFrom the time the physician greets the patient he or she can 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 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 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 obtained 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 ExaminationIf 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. System IntegrationWhen 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. 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. The development of erector tone, which has provided the supporting framework, and initiation of voluntary movements are, still rudimentary and uncoordinated. What is needed is a system, which monitors motor activity and then smoothes out irregularities in the desired action. The cerebellum occupies a large portion of the posterior fossa, and is in a unique position to monitor impulses entering and leaving the brain. Its foreboding anatomical structure, with its many lobes and folia, often discourages students from 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 the pilot has entered. Any discrepancy between the desired and actual readings will be corrected by output from the computer. 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 these systems that produces 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 arm’s position can only be determined by the patient 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 ReviewCranial 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.
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 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 Problems 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. The patient should wear corrective lens, if available, 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. If the patient fails this test, 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. 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. 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 Problems)
The trochlear nerve (cranial verve IV) nucleus lies in the medial midbrain, at the level of the inferior colliculi, and wraps around the midbrain dorsally, alongside the cerebral peduncles, and courses between the posterior cerebral and superior cerebellar arteries (Figure 2-7). 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. 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). 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 masseters, temporalis and medial and lateral pterygoids. There are three nuclei of the trigeminal nerve, which span from the midbrain to the upper cervical cord. The mesencephalic nucleus of V lies in 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. 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 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 after which an attempt is made 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. |
The nuclei of the somatic,
(homologous to spinal nerves), cranial nerves (III, IV, VI, and XII)
are located just off the midline of the brainstem (Figure 2-1).
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.
The
oculomotor (III), trochlear (IV), and abducens (VI),
nerves together innervate the extraocular muscles (Figure 2-4).
The primary action of the medial rectus is adduction and that
of the lateral rectus is abduction. The superior rectus
and inferior oblique primarily elevate the eye while the inferior
rectus and superior oblique primarily depress the eye.
