1 Bedside Neurologic Exam
Abstract
The bedside neurologic exam is the most sensitive test to determine the condition of the patient in the neurosurgical intensive care unit. It should be conducted frequently and consistently, whether the person is in a coma or not. Each part of the neurologic exam, from higher mentation to the cranial nerve exam and motor, sensory, and reflex exam, pinpoints the astute clinician to a specific pathology and anatomy.
Case Presentation
A 46-year-old woman presented to the emergency room with a spontaneous unilateral third nerve palsy manifested as a large, nonreactive pupil and minimal or no eye movement abnormalities. The patient had had a severe, and uncharacteristic, headache 2 days earlier, and she came to the emergency room only because of blurred vision. Other than the eye finding, the patient was awake and alert and in no acute distress, with a normal neurologic exam.
See end of chapter for Case Management.
1.1 Introduction
Patients admitted to the neurosurgical intensive care unit (NICU) are among the most critically ill and unstable. Many are admitted for traumatic brain injury, aneurysmal subarachnoid hemorrhage, spinal cord injury, postoperative craniotomies, stroke, and much more. With the advent of improved laboratory data and advanced imaging techniques, the physical examination has become less emphasized in training. While imaging and laboratory data augment our clinical decision making, the decision to order these tests and their interpretation should be influenced by the patient’s physical exam. A detailed physical examination, with attention to all of the subtleties, is necessary to guide the treatment of a patient and the decision to order tests. Knowledge of the physical examination and its terminology also allows for more effective communication among health care workers whose clinical decision making will rely on the information passed down to them.
1.2 The Power of Observation
In the NICU, as elsewhere, the art of medicine should never be underestimated. While in many NICU patients, the neurologic exam is rendered more difficult by sedation, intubation, and paralytics, leaving the neurosurgeon and his or her team to rely on invasive monitoring data, serial neuroimaging, and intermittently withholding sedation to assess the patient, observation is still an important component of the patient’s examination. For example, the obtunded or comatose patient breathing rhythmically in a specific pattern offers important lesion-localizing clues to the astute neurosurgeon (► Table 1.1). Observation of asymmetric spontaneous movements of the extremities, or change in their frequency, can be another clue to evolving brain or spinal cord lesions.
In the smaller number of awake patients in the NICU, the neurosurgeon has greater leeway to observe and converse with the patient. In these patients, observing whether they show any subtle localizing signs may betray early and enlarging focal lesions in the brain. For example, the patient who complains of a focal headache and who holds his hand over his head in the same area repeatedly, and on request is able to point to a specific area of his head as the site of most discomfort, may be helping the neurosurgeon with localization of an existent or developing lesion (tumor, hematoma, abscess, edema, etc.). This ability of the awake patient to localize the lesion for the neurosurgeon by effectively putting a finger on where it hurts the most, or showing the “Siddiqi sign,” constitutes an observation and communication component of the neurologic exam with significant interobserver reliability (in patients without the confounding variables of recent soft tissue bruising or incision on the head). The value of focality of the Siddiqi sign is lost when the patient complains of a global headache, or pain “all over.” A conscious attempt should be made in the NICU to not dismiss the initial observation of the patient in favor of exhaustive analyses of numerous data sets generated by an ever-increasing number of invasive monitoring techniques.
1.3 Coma
1.3.1 Glasgow Coma Scale
First published in 1974 by Graham Teasdale and Bryan Jennett, the Glasgow Coma Scale (GCS) has become a universally used tool for measuring a patient’s overall state of alertness. Its score often guides medical decision making in neurointensive care. Despite its seeming simplicity there exists significant interrater variability. In an attempt to decrease this variability, a discussion will follow detailing the subtleties of this scale.
The GCS is calculated by adding up the points from each category, with motor receiving 6 points, verbal receiving 5, and eyes receiving 4. During an examination, the best scores for all three categories will be added together (► Table 1.2, ► Table 1.3). Patients are considered to be in a coma with a GCS of 8 or less.
1.3.2 Motor Score
The motor score is measured out of a total of 6 points. A score of 6 points is given when a patient follows commands. Standard commands include asking patients to give a thumbs up, show two fingers, stick out their tongue, or wiggle their toes. Caution should be given when asking a patient to squeeze the examiner’s hand during this part of the exam because this can often represent a frontal release sign in patients with lesions of the frontal lobe and may not indicate true command following. Because of this, it is not recommended to use hand squeeze as a command. A score of 5 is given for localization. This can be interpreted as any purposeful movement performed by the patient, such as a limb crossing the midline to reach for painful stimuli or an endotracheal tube, to scratch an itch, or to fix the blanket. A score of 4 is given for withdrawal from painful stimuli. This can be given for a patient who tries to move away from a painful stimulus or who grimaces with pain. It is important not to confuse withdrawal with a spinal reflex. Withdrawal is held, whereas spinal reflexes return to a normal position while the stimulus is still being applied. The best location to perform a painful stimulus to determine withdrawal versus reflex is on the inner aspect of the upper arm. In withdrawal, the patient will move the arm away from the torso, or abduct the arm. In a reflex response, the patient will bring the arm closer to the torso, or adduct the arm. A score of 3 is given for abnormal flexion in response to painful stimuli. This is called the decorticate response and can include flexion at the biceps, wrist, or thighs or dorsiflexion without localizing to the stimuli. Decorticate posturing localizes the lesion in the brain to be above the red nucleus. Special attention should be given to the triple flexion response, which is often misinterpreted. It occurs in response to painful stimuli of the toes when a patient will dorsiflex the foot, flex at the knee, and flex at the thigh and is a form of decorticate posturing. A score of 2 is given for extensor posturing, also known as decerebrate posturing. In decerebrate posturing, there is disruption between the superior colliculi or the decussation of the rubrospinal pathway and the rostral portion of the vestibular nuclei. Decerebrate posturing consists of extension of the upper or lower extremities in response to painful stimuli. A score of 1 is given for no motor response to stimulation.
1.3.3 Verbal Score
The verbal score is measured with a total of 5 points. A score of 5 is given to patients who are oriented to name, where they are at, the date or year, and the reason they are in the hospital. Inability to answer these questions reliably constitutes a disoriented patient. A score of 4 is given when a patient is unable to answer all questions regarding orientation. However, the patient must be able to attempt to answer questions with a response that is appropriate to the question being asked. A score of 3 is given when a patient’s response to a question is inappropriate to what was asked. A score of 2 is given when a patient’s verbal responses are inaudible. This is constituted by mumbling, grunts, or other produced sounds. A score of 1 is given when a patient is nonverbal despite stimulation or questioning. All intubated patients receive a score of 1. However, to signify that their poor GCS score is a reflection of intubation and not neurologic injury a T will be placed at the end of the score to signify the patient cannot receive those points.
1.3.4 Eye Score
The eye score is measured with a total of 4 points. A score of 4 is given to patients who can open their eyes spontaneously or who, after being awakened, continue to keep their eyes open. It is important that patient not be given a score of 4 if the patient’s eyes are stuck open. A score of 3 is given to patients who are able to open their eyes to voice or their name. A score of 2 is given to patients who are able to open their eyes only when stimulated with pain. A score of 1 is given to patients who do not open their eyes despite the level of stimulation given.
1.4 Cranial Nerves
The neurosurgical patient’s cranial nerves may be examined quickly at bedside. Cranial nerve examination is important in identifying and localizing lesions. Multiple pathologies result in cranial neuropathies, including stroke, Chiari malformations with or without syringobulbia, fungal meningitis, posterior fossa surgery, cerebellopontine angle surgery, microvascular decompression of the trigeminal nerve, glomus jugulare tumors, and leptomeningeal carcinomatosis.
1.4.1 Cranial Nerve I: Olfactory Nerve
Olfaction is tested by supplying the patient with different odors and asking the patient to identify them. Each nostril should be tested individually. Allergic rhinitis is the most common cause of a loss or a decrease in smelling capacity. The most common neurologic cause results from significant head trauma that causes shearing of the olfactory bulb/fibers off the cribriform plate. Other causes include congenital diseases, such as Kallman syndrome, or tumors causing local compression.
1.4.2 Cranial Nerve II: Optic Nerve
Pupillary Light Reflex
The pupillary light reflex is perhaps the single most important neurologic reflex and the quickest way to get a neurosurgeon’s attention. The reflex arc involved in the pupillary light reflex starts as light enters the retina and is transmitted along the optic nerve and synapses in the pretectal nucleus. Fibers from the pretectal nucleus then travel bilaterally to each Edinger–Westphal nucleus. From there, preganglionic parasympathetic fibers arise and travel with the oculomotor nerve and synapse in the ciliary ganglion and then travel in the short ciliary nerve to the sphincter muscle of the iris, leading to constriction of the pupil.
Afferent Pupillary Defect: Marcus Gunn Pupil
Afferent pupillary defect is caused by damage to the optic nerve. It can be identified by using the swinging light test. When light is directed toward the functional optic nerve the contralateral pupil will constrict normally. However, when the light is switched to the affected optic nerve, the pupil will dilate due to the pretectal nucleus receiving less light input from the damaged optic nerve.
Anisocoria
Differing pupillary diameters is termed anisocoria and is defined as a difference in pupillary size of at least 0.4 mm. 2 Anisocoria is present in 20% of the population and is generally not pathological until the difference is greater than 1 mm. 3
Papilledema
Papilledema can be best viewed by funduscopic exam with pupillary dilation and is graded from 0 to 5 using the Frisen scale. Papilledema is characterized by haloing around the optic disc, elevation of the borders of the optic disc, and, at more severe stages, obscuration of the vessels at the optic disc. In studies it has been found to have a sensitivity of 100% and specificity of 98% for elevated intracranial pressure. However, this finding is age dependent, and in patients younger than 8 years old it indicates increased intracranial pressure in only 22% of patients. 4
Visual Fields
Checking the visual fields is part and parcel of the cranial nerve II examination (see the discussion later in this chapter on this topic).
1.4.3 Cranial Nerve III: Oculomotor Nerve
The oculomotor nerve originates in the midbrain just anterior to the periaqueductal gray matter. The oculomotor nerve is responsible for innervation of the levator palpebrae superioris, medial rectus, inferior rectus, superior rectus, inferior oblique, and iris sphincter muscles. Loss of function of the oculomotor nerve can lead to pupillary dilation and an eye that deviates downward and laterally.
Pupil-Sparing Third Nerve Palsy
The nerve fibers that innervate the extraocular muscles travel on the periphery of the nerve and are subject to damage by microvascular pathology, such as hypertension, diabetes, or dyslipidemia. These palsies are typically incomplete and temporary, usually resolving within 3 months. 5
Non-Pupil-Sparing Third Nerve Palsy
Multiple etiologies exist that result in unilateral dilation of a pupil, ranging from benign to life threatening and requiring emergent intervention. Although it is more typical of a neurocritical care patient to have malignant underlying pathologies, knowledge of the other causes is important to keep in mind when composing a differential diagnosis.
Mass Lesion
A mass lesion that results in uncal herniation and compression of the oculomotor nerve will lead first to a dilated pupil, followed by a nonreactive pupil. Causes include intracerebral hemorrhage, cytotoxic edema from a stroke, subdural or epidural hematomas, and tumor. A special circumstance involving unilateral pupil dilation includes a posterior communicating artery aneurysm exerting local pressure on the oculomotor nerve.
Traumatic Mydriasis
Traumatic mydriasis arises from traumatic injury to the globe and results from either tearing of the iris sphincter muscle fibers or its nerve fibers innervating it.
Horner’s Syndrome
Horner’s syndrome consists of unilateral miosis, ptosis, enophthalmos, and anhidrosis. This is caused by a disruption at any point in the sympathetic innervation to the eye. Ptosis and enophthalmos are due to paralysis of Müller’s muscles of the tarsal plates. Anhidrosis is due to sympathetic chain disruption in the carotid sheath. 6 Etiologies are numerous, but include Pancoast’s tumor, lower cervical cord lesion, carotid injury/dissection, posterior inferior cerebellar artery occlusion (as a part of Wallenberg’s syndrome), syringobulbia, and others. 7
Adie’s Pupil
Adie’s pupil presents as a dilated pupil that is slow to react with light, but with almost normal response to accommodation. Adie’s tonic pupil is thought to be caused by either a viral or a bacterial infection that leads to damage of the ciliary ganglion. Because patients with an Adie’s pupil have damage only to the ciliary ganglion, the pupil will respond to parasympathomimetics, such as pilocarpine.
1.4.4 Cranial Nerve IV: The Trochlear Nerve
The trochlear nerve (CN IV) supplies the superior oblique muscle of the eyeball. It completely decussates in the superior medullary velum at the level of the inferior colliculus before exiting the brainstem posteriorly. Patients with trochlear nerve palsy will complain of double vision with downward gaze. On exam, the patient’s pathological eye will be slightly more superior on downward medial gaze. Asking the patient to tilt the head to the contralateral side will improve the diplopia, whereas tilting the head to the ipsilateral side will worsen the diplopia. 8
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